Regulation of ontogenesis differentiation. Individual development (ontogenesis), periodization of ontogenesis
Department of Biology with Ecology and Coursepharmacognosy
Lecture
PRINCIPLES AND
MECHANISMS
REGULATIONS
ONTOGENESIS
Associate Professor DEGERMENDZHI N.N. Questions:
Levels of regulation
ontogeny
Determination of ontogeny,
embryonic induction
Gene and cellular mechanisms
regulation of ontogenesis
Levels of regulation of ontogenesis
Ontogeny is a setinterrelated and chronologically
deterministic events in the process
the body's life
cycle. At every stage of the individual
development is being implemented
hereditary information in close
interaction with the environment
Levels of regulation of ontogenesis
GeneticCellular
Organismic
genes,
regulating
course of ontogeny
Cellular
mechanisms
Neurohumoral
regulation
Levels of regulation of ontogenesis
pre-embryonic periodGene amplification-
making copies of genes
that leads to
emergence
repeating sections
DNA and volume expansion
genome.
Levels of regulation of ontogenesis
pre-embryonic periodOoplasmic segregation -
specific organization of the egg,
in which in the eggs before
fertilization occurs
movement of the cytoplasm. And in
different parts of the cytoplasm
various: on animal pole
an increase in RNA concentration
glycogen, along the equator -
ascorbic acid
Formation and accumulation in the cytoplasm
nutrients
Levels of regulation of ontogenesis
Embryonic periodDetermination is the occurrence
qualitative differences between parts
developing organism, predetermines
further fate these parts before
there are morphological differences between
them
Potencies - the maximum possibilities of the elements
germ. Normally, one of them
determination
Embryonic periodTotipotency -
equally hereditary
ness. germ
has broad
potency
Labile determination
the embryo has blastomeres
behave during transplantation
according to the place
transplants
determination
Labile determinationExperiments by Tarkovsky and Mintz
determination
Stable determination -rudiments of the embryo
determined and give rise
authorities, regardless of location.
transplants
determination
Stable determinationdetermination
Sewer developmentEmbryonic induction
This interaction of partsdeveloping embryo, while
one site of the embryo affects
the fate of another
Spemann experience EMBRYONAL
INDUCTION
is the effect of a group of embryonic cells
for differentiation near
located cells
is the influence of some rudiments on
others with allocated
cells of substances-regulators G. Driesch (1891) - phenomenon
embryonic regulation
Ontogeny is a holistic
process, NOT simple
single digit sum
causal
links! Chordomesodermal
germ - primary
embryonic
organizer EMBRYONAL
INDUCTION due to
SPECIFIC
INDUCTORS
ON AND OFF
GENE BLOCKS IN NEARBY
LOCATED CELLS
Embryonic period
Thus, the mainmethods of embryonic
development
are: differentiation,
determination, and all this
takes place in conjunction with all
parts of the embryo, i.e. integration
In 1985, the genes that control the course of
ontogeny
Chronogens - control
Manage all processes
cleavage to gastrulation
time of occurrence of events.
The earliest of the chronogens
genes with maternal effect.
Produced in the ovum
gene amplification.
As a result, there appears
a large number of copies
genes. Some of them
transcribed and created
a lot of mRNA
which starts
broadcast immediately after
fertilization.
Genes with maternal effect
early genes embryonic development DrosophilaMessenger RNA distribution
Genes that regulate the course of ontogeny
At the stage of gastrulation, genes begin to actspatial organization are their own
organism's genes.
They are divided into genes:
Segmentation - responsible for the formation of segments.
Act up to the stage of late gastrula.
Compartmentalizations are responsible for
segment differentiation and education
compartments
Homeotic genes - provide normal
the formation of structures and their location in the right place.
Segmentation genes
Segmentation genes
Segmentation genes
Mutations in segmentation genes in DrosophilaNobel
1995 laureates:
E. Lewis; TO.
Nüsslein-Wolhard;
E. Vishuas - for
opening
genetic control
early
embryonic
development
Homeotic genes (HOM)
Supports organ developmenttissue in a specific location
In the structure of homeotic genes,
regions that have a similar nucleotide
sequence is the so-called
HOMEOBOXES
Homeoboxes encode the sequence
amino acids called homeodomain
Homeotic genes (HOM)
HomeodomainMouse
Frog
ANTENNAPEDIA
FUSHITARASU
ULTRABITHORAX
Tri, glu, arg, gli, ile, liz, ile, tri, fen, gli, asn, arg, arg, meth, liz, tyr, liz, liz, asp, glu
Tri,glu,arg,gli,ile,liz,ile,tri,phen,gli,asn,arg,arg,meth,liz,tri,liz,liz,glu,asp
Ser, glu, arg, gli, ile, liz, ile, tri, fen, gli, asn, arg, arg, meth, lys, ser, liz, liz, asp, arg
Tri, glu, arg, gli, ile, liz, ile, tri, fen, glu, asn, arg, arg, met, liz, ley, liz, liz, glu, ile
The homeodomain is more similar,
than homeobox
Homeobox is recognized by homeodomain
Homeotic genes (HOM)
Mutations in homeotic genes
Mutations in homeotic genes
Silkworm larvaMutations in homeotic genes
Homeotic genes in humans
- Genes of the PAX group (play an important rolein development nervous system).
- MSX genes (when mutated, premature overgrowth of sutures in
skull).
- EMX (with mutation - a cleft brain in
one or both hemispheres).
- SOX (role in the primary determination of sex
and etc.
determination
Genetic sex determinationZinc finger regulation
Diagram of a set of gene switches
morphogenB
E
G
A
C
morphogen
F
H
D
Kaufman, 1972
Homology of genes controlling early development
Levels of regulation of ontogenesis
Gene mechanismsCellular mechanisms
With maternal effect
Proliferation
segmentation
Differentiation
Compartmentalization
homeotic
Sorting
moving
Adhesion
Proliferation
Differentiation
Sorting
moving
Adhesion
apoptosis
Cellular mechanisms of regulation
Splitting upGenes - with maternal
effect
Cellular mechanisms of proliferation
gastrulation
Genes - segmentation
Cellular mechanisms of proliferation,
moving,
sorting
Cellular mechanisms of regulation
Genes: compartmentalizationsCellular Mechanisms:
Proliferation
Differentiation
Sorting
moving
Adhesion
Cellular mechanisms of regulation
In 1987 they were discovered by Edelmanseveral groups of proteins that determine
cell interaction in the embryo.
CAM - determine the interaction of cells in
embryo. Found on the surface of cells
interact with the same molecules
neighboring cells. Participate in the formation
tight and gap contacts.
SAM- determine the relationship of cells with
substrate
CJM - Cell Contact Molecules
Cellular mechanisms of regulation
Histo- and organogenesisGenes: homeotic
Cellular Mechanisms:
Proliferation
Differentiation
Sorting
moving
Adhesion
apoptosis
Epigenetic control
Epigenetic control of strokeontogeny is carried out
the following mechanisms:
Nucleosomal organization
DNA - protein
interactions
Alternative splicing
DNA methylation
Imrinting
Epigenetic control
Morphogenesis determinedgenetically, but
thanks to
epigenetic
cell interdependence and
their complexes.
Unregulated distortion
morphogenesis lead to
developmental anomalies
(Teratoma). Birth defects in populations
human (1-2%) are divided into
-
aplasia, agenesis
atresia
hypoplasia
hyperplasia
heterotopias
cleft
persistence
stenoses
gametopathies
embryopathies Development of the organism
determine:
-genetic factors
-interaction of parts
germ
- external factors
environments
Ontogeny is the name given to the individual development of an individual (E. Haeckel, 1866).
The main question of biology: how many different types of cells arise from one egg! And from one genotype - several thousand different phenotypes? In mammals, more than 1000 different types of cells are formed from one zygote.
Development- a continuous process of change, usually accompanied by an increase in weight, size, change in function. Almost always involves growth, which may be due to an increase in cell size or number. The weight of the egg is 1*10x(-5)g, the spermatozoon is 5x10(-9)g. In a newborn - 3200 g.
One increase in mass is impossible to ensure the formation of signs characteristic of the body.
Stages of development.
Cell determination
Cell differentiation
Formation of a new form, morphogenesis.
Violation of any stage can lead to malformations and deformities.
determination- limitation, definition - progressive limitation of the ontogenetic possibilities of embryonic cells. This means that at the stage of determination, cells differ in their morphological features from embryonic cells, but the functions are still performed by embryonic cells. Those. determined cells are not yet capable of performing special functions. In mammals, determined cells appear at the eight blastomere stage. Chimeric, allopheric organisms. As an object of study of the mouse. The embryos of mice at the stage of 8 blastomeres are extracted with the help of the enzyme pronase and broken into separate blastomeres, blastomeres from different animals are mixed in a test tube, and then sewn into the uterus. The result is normal animals, but the color of the parts is different, because. the original forms were different colors. If such an operation is carried out at later stages of embryogenesis, the death of animals, which proves the determination of cells at this stage.
The process of determination is under genetic control. This is a stepwise, multi-stage process that has not yet been well studied. Apparently, the basis of determination is the activation of certain genes and the synthesis of various mRNAs and, possibly, proteins.
Determination can be violated, which leads to mutations. A classic example is the development in mutants of Drosophila instead of antennae of the mouth apparatus - limbs. Formation of limbs in uncharacteristic places.
Differentiation. Deterministic cells gradually enter the path of development (non-specialized embryonic cells turn into differentiated cells of the body). Differentiated cells, unlike deterministic ones, have special morphological and functional organizations. Strictly defined biochemical reactions and the synthesis of special proteins occur in them.
Liver cells - albumin.
The epidermal cells of the skin are keratin.
Muscles - actin, myosin, myelin, myoglobin.
Mammary glands - casein, lactoglobulin.
The thyroid gland is thyroglobulin.
The mucous membrane of the stomach is pepsin.
Pancreas - trypsin, chymotrypsin, amylase, insulin.
As a rule, differentiation occurs in the embryonic period and leads to irreversible changes in the pluripotent cells of the embryo.
The synthesis of special proteins begins at very early stages of development. Regarding the stage of crushing: blastomeres differ from each other in the cytoplasm. The cytoplasm of different blastomeres contains different substances. The nuclei of all blastomeres carry the same genetic information, because have the same amount of DNA and the same order of base pairs. The question of specialization has not yet been answered.
1939 Thomas Morgan hypothesized: "Cell differentiation is associated with the activity of different genes in the same genome." Currently, it is known that about 10% of genes work in differentiated cells, while the rest are inactive. Because of this, specific genes function in different types of specialized cells. Special experiments on the transplantation of nuclei from tadpole intestinal cells into a nuclear-free ovum have shown that genetic material is preserved in differentiated cells and the cessation of the functioning of certain genes is reversible. The nucleus was removed from the frog egg, the nucleus was taken from the intestinal cell of the tadpole. Development did not occur, sometimes embryogenesis occurred normally. The structure of an adult frog was completely determined by the nucleus.
The functioning of genes during the development of a multicellular organism is influenced by complex and continuous interactions between the nucleus and cytoplasm and intercellular interactions.
Differentiation is regulated at the level of transcription and at the level of translation.
Levels of regulation of cell differentiation .
at the level of transcription.
The participation of proteins - histones, which form a complex with DNA.
DNA regions covered with histone are incapable of transcription, while regions without histone proteins are transcribed. Thus, proteins are involved in the control of readable genes.
Hypothesis of differential activity of genes: “The assumption that in different genes of differentiated cells different DNA regions are repressed (closed for reading) and therefore different types of mRNA are synthesized.”
at the broadcast level.
It is known that during the development of the organism, the laying of organs occurs simultaneously.
heterochrony- a pattern that implies non-simultaneous development.
The process of cell differentiation is associated with the depression of certain cells. In the process of gastrulation, gene depression depends on the influence of unequal cytoplasm in embryonic cells. In organogenesis, intercellular interactions are of primary importance. Later, the regulation of gene activity is carried out through hormonal connections.
In the embryo, different regions influence each other.
If the newt embryo is divided in half at the blastula stage, then a normal newt develops from each half. If the same is done after the beginning of gastrulation, a normal organism is formed from one half, and the other half degenerates. A normal embryo is formed from the half where the dorsal lip of the blastopore was located. This proves that
cells of the dorsal lip have the ability to organize the development program of the embryo
no other cells are capable of doing this.
Morphogenesis- formation of a form, the adoption of a new form. Form formation most often occurs as a result of differential growth. Morphogenesis is based on the organized movement of cells and groups of cells. As a result of the movement, the cells enter a new environment. The process takes place in time and space.
Differentiated cells cannot exist independently; they cooperate with other cells, forming tissues and organs. In the formation of organs, the behavior of cells, which depends on cell membranes, is important.
The cell membrane plays a role in the implementation
cell contacts
adhesion
Aggregations.
Intercellular contact– mobile cells come into contact and diverge without losing mobility.
Adhesion- cells that come into contact long time pressed against each other.
Aggregation - special connective tissue or vascular structures appear between adherent cells, i.e. the formation of simple cellular aggregates of tissues or organs.
For the formation of an organ, the presence in a certain amount of all cells with a common organ property is necessary.
Experiment with disaggregated amphibian cells. 3 tissues were taken - the epidermis of the neural plate, the area of the neural folds, the cells of the intestinal ectoderm. Cells are randomly disaggregated and mixed. Cells begin to gradually sort out. Moreover, the sorting process continues until 3 tissues are formed: on top is a layer of epidermal tissue, then the neural tube, and below is an accumulation of endodermal cells. This phenomenon is called cell segregation - selective sorting.
Cells of eye rudiments and cartilage were mixed. Cancer cells are incapable of segregation and are inseparable from normal cells. The remaining cells are subject to segregation.
Critical periods of development.
The critical period is a period that is associated with a change in metabolism (genome switching).
In human ontogenesis, there are:
1. development of germ cells
2. fertilization
3. implantation (7-8 weeks)
4. development of axial organs and formation of the placenta (3-8 weeks)
5. stage of brain growth (15-20 weeks).
6. formation of the main functional systems of the body and differentiation of the reproductive apparatus (10-14 weeks).
7. birth (0-10 days)
8. the period of infancy - the maximum intensity of growth, the functioning of the energy production system, etc.
9. preschool (6-9 years old)
10. pubertal - for girls 12. for boys 13 years old.
11. the end of the reproductive period, for women - 55, for men - 60 years.
During critical periods of development, mutations appear, so one must be attentive to these periods.
CELLULAR MECHANISMS OF ORIGIN OF CONGENITAL DEFECTS.
The formation of congenital malformations is the result of deviations from the normal development of an individual. This development takes place over a long period of time and is carried out through a chain of successive and interconnected events. A single process of individual development can be represented by the main stages:
gametogenesis,
fertilization,
embryonic morphogenesis,
postembryonic development.
The main content of gametogenesis (the formation of germ cells), according to the figurative expression of S. Raven, is “coding of morphogenetic information”, in the process of implementation of which a multicellular organism develops from a unicellular embryo (zygote). Morphogenetic information is carried by nuclear genes localized in the chromosomes of gametes (genotypic information), and cytoplasmic factors - cytoplasmic proteins (cytoplasmic information). Both types of information form a single nuclear-cytoplasmic system that determines the development of the organism.
Embryonic morphogenesis , i.e. the formation of the morphological structures of the embryo, includes embryonic histogenesis - the emergence of specialized tissues from poorly differentiated cells of the embryonic germ, and organogenesis - the development of organs and body systems. Embryonic morphogenesis is carried out with the interaction of the genome of the embryo and the mother's body, especially its hormonal and immune systems, and is associated with the processes of reproduction, growth, migration, differentiation and death of cells and the formation of organs and tissues.
These processes are controlled by a complex interaction of genetic, epigenomic, and environmental factors that ultimately determine the temporal and spatial sequence of gene expression and, thus, cytodifferentiation and morphogenesis. The inclusion of some and the exclusion of other genes occurs throughout the entire embryogenesis. Accordingly, these processes change the temporary structures of the embryo, of which there are hundreds during embryogenesis, and they are formed at the intracellular, cellular, extracellular, tissue, intertissue, organ and interorgan levels. Violation of any of the above mechanisms in the discrete process of embryogenesis entails a deviation from normal development and, therefore, can be realized in a congenital defect. At the intracellular level, “triggering” mechanisms of developmental disorders include changes in molecular processes involved in replication, changes in the pathways of biosynthesis and protein nutrition of embryos, disturbances in energy metabolism and other intimate mechanisms that determine the vital activity of cells.
To the main cellular mechanisms of teratogenesis include changes in reproduction, migration and differentiation.
Reproduction disorders are mainly associated with a decrease in the mitotic activity of cells and are manifested by inhibition of the preliferative activity of cells up to its complete stop. The result of such changes can be hypoplasia or aplasia of any organ or part of it, as well as a violation of the fusion with each other of individual embryonic structures that form the organ, since fusion occurs at strictly defined periods.
As a result of low proliferative activity, the contact between embryonic structures is broken (late). Such a mechanism, obviously, underlies many dysraphia (some cleft lip, palate, spinal hernia). Thus, any factor (genetic or environmental) that can reduce mitotic activity during embryogenesis (for example, DNA synthesis inhibitors, chloridine, oxygen deficiency in cells and tissues, rubella virus, numerical aberrations of chromosomes) can lead to the development of congenital malformation. As a result of impaired cell migration, heterotopias, agenesis and other defects may develop. In an experiment conducted on rats with the introduction of an excess amount of vitamin A, it was shown that severe symmetrical facial clefts are formed as a result of a violation of the migration of cells of the peiroectodermal ridge into the embryonic maxillary processes. In most chromosomal diseases, heterotopy of neurons is found in the white matter of the brain, due to a violation of migration processes. The origin of the Robinov and DiGeorge syndromes is associated with impaired migration.
Differentiation, i.e., the formation of heterogeneous cells, tissues and organs from a homogeneous embryonic primordium, consistently occurs throughout the entire embryogenesis. Such differentiation can stop at any stage of development, which will entail the growth of a shapeless mass of undifferentiated cells (as is observed in early abortions), agenesis of an organ or organ system, their morphological and functional immaturity, and persistence. embryonic structures. The key positions in the specialization of cells are occupied by the differential activity of genes, as a result of which, in different phases of embryogenesis, isoenzymes specific for each stage are synthesized, with which the induction of cells and tissues in a certain direction is mainly associated. This process involves at least two objects - the donor of the enzyme or hormone and their recipient. Developmental disorders can occur both with insufficient function or the absence of genes and cells producing these substances, and with changes in target cells. For example, the lack of androgen activity in the target cells of the rudiments of the male genital organs, due to receptors capable of “recognizing” the corresponding hormone, leads to various defects in these organs. The absence of testicular hormones in fetuses with a genetic male sex leads to the development of the genital organs according to the female type.
Extracellular factors regulating embryogenesis include components of the extracellular matrix - glycosamino-glycans, proteoglycans, collagen proteins, fibroectin, which are involved in all processes of organogenesis. Violations of the normal functioning of the components of the extracellular matrix may be due to genetic and teratogenic factors. For example, such chemical teratogens as salicylates and aminonicotine, thalidomide and dilantin, respectively, disrupting the synthesis and processing of proteoglycans and collagen, cause a number of defects in the limbs, heart, eyes, and palate.
The main mechanisms of teratogenesis at the tissue level include the death of individual cell masses, slowing down the decay and resorption of cells that die during normal embryogenesis, as well as impaired tissue adhesion. Physiological cell death occurs under the influence of lysosomal enzymes in many organs in the process of their final formation. Such "programmed" (primary) cell death occurs when primary anatomical structures (eg, palatine processes, musculoendocardial protrusions) merge, intestinal tube recanalization, natural openings open, or, for example, regression of the interdigital membranes during the formation of fingers. In some cases, excessive cell breakdown is observed, which can lead to some dysmelia, heart septal defects, fistulas. Secondary death of cells and tissues is associated with circulatory disorders (thrombosis of blood vessels, their compression, hemorrhages) or the direct cytolytic effect of a damaging factor, such as the rubella virus.
A delay in the physiological breakdown of cells or a slowdown in their resorption due to insufficient macrophage response or dysfunction of the components of the extracellular matrix can lead to syndactyly, atresia, displacement of the aortic orifice, combined with a ventricular septal defect. A similar mechanism is the delayed involution of some embryonic structures, for example, the prolongation of the functioning of the apical ectodermal ridge, leading to the development of preaxial polydactyly.
Violation of the adhesion mechanism, i.e. processes of "gluing", "retention" and "growth" of embryonic structures, can lead to the development of a defect even in cases where the proliferation of tissues and the growth of embryonic organ structures were normal. Violation of the adhesion mechanism, as well as insufficiently active proliferation, underlie many defects such as dysraphia (for example, defects associated with non-closure of the neural tube).
Congenital malformations after the end of the main organogenesis are mainly developmental arrest (for example, hypoplasia), a delay in the movement of the organ to the place of its final localization (pelvic kidney, cryptorchidism), secondary changes associated with compression (for example, deformity of the limbs with oligohydramnios, amniotic constriction ) .
A progressive role in understanding the pathogenesis and in establishing the causes of congenital malformations was played by the teachings of S. Stockard and P. G. Svetlov (1937, 1960) on critical periods, as well as the teachings of E. Schwalbe on teratogenetic termination periods. These periods are often identified, which is not true. The term “critical periods”, introduced into the scientific literature in 1897 by P. I. Brounov, is understood as periods in embryogenesis, characterized by an increased sensitivity of the embryo to the damaging effects of factors external environment. In mammals, critical periods coincide with the periods of implantation and placentation. The first critical period in humans occurs at the end of the 1st - the beginning of the 2nd week of pregnancy. The impact of the damaging factor at this time mainly leads to the death of the embryo. The second period covers 3-6 weeks, when a similar factor often induces a malformation.
Critical periods coincide with the periods of the most intensive formation of organs and are associated mainly with the frequency of manifestations of the morphological activity of the nuclei.
The term teratogenetic termination period is understood as a deadline (from Latin terminus - limit, border), during which damaging factors can cause malformation. Since a teratogenic factor can lead to the development of a defect only if it acted until the end of the formation of an organ, and the formation of organs (especially various defects) does not coincide in time, each defect has its own termination period. For example, this period for undivided twins is limited by the first two weeks after fertilization, for a two-chamber heart - up to the 34th day, for aplasia of the interventricular septum - up to the 44th day, for an atrial septal defect - up to the 55th day of pregnancy. For persistence of the arterial duct or foramen ovale, cryptorchidism, many malformations of the teeth, the duration of this period is not limited to pregnancy.
Knowledge of the termination periods of malformations in clinical teratology is of exceptional importance, since it can assist in determining the cause of the development of a congenital malformation. If the time of action of the detected damaging factor coincides with the terms for a different period, then this factor can be accepted as a probable cause of a congenital defect. If the damaging factor acts later than the termination period, it certainly cannot be the cause of the defect. However, it must be remembered that the termination periods are only important for establishing the causes of congenital malformations induced by teratogenic factors, since hereditary malformations are associated with mutations that, as a rule, occurred in parents or more distant ancestors, and not in a child with a congenital malformation. If congenital malformations cause secondary changes in the organ (for example, the hydroureter due to aplasia of the muscle layer or the nervous apparatus of the ureter), then the termination period should be determined for the primary malformation (in this case, the 12th week of embryonic development), and not for the secondary - in the given example for the hydroureter, the termination period of which can last until the end of the second trimester of pregnancy.
In experimental teratology, it is known that the type of defect depends not only on the nature of the teratogen, but also on the time of its exposure. Thus, exposure to the same teratogenic factor at different periods of embryogenesis can lead to various defects and, on the contrary, various teratogens (for example, thalidomide and aminopterin), applied at the same time, can give the same type of defects. A certain specificity of teratogenic factors is also known in humans. For example, thalidomide affects the rudiments of predominantly mesodermal origin, inducing various dysmelia, anticonvulsants more often - cleft palate and heart defects, the anticoagulant warfarin damages the epiphyses tubular bones, alcohol predominantly damages 11HC and facial structures.
It should be noted that just as there are no periods when the embryo would be equally sensitive to various agents, so there are no stages when the embryo would be resistant to all damaging effects.
TERATOGENESIS
Teratogenesis is the occurrence of malformations under the influence of environmental factors (teratogenic factors) or as a result of hereditary diseases.
Teratogenic factors include medicines, drugs and many other substances. They are described in more detail in the section on teratogenic factors. The following features of the influence of teratogenic factors are distinguished.
1. The effect of teratogenic factors is dose-dependent. In different biological species, the dose-dependence of the teratogenic effect may vary.
2. For each teratogenic factor, there is a certain threshold dose of teratogenic effect. Usually it is 1-3 orders of magnitude lower than the lethal one.
3. Differences in teratogenic effects in different biological species, as well as in different representatives of the same species, are associated with the characteristics of absorption, metabolism, the ability of a substance to spread in the body and penetrate the placenta.
4. Sensitivity to various teratogenic factors during fetal development may vary. The following periods of intrauterine development of a person are distinguished.
The initial period of intrauterine development lasts from the moment of fertilization until the implantation of the blastocyst. The blastocyst is a collection of cells called blastomeres. Distinctive feature the initial period - great compensatory-adaptive capabilities of the developing embryo. If a large number of cells are damaged, the embryo dies, and if individual blastomeres are damaged, the further development cycle is not violated (the "all or nothing" principle).
The second period of intrauterine development is embryonic (18-60 days after fertilization). At this time, when the embryo is most sensitive to teratogenic factors, gross malformations are formed. After the 36th day of intrauterine development, gross malformations (with the exception of malformations of the hard palate, urinary tract and genital organs) are rarely formed.
The third period is fetal. Malformations for this period are not typical. Under the influence of environmental factors, growth inhibition and death of fetal cells occur, which is further manifested by underdevelopment or functional immaturity of organs.
5. In cases where infectious agents have a teratogenic effect, the threshold dose and the dose-dependent nature of the action of the teratogenic factor cannot be assessed.
Literature
1. Ayala F., Kyger J. Modern genetics. M., 2004
2. Alikhanyan S.I., Akifiev A.P., Chernin L.S. General genetics. M.,
3. Bochkov N.P. Clinical genetics. M., 2011
4. Introduction to molecular medicine. Ed. Paltseva M.A. M., Zhimulev I.F. - 2011
5. General and molecular genetics. Novosibirsk, Genetics. Ed. Ivanova V.I. M., 2010
6. Introduction to developmental genetics. M., Nurtazin S.T., Vsevolodov E.B. Biology of individual development. A., 2005.
Ontogenesis(from Greek. ontos- existent and genesis- development) - the individual development of each individual. This is a set of successive interrelated events that naturally take place in the process of the life cycle of each organism.
The life cycle of unicellular begins from the division of the mother cell and continues until the next division of the daughter.
The life cycle of multicellular organisms begins with one or a group of cells (during vegetative reproduction), from a zygote (during sexual reproduction) and ends with death.
In the ontogeny of multicellular organisms with sexual reproduction, three periods are distinguished.
1. Progenesis(prezygotic) - the period of formation of germ cells and fertilization.
2. Embryogenesis(embryonic) - the period from the zygote to birth or exit from the egg membranes.
3. Postembryonic(post-embryonic), including the periods:
Pre-reproductive - before puberty;
reproductive - adulthood, in which the organism performs its main biological task - the reproduction of individuals of a new generation; in this period, the life cycles of descendants begin;
Post-reproductive - aging and death of the body. Features of the ontogeny of individuals of each species have developed in the process
historical development of the species - in the process of phylogenesis.
However, the ontogeny of each multicellular organism is based on the general mechanisms of growth and development, which are carried out through the processes of cell division, their differentiation, and morphogenetic movement.
The two main principles of ontogenesis are differentiation (specialization of its individual parts) and integration - the unification of individual
parts and their subordination to a single organism, are manifested at all stages of ontogenesis and at all levels of the organism.
According to modern concepts, the cell that gives rise to a new organism contains the entire genetic program of one (in asexual reproduction) or two parents (in sexual reproduction).
Ontogeny is a consistent implementation of a genetic program under specific environmental conditions, so the final result depends not only on the genotype, which determines the general direction of morphogenetic processes, but also on environmental factors.
Ontogenetic processes are controlled by the interaction of many factors: genetic, inductive interaction of cells, tissues, organs of the embryo, endocrine, nervous and immune systems.
Topic 3.1. Ontogenesis. General patterns
progenesis
Target. Know the features of gametogenesis in humans, the biological significance and essence of meiosis, the structure of germ cells, the stages of fertilization.
Task for students
Work 1. Gametogenesis
Disassemble the scheme of gametogenesis, noting the similarities and differences in the processes of maturation of male and female gametes. Fill in and rewrite the table, indicating in each period of gametogenesis the type of division, the name of the cells, the set of chromosomes and the amount of DNA in them.
Gametogenesis. Features and differences
Work 2. Ovo- and spermatogenesis in humans
Study and rewrite the table, paying attention to the characteristics of the maturation of male and female gametes in humans.
Features of ovo- and spermatogenesis in humans
Period | spermatogenesis | Ovogenesis |
reproduction | Proliferation of spermatogonia begins in the early embryonic period, the most intense - from the period of puberty, periodic waves of mitosis occur throughout the reproductive period | Proliferation of oogonia begins in the early embryonic period, the most intense - between the 2nd and 5th months of embryogenesis. By the 7th month, there are about 7 million ovogonia in the embryonic ovary. Later, part of the oogonia degenerates |
Preparation for meiosis - autosynthetic interphase can be traced throughout the reproductive period | Preparation for meiosis - autosynthetic interphase begins at the 3rd month of embryogenesis, ends at birth - 3 years after birth. By the time of birth, there are about 100,000 oocytes of the first order in the ovary of a girl |
|
maturation (meiosis) 1 - reduction division | 1st meiotic division begins at puberty, lasts 7-8 weeks, ends with the formation of 2 spermatocytes of the 2nd order | The 1st meiotic division begins at the 7th month of embryogenesis, is characterized by a long prophase with periods of "small" and "large" growth. During the period of “small” growth, chromosomes acquire the structure of “lamp brushes”, extracopying (amplification) of genes, increased synthesis of mRNA, tRNA, proteins, enzymes, vitamins, ribosomes, membranes, mitochondria, and accumulation of endogenous yolk produced by the oocyte are observed. |
The end of the table.
Period | spermatogenesis | Ovogenesis |
2 - equational | Lasts 8 hours, ends with the formation of 4 spermatids | During the period of "great" growth, there is an intensive storage of exogenous yolk produced by the liver, which enters through the follicular cells. At the stage of diakinesis, division is blocked - block-1. During puberty (under the influence of sex hormones), block-1 is removed. The 1st meiotic division ends with the formation of a large oocyte of the 2nd order and the first reduction body. The 2nd meiotic division begins, which is blocked at the metaphase stage - block-2, going on ovulation. The process is repeated at monthly intervals for each subsequent oocyte until the onset of the menopause. For the entire productive period, ovulates 300-400 oocytes. The 2nd meiotic division ends after fertilization with the formation of an ovotid and a second reduction body |
Formation | It lasts 10 days, cell differentiation occurs, the formation of the head, neck, tail, acrosomes, the concentration of mitochondria in the middle part |
Work 3. Spermatogenesis in the testes of rats
Examine under a high magnification microscope a cross section of the seminiferous tubule of rats. Compare the preparation with the attached drawing, find the cells at different stages of spermatogenesis.
Rice. 1. Section of the cross section of the rat seminiferous tubule: 1 - limiting membrane; 2 - spermatogonium type (A) - "long-term reserve"; 3 - spermatogonium type (B) - "mitotically active cells"; 4 - spermatocyte of the first order; 5 - spermatocyte of the second order; 6 - spermatids at an early stage of development; 7 - spermatids at a late stage of development; 8 - spermatozoa; 9 - Sertoli cell
Work 4. The structure of spermatozoa of various vertebrates
Examine the external structure of spermatozoa under a high magnification microscope:
b) guinea pig;
c) a rooster.
Work 5. Ultramicroscopic structure of the sperm
Sketch the structure of a spermatozoon (Fig. 2). Label the main structures.
Rice. 2. Human spermatozoon according to electron microscopy (scheme): 1 - head; 2 - acrosome; 3 - outer membrane of the acrosome; 4 - inner membrane of the acrosome; 5 - nucleus (chromatin); 6 - tail (fibrous sheath; 7 - neck (transitional section); 8 - proximal centriole; 9 - middle section; 10 - mitochondrial helix; 11 - distal centriole (terminal ring); 12 - axial filaments of the tail
Work 6. The structure of the mammalian egg
Examine a cat's ovary under a high magnification microscope. Find a mature follicle with a 1st order oocyte. Compare the specimen with the attached drawing. Sketch the structure of a mammalian egg, noting the main structures.
Rice. 3. The structure of the egg cell of mammals:
1 - core; 2 - nucleolus; 3 - cytoplasmic membrane (ovolemma); 4 - microvilli of the cytoplasmic membrane - microvilli; 5 - cytoplasm; 6 - cortical layer; 7 - follicular cells; 8 - processes of follicular cells; 9 - shiny shell; 10 - yolk inclusions
Work 7. Types of eggs in chordates and vertebrates
Complete the table of egg types in chordates and vertebrates, indicating the amount and distribution of the yolk in the cytoplasm.
Oocyte types in chordates and vertebrates
Work 8. Fertilization
Consider and draw a diagram (Fig. 4) of the stages of fertilization in animals. Pay attention to the acrosomal and cortical reactions, to the formation of the fertilization membrane.
Rice. 4. Fertilization stages:
1 - sperm nucleus; 2 - proximal centriole; 3 - acrosome; 4 - acrosome enzymes; 5 - shiny shell; 6 - cytoplasmic membrane; 7 - cortical layer; 8 - yolk membrane; 9 - acrosome thread; 10 - fertilization shell; 11 - hyaline shell; 12 - perivitelline space; 13 - spermatozoa
Work 9. Internal phase of fertilization
Examine under a high magnification of the microscope the preparation - the fertilization of the roundworm egg, find, shade and designate:
a) the stage of two pronuclei;
b) the stage of synkaryon.
Rice. 5. Fertilization phases:
1 - egg shell; 2 - cytoplasm; 3 - male pronucleus; 4 - female pronucleus; 5 - pronuclei at the synkaryon stage; 6 - reduction bodies
Annex 1
Lampbrush chromosomes
(after Alberta, Bray, Lewis, 1994)
In the long diplotene of meiosis of the oocyte, a special phase of dictyoten is distinguished, in which the chromosomes acquire a “lampbrush” structure. Each bivalent consists of 4 chromatids forming symmetrical chromatin loops of different sizes, 50-100 thousand bp long, RNA synthesis takes place along the loops. Lampbrush chromosomes are actively transcribed for the accumulation of gene products in the oocyte cytoplasm. These chromosomes are found in the oocytes of fish, amphibians, reptiles, and birds.
Annex 2
Differentiation of the egg cytoplasm after fertilization
Map of the presumptive organs of the egg:
a - fish; b - reptiles and birds; in - amphibians
Topography of the anlages of the organs of the amphibian embryo to the beginning of gastrulation:
1 - ectoderm; 2 - neural plate; 3 - chord; 4 - intestinal ectoderm; 5 - mesoderm
Topography of the organs of the amphibian embryo at later stages of development: 1 - integumentary tissue (epidermis); 2 - neural tube with brain; 3 - chord; 4 - intestine with gill slits; 5 - chord shell; 6 - heart
Questions for self-study
1. What is ontogeny? Ideas about ontogenesis: epigenesis, preformism, modern.
2. Name the main periods of human ontogenesis.
3. What is the essence and significance of the prezygote period - progenesis?
4. Name the periods of gametogenesis.
5. What is the difference between spermatogenesis and oogenesis?
6. What are the types of eggs according to the number and distribution of yolk?
7. What is the reason for the change in the amount of yolk in the eggs in the process of vertebrate phylogenesis?
8. Fertilization. biological entity. Parthenogenesis. Gynogenesis. Androgenesis.
9. Biological meaning of acrosomal and cortical reactions in the process of fertilization.
10. Genetic processes in the pronuclei of the internal stage of fertilization.
11. What is ooplasmic segregation? What is its role in the further development of the egg?
12. What are the main problems characteristic of human progenesis? What are the current possibilities for their resolution?
Test tasks
1. MEIOSIS CORRESPOND TO THE STAGE OF GAMETOGENESIS:
1. Breeding
3. Maturing
4. Formations
2. OVULATION IS CARRIED OUT AT THE STAGE:
1. Ovogonia
2. Oocyte of the 1st order
3. Oocyte of the 2nd order
4. Ovotids
5. Differentiated ovum
3. IN MAMMALS AND HUMANS, FERTILIZATION OCCURRS AT THE STAGE:
1. Ovogonia
2. Oocyte of the 1st order
3. Oocyte of the 2nd order
4. Ovotids
5. Mature differentiated ovum
4. THE GROWTH STAGE IN SPERMATOGENESIS ENDS
EDUCATION:
1. Spermatogonia
2. Spermatocyte of the 1st order
3. Spermatocyte of the 2nd order
4. Spermatids
5. Sperm
5. BIOLOGICAL MEANING OF THE CORTICAL REACTION:
1. Contact of gametes of organisms of the same species
2. Penetration of the sperm into the egg
3. Rapprochement of pronuclei
4. Formation of the fertilization membrane, ensuring monospermia
5. New combinations of hereditary material
6. FEATURES OF THE FEMALE GAMETES OF MAMMALS:
1. Mobility
2. Pronounced cortical layer
3. High nuclear cytoplasmic index
4. Acrosome
5. Yolk in the cytoplasm
6. Shiny shell
7. FORMS OF SEXUAL REPRODUCTION WITHOUT FERTILIZATION:
1. Copulation
2. Conjugation
3. Gynogenesis
4. Polyembryony
5. Androgenesis
Set a match.
8. TYPES OF EGGS:
1. Isolecithal
2. Telolecithal moderately
3. Telolecithal abruptly
CHORDS AND VERTEBRATES:
a) Placental mammals and humans
b) Oviparous mammals
c) Reptiles
d) Amphibians
e) Cartilaginous fish
f) Bony fish
9. IN CELLS AT DIFFERENT STAGES OF OVOGENESIS:
1. Ovogonia
2. Oocytes of the 1st order
3. Oocytes of the 2nd order
4. Ovotids
SET OF CHROMOSOMES AND Amount of DNA:
10. SET OF CHROMOSOMES AND QUANTITY OF DNA:
IN CELLS AT DIFFERENT STAGES OF SPERMATOGENESIS
a) Spermatogonia after mitosis
b) Spermatocytes of the 1st order
c) Spermatocytes of the 2nd order
d) Spermatogonia before mitosis
e) spermatozoa
Literature
Main
Guide to practical exercises in biology / Ed.
V.V. Markina. - M.: Medicine, 2006. - S. 96-104.
Biology / Ed. N.V. Chebyshev. - M.: VUNMTs, 2000.
Biology / Ed. V.N. Yarygin. - M.: Higher school, 2007.
Additional
Gilbert S. Developmental biology: in 3 volumes - M.: Mir, 1998.
Vogel F, Matulski A. Human genetics: in 3 volumes - M .: Mir,
Topic 3.2. General patterns of embryogenesis
Target. To study the stages of animal and human embryogenesis, methods of cleavage and gastrulation, the formation of germ layers, the formation of tissues and organs, provisional organs in anamnia and amniotes and their functions.
Task for students
Work 1. The main stages of embryogenesis in chordates and humans
Using dummies, micropreparations, tables, study the main stages of embryogenesis in animals. Note the features of the development of chordates. Draw the main stages of embryogenesis using the example of the lancelet embryo (Fig. 1), mark the parts of the embryo at different stages of development.
Rice. 2. Stages of human development (from various sources):
a - crushing; b - blastocyst; c - 8-day embryo; d - 13-14-day embryo; e - 30-day embryo; e - embryo 5 weeks (in the uterine cavity); g - the fetus in the uterine cavity;
1 - large blastomeres; 2 - small blastomeres; 3 - embryoblast; 4 - blastocoel; 5 - trophoblast; 6 - endoderm; 7 - amnion cavity; 8 - amnion; 9 - embryo; 10 - yolk sac; 11 - stalk; 12 - villi of the chorion; 13 - placenta; 14 - allantois; 15 - umbilical cord; 16 - fetus; 17 - cervix
Work 3. Histo- and organogenesis. Derivatives of the germ layers
Study and rewrite the table.
Derivatives of the germ layers
Work 4. Organogenesis on the example of the development of the initial section of the digestive system
Using drawings, lecture materials and a textbook, study the developmental features of the initial section of the human digestive system.
Development of the oral cavity
The first germ oral cavity is the ectodermal cavity - oral fossa (stomodeum, stomodaeum). It is initially separated from the pharyngeal cavity by the oropharyngeal membrane, which then breaks through. The oral fossa is not only the bookmark of the oral cavity, but also the nasal cavity. The oral cavity and the nasal cavity are separated by the hard and soft palate, this occurs at the 7th week of embryogenesis.
The epithelium of the roof of the stomodeum forms an invagination towards the diencephalon - Rathke's pouch - the future anterior lobe of the pituitary gland. Subsequently, Rathke's pouch is completely separated from the stomodeum and forms the anterior (adenohypophysis) and intermediate lobes of the pituitary gland (endocrine gland).
Rice. 3. Facial area in human embryos:
a - a four-week embryo; b - a five-week embryo; c - embryo at the age of 5.5 weeks;
1 - protrusion due to the middle cerebral bladder; 2 - olfactory placode; 3 - frontal process; 4 - maxillary process; 5 - primary mouth opening; 6 - mandibular process; 7 - sublingual gill arch; 8 - third gill arch; 9 - laying the nose hole; 10 - eye tab
Tooth development
In front, the oral cavity is limited by the oral opening, along the edges of which a horseshoe-shaped strip of epithelial thickening is laid - the labio-gingival strip. A groove forms in it, which separates the lip area from the gum area. The vestibule of the mouth is formed from the cavity of this groove. The second (also horseshoe-shaped) thickened epithelial strip - the periodontal (dental plate) begins to grow into the mesenchyme of the gingival region, from which the epithelial elements of the teeth originate.
The epithelium of the dental plate grows into the mesenchyme of the jaw anlages (usually at the 7th week). Flask-shaped outgrowths appear on its inner surface, from which enamel organs later arise (each enamel organ is the germ of a separate tooth). The mesenchymal dental papilla grows into the enamel organ.
The cells of the enamel organ form the enamel, and the dental papillae form the dentin and pulp.
First, the crown of the tooth is formed. Root development begins after birth.
As with milk teeth, in permanent teeth, the rudiments are laid during embryogenesis.
Development salivary glands
The large salivary glands (parotid, submandibular, sublingual), which open into the oral cavity, are laid at the 2nd month of embryonic development, the small glands of the oral cavity - at the 3rd month, are of ectodermal origin. Initially, they are laid in the form of epithelial cords, which grow into the mesenchyme, where they begin to branch. Complete differentiation of the glands occurs shortly after the birth of the child.
Language development
The tongue tab consists of three tubercles. Two of them - the right and left hyoid tubercles - are located in pairs, the third - the middle lingual tubercle - is unpaired. Between the individual rudiments of the language, a process begins, leading to their fusion.
Rice. 4. Sections of the tooth at various stages of development (according to Kollman): 1 - enamel; 2 - dentin; 3 - mesenchyme; 4 - the remains of a tooth strip; 5 - enamel pulp; 6 - dental papilla; 7 - bookmarks of the dental alveoli; 8 - dental pulp; 9 - epithelial pearls; 10 - bookmark mandible with alveolar process; 11 - laying of the final tooth; 12 - dental pouch; 13 - epithelium of the oral cavity; 14 - tooth strip; 15 - language tab; 16 - enamel organ
Rice. 5. Language development. Inside view of the base of the pharyngeal region: a - a six-week embryo; b - a seven-week embryo; in - in an adult; 1 - lingual lateral tubercle; 2 - lingual middle tubercle (unpaired); 3 - blind hole; 4 - copula; 5 - bookmark of the epiglottis; 6 - arytenoid tubercles; 7 - lower lip; 8 - median groove of the tongue; 9 - palatine tonsil; 10 - the root of the tongue with the lingual tonsil; 11 - epiglottis
Development of the pharynx
The pharynx is located immediately behind the oral cavity.
In humans, 5 pairs of gill arches are laid here, between which there are 4 pairs of gill pockets. Gill slits form from the ectoderm of the cervical region towards the gill pockets.
In animals that breathe with gills, they connect, forming through slits through which oxygen enters from water into the blood circulating in the capillary networks of the vessels of the gill arches. In lung-breathing amniotes, including humans, the gill slits and pouches are folded but not connected. In humans, all gill pockets are overgrown. In the future, they will be transformed into other structures.
Transformation of gill pockets
From the first pair of gill pockets in humans, tympanic cavities and auditory tubes are formed, connecting these cavities with the nasopharynx. From the first pair of gill slits, external auditory canals are formed.
An invagination of the external ectoderm begins to grow to the location of the auditory ossicles from the outside, the lumen of which gives rise to the external auditory meatus. The invagination adjoins the rudiment of the middle ear cavity. Later, a tympanic membrane forms in this place.
Rice. 6. Development of the pharynx (side view, borrowed from Patten): 1 - first gill pocket; 2 - second gill pocket; 3 - third gill pocket; 4 - fourth gill pocket; 5 - bookmark of the thyroid gland; 6 - bookmark of the pituitary gland; 7 - esophagus
From the material of the II pair of gill pockets palatine tonsils are formed.
From the material of III and IV pairs of gill pockets are formed:
Thymus, the laying of which occurs at the end of the 1st - the beginning of the 2nd month of intrauterine life. Soon, the cavities overgrow and dense epithemal nodes appear;
Parathyroid glands. They are laid in the form of epithemal nodules, which are later separated from the endoderm of the gill pockets and superficially located in the capsule of the thyroid gland;
Ultimobronchial bodies. In humans, they are in the form of C-cells are part of the thyroid gland.
II, III, IV pairs of gill slits are reduced.
Work 6. Provisional organs of anamnia and amniotes
Study the tables, macropreparations and drawing, compare provisional organs and their functions in different groups of animals. Rewrite and complete the table.
Work 7. Histological types of placentas(Tokin B.P., 1987)
Learn the classification and functions of the placenta. Note the peculiarity of the human placenta (Fig. 7).
The placenta is a provisional organ, it distinguishes germinal, or fetal, part And maternal, or uterine. The fetal part is represented by a branched chorion, and the maternal part is represented by the mucous membrane of the uterus.
The placenta differs anatomically (in shape) and histologically. There are several histological types of placentas according to the degree of relationship between the chorionic villi and the uterine mucosa.
Rice. 7. Types of placenta:
1 - chorion epithelium; 2 - epithelium of the mucous membrane of the uterus; 3 - connective tissue of the chorionic villus; 4 - connective tissue of the mucous membrane of the uterus; 5 - blood vessels of the chorionic villi; 6 - blood vessels of the uterus; 7 - gaps
Annex 1
The main stages of human embryogenesis and the formation of the structures of the visceral skull and the initial section of the digestive tract
Annex 2
Rice. 1. Changes in the appearance of the human embryo in the early stages of development (Sadler, 1995):
a - stage 25 somites (28 days of development); b - 5 weeks of development; c - 6 weeks of development; d - 8 weeks of development;
1 - visual placode; 2 - auditory placode; 3 - gill arches; 4 - somites; 5 - umbilical cord; 6 - cardiac ledge; 7 - bookmark of the upper limb; 8 - bookmark of the lower limb; 9 - tail; 10 - cervical bend; 11 - emerging auditory meatus; 12 - development of the fingers; 13 - toe development
Appendix 3
Rice. 1. Provisional organs of vertebrates:
a - anamnia; b - non-placental amniotes; c - placental amniotes; 1 - embryo; 2 - yolk sac; 3 - amnion; 4 - allantois; 5 - chorion (serous membrane); 6 - villi of the chorion; 7 - placenta; 8 - umbilical cord; 9 - reduced yolk sac; 10 - reduced allantois
Questions for self-study
1. Name the main processes occurring in embryogenesis.
2. What are the main stages in the development of the embryo?
3. What is the essence of the crushing process? Name and describe the main types of crushing.
4. Describe the embryo at the stage of morula, blastula, gastrula.
5. Name the main ways of gastrulation.
6. What are the ways of mesoderm formation?
7. Describe the methods of cleavage and gastrulation in placental mammals.
8. Name the derivatives of the three germ layers.
9. Describe the main stages in the formation of the initial section of the human digestive system.
10. Name provisional bodies, their functions. How do they differ between anamnia and amniotes?
11. What is the structure of the placenta? What is its function? Describe the structural features of the placenta in humans.
Test tasks
Choose one correct answer.
1. SET OF CHROMOSOMES IN THE ZYGOTE:
2. CHARACTERISTIC FOR HUMAN TYPE OF CRUSHING:
1. Full uniform
2. Complete uneven
3. Incomplete superficial
4. Incomplete discoidal
3. TYPE OF BLASTULA CHARACTERISTIC FOR HUMANS:
1. Coeloblastula
2. Discoblastula
3. Blastocyst
4. Amphiblastula
4. HUMAN PLACENTA:
1. Desmochorionic
2. Hemochorionic
3. Endotheliochorial
4. Epitheliochorial
Choose multiple correct answers.
5. DURING GASTRULATION IN CHORDS, THE FOLLOWING HAPPENS:
1. Bookmark mesoderm
2. Bookmark of the digestive glands
3. Bookmark of axial organs
4. Formation of a two-layer nucleus
6. FROM THE FIRST GILL POCKET AND GILL SLISTURE ARE FORMED:
1. Tympanic cavity
3. Ultimobranchial body
4. Ear canal
6. IN THE LATER STAGES OF HUMAN EMBRYO DEVELOPMENT THE PROVISORY ORGANS FUNCTION:
2. Yolk sac
3. Placenta
4. Allantois
Set the correct sequence. 7. STAGES IN THE EMBRYOGENESIS OF CHORDS:
1. Gastrula
4. Blastula
Set a match.
8. IN PERIODS
EMBRYOGENESIS:
1. Crushing
2. Histo- and organogenesis
3. Gastrulation
MAIN EVENTS:
a) Formation of tissues and organs
b) Formation of germ layers
c) Successive mitotic divisions leading to the formation of a single-layer embryo
Set a match.
9. IN HUMAN GERMAN LEAMS:
1. Ectoderm
2. Mesoderm
3. Endoderm
DEVELOPING:
a) Glandular epithelium of the salivary glands
b) Dental pulp
c) Epithelium of the middle part of the digestive tract
d) Tooth enamel
e) Dentin of teeth
Literature
Main
Biology / Ed. V.N. Yarygin. - M.: Higher school, 2001. - Book. 1. - S. 276-284, 287-317.
Pekhov A.P.
Additional
Gazaryan K.G., Belousov L.V. Biology of individual development of animals. - M.: Higher school, 1983
Gilbert S. Biology of development. - M.: Mir, 1993. - T. 1.
Carlson b. Fundamentals of Embryology according to Patten. - M.: Mir, 1983.
Stanek I. Human embryology. - M.: Veda, 1977.
Danilov R.K., Borovaya T.G. General and medical embryology. -
M.-SPb.: SpecLit, 2003.
Topic 3.3. Patterns of the postembryonic period of ontogenesis
Target. Know the types of postembryonic development of animals. To study the periods and features of human postnatal ontogenesis.
Task for students
Work 1. Types of development of organisms in the postembryonic period
The postembryonic period of ontogeny begins after the release of the embryo from the embryonic membranes or after birth. It is divided into three periods: pre-reproductive (juvenile), reproductive (adult state) and post-reproductive (not present in all species). The duration of these periods, their time ratio - are species-specific. The main processes occurring in the post-embryonic period of ontogenesis are growth, the formation of definitive (final) organ structures, puberty, and aging. The postembryonic period ends with the biological death of the individual.
There are two types of postembryonic development: direct and development with metamorphosis.
With direct development in the juvenile period, the forming individual has all the main features of the organization of an adult organism and differs mainly in smaller sizes, body proportions and underdevelopment of some organ systems. Direct development occurs in invertebrates, vertebrates, and humans.
During development with metamorphosis, a larva emerges from the egg, which differs from the adult animal in structure and way of life. Larval development is typical for species that lay small eggs with insufficient nutrients for the development of all structures characteristic of individuals of this species. The larvae are more similar in structure to the ancestral forms, and may have organs that are not characteristic of adults. They move freely and are able to feed on their own. Development with metamorphosis is widespread in the animal kingdom: sponges, scyphoid and coral polyps, most arthropods, many echinoderms, sea squirts, cyclostomes, lungfish and bony fish, amphibians.
Study the table, rewrite and complete it with examples.
Work 2. Features of the postnatal period of human ontogenesis
Study and rewrite the table.
Periods | Core Processes | Disease risk |
|
1. Newborn? up to 1 month | The first stage of adaptation to less favorable environmental conditions than in the mother's body: non-sterile conditions, lower temperature, changes in external pressure. The umbilical cord falls off. The child begins to suckle the mother's breast (4 days - colostrum, then milk), which requires effort and is accompanied by a weight loss of 150-200 g. Pulmonary breathing begins. The extrauterine circulation is established, the ductus arteriosus and the foramen ovale between the atria are overgrown. The functions of individual organs change. Set your own daily biorhythms | Reduced due to the immaturity of the immune nervous and other systems. Immunity is passive due to antibodies obtained from the mother's body through the placenta and with colostrum. Needs mother's care and protection. Critical period | Nonspecific infections, overheating, hypothermia, pathology of various organs and systems, especially digestive, due to insufficiency of their own enzymes. Increased chance of death |
2. Infant (thoracic) up to 1 year | Intensive growth and development: body length increases 1.5 times, weight - 3 times. Fontanelles close, curves of the spine appear | Reduced due to rapid growth, morphological incompleteness of the structure and |
Continuation of the table.
Periods | Core Processes | The adaptive capacity of the body | Disease risk |
|||
The brain is rapidly growing and developing, numerous conditional connections are being developed, a second signaling system is being formed, and static functions are developing. Intensive psycho-emotional development. Own digestive enzymes are produced less than in an adult. Milk teeth erupt. Passive immunity gradually weakens, acquired immunity is weakly expressed | functional imperfection of organ systems | Tendency to convulsions and other disorders of the nervous system. 3. Early childhood up to 4 years | The growth and development of the child continues, but the intensity of growth decreases. All 20 milk teeth erupt. The intellect develops especially rapidly. Speech includes many words, speaks in sentences | Rise gradually | Often - acute infections: measles, whooping cough, chicken pox, etc. Dentomaxillofacial anomalies due to early removal of milk teeth. is increasing infection tuberculosis |
Continuation of the table.
Periods | Core Processes | The adaptive capacity of the body | Disease risk |
4. First childhood 4 years - 7 years | The first growth jump. Large molars erupt. Gender differences appear in the structure of the skeleton, the deposition of fat, the formation of the psyche | Increases gradually | Dentofacial anomalies due to early extraction of milk teeth |
5. Second childhood (prepubertal) 7-12 years | Strong growth, especially muscular system. The development of the liver, the respiratory system ends. The change of milk teeth to permanent ones begins. Increased secretion of sex hormones. The beginning of the development of secondary sexual characteristics (in girls earlier) | Rise gradually | Injury is on the rise. Pathology of the cardiovascular and other systems. Anomalies of eruption of permanent teeth and bite |
6. Teenage (pubertal) 12-15-16 years | Growth jump. The formation of the circulatory and a number of organs of the digestive and other systems ends. All milk teeth are replaced by permanent ones. Intensive puberty: the production of sex hormones increases, the sexual characteristics of the body are formed, the development of secondary sexual characteristics ends, menarche appears in girls, wet dreams in boys. Puberty is characterized by radical biochemical, hormonal, physiological, morphological, neuropsychological changes in the body. | Critical | Possible manifestation of hereditary diseases, metabolic disorders (obesity or malnutrition). Pubertal behavioral crises, aggressiveness |
Continuation of the table.
Periods | Core Processes | The adaptive capacity of the body | Disease risk |
7. Youth period (post-puberty) 15-16 - 18-21 years | By the end of the period, body growth stops. The formation of all organ systems ends. Completion of puberty. Boys have facial hair. There is an intensive development of intelligence | Can be reduced | Violations of the functions of various organs and systems due to unbalanced growth of the body and development of organ systems (especially in connection with acceleration). Psychoneuroses |
8. First maturity 18-21-35 years | development of the adult organism. stable homeostasis. Ability to reproduce full-fledged offspring | Maximum | |
9. Second maturity up to 55-60 years | Physiological changes in organs, metabolism, preceding involution. Slowing down the speed of responses. Decreased production of hormones, especially sex hormones. The manifestation of noticeable signs of aging of the body at the end of the period. Gradual fading of reproductive function | Gradually decrease due to a decrease in the function of the immune and other systems. Critical period | The risk of developing somatic and mental illnesses increases. Increasing incidence of tumors. Menopausal syndrome, mental disorders may occur |
Continuation of the table.
Periods | Core Processes | The adaptive capacity of the body | Disease risk |
10. Old age up to 75 years | Gradual involution of organs and tissues of the body. The rate of aging in different organ systems is not the same. Flabbiness of the skin. Limitation of mobility in the joints, decrease in mass and muscle tone. Often - obesity or a sharp weight loss. Decreased physical activity. Fatigue | Weak resistance and adaptation to environmental factors | An increase in the incidence of age-related diseases: atherosclerosis, diabetes, gout and others. Psychoneuroses |
11. Senile age up to 90 years | Involution of all systems. Decreased hearing, visual acuity, memory, will, emotions, mental reactions | May have dementia, depression |
|
12. Longevity over 90 years | A biological phenomenon caused by a complex of various factors, both biological (heredity, body type) and social (traditions of correct behavior in stressful situations), an active lifestyle and rational nutrition |
Work 3. The final formation of the structures of some human organs in the postembryonic period
After the birth of a person, the laying and formation of structural and functional units of organs continues. The maturity of individual body structures occurs asynchronously. All organs and systems in structure and function become like in an adult organism by about 20-21 years.
Study and rewrite the table
Work 4. Dental and maxillofacial anomalies of a person developing in the postnatal period of life
Study and rewrite the table.
Type of anomaly | Cause |
Underdevelopment of the lower jaw | One of the reasons for underdevelopment of the jaw may be improper artificial feeding of the child, since there is no normal functional load necessary to remove the lower jaw from the distal position. |
Narrowing of the upper jaw | With a long-term violation of proper nasal breathing (non-closure of the bone palate, inflammation in the nasal cavity), the child breathes through the mouth, which changes the position of the elements of the oropharynx |
Displacement of the lower jaw forward or its lag in development | If the head position is too high, conditions are created for the jaw to move forward. If a child throws his head back during sleep, then prerequisites are created for the jaw to sag and its developmental lag |
malocclusion | The reason may be - early removal of milk teeth. This leads to the movement of the rudiments of permanent teeth anteriorly, which shortens the jaw arch; transferred inflammatory diseases of the jaws and teeth; endocrine pathologies, etc. |
jaw deformity | Bad habits - sucking a finger, lips, cheeks and various objects (diaper, pencil, etc.), placing palms under the cheek, etc. |
Formation of a high palate | Thyroid dysfunction; prolonged breathing through the mouth, for example, with inflammatory processes in the nasal cavity |
Facial asymmetry | Measles, diphtheria, whooping cough, rickets, scarlet fever |
Slow teething, enamel hypoplasia | It is possible with dysfunction of the thyroid and parathyroid glands, impaired mineral metabolism, etc. |
Inflammation of the salivary glands | Hypothermia, insufficient sanitation of the oral cavity |
Work 5. Manifestations of aging processes on various levels individual organization
Complete the table using textbook and lecture material.
Questions for self-study
1. What is postembryonic development?
2. What are the types of postembryonic development?
3. What are the differences between direct development and development with metamorphosis?
4. What distinctive features complete metamorphosis and what causes it?
5. What causes the metamorphosis of amphibians?
6. What are the periods of postnatal human development?
7. What factors determine the development of the human body in the postnatal period?
8. What stages of human ontogenesis are included in the pre-reproductive, reproductive and post-reproductive periods?
9. What are they characterized by?
10. Name the critical periods of postnatal human development; explain what causes them.
11. The concept of theories and mechanisms of aging.
Test tasks
Choose one correct answer.
1. CHANGING THE TEETH IN A HUMAN STARTS AT THE AGE:
2. HUMAN AGING GENE:
1. Located on the sex chromosomes
2. Located in the first pair of autosomes
3. Available in every pair of chromosomes
4. Appears as a result of mutations
1. Children's
2. Teenage
3. Reproductive
4. Post-reproductive
4. MAXIMUM LIFE
PERSON IS MAINLY DEFINED BY:
1. Lifestyle
2. Nutrition
3. Genotype
4. Environmental conditions
Choose multiple correct answers.
5. DIRECT TYPE OF DEVELOPMENT IS OCCURRED:
1. Growth of a juvenile
2. Reduction of larval organs
3. Formation of final organ structures
4. Changing the proportions of the body of an individual
6. DURING DEVELOPMENT WITH COMPLETE METAMORPHOSIS IN YOUNG
1. Body shape like an adult
2. Body shape different from adult
3. Larval organs are available
4. No reproductive system
7. DISTURBANCE OF THE FUNCTIONS OF VARIOUS ORGANS IN THE JUVENILE PERIOD OF POSTNATAL
OF ONTOGENESIS DUE TO:
1. Unfinished development of the immune system
2. Imbalance of nervous regulation
3. Intensive body growth
4. The work of aging genes
8. HUMAN GROWTH IS CONTROLLED BY HORMONES:
1. Somatotropin
2. Sexual
3. Parathyroid hormone
4. Thyroxine
9. IN THE POSTNATAL STAGE OF HUMAN ONTOGENESIS
CRITICAL PERIODS ARE:
1. Newborns
2. Infant
3. Teenage
4. Youthful
Set a match.
10. THEORIES OF AGING:
1. Overvoltage of the nervous system
2. Intoxication of the body
3. Accumulation of mutations in somatic cells
a) I.I. Mechnikov
b) A.A. Bogomolets
c) M. Szilard
d) I.P. Pavlov
e) L. Hayflick
Literature
Main
Biology / Ed. V.N. Yarygin. - M.: Higher school, 2001. -
Book. 1. - S. 276-278, 368-372, 381-409.
Pekhov A.P. Biology and general genetics. - M.: Publishing house of RUDN University, 1993. -
Additional
Gazaryan K.G., Belousov M.V. Biology of individual development of animals. - M.: Higher school, 1983.
Gilbert S. Biology of development. - M.: Mir, 1996.
Topic 3.4. Regulation of ontogeny
Target. To study the main mechanisms of ontogeny regulation; the influence of harmful factors on the human body and the mechanisms of formation of malformations.
Individual development and growth are genetically determined; the genotype of an individual determines a certain sequence of stages of development and growth, as well as the type of development at different stages of ontogenesis. In development, there is a unity of continuous and intermittent, gradualness and cyclicality. Periods alternate in ontogeny accelerated development with stages of relative stabilization. Ontogenesis is characterized by heterochrony in the initiation and maturation of different systems and tissues of the body, as well as different characters in one system. The postembryonic period of vertebrates is characterized by individual diversity of age dynamics due to the interaction of genetic and environmental factors. The specificity of the biology of human development is the indirect impact of environmental factors through socio-economic and socio-psychological conditions.
Task for students
Work 1. Main factors regulating the development of placental mammals
Rewrite the table.
Work 2. Genetic regulation of organism development
At all stages of ontogenesis, genes regulate and control the development of the organism.
During oogenesis, cells synthesize a large amount of different types messenger and ribosomal RNA, which are activated after fertilization and control the development of the embryo from the zygote to the blastula stage. The genes of the embryo itself begin to function in different vertebrate species at different stages of fragmentation (for example,
in humans at the stage of two blastomeres), and the products of their activity begin to regulate the development of the embryo. Thus, the early stages of development are regulated by maternal and germinal genes. Starting from the gastrula stage in many vertebrate species, the development of the organism is regulated only by the products of activity own genes embryo (Fig. 1).
The regulation of gene expression during the development of organisms is carried out at all stages of protein synthesis, both by the type of induction and by the type of repression, and control at the transcription level determines the time of functioning and the nature of transcription of a given gene.
On fig. 1 shows some models of genetic regulation of development at the level of transcription. Model 1 of cascade embryonic induction (Fig. 1) explains a certain change in the stages of ontogeny by sequential activation of the corresponding stage-specific genes. So, inducer 1 interacts with the sensor gene (C), activating the integrator gene (I), the product of which acts through the promoter (P 1) on structural genes (SG 1, SG 2, and SG 3) In turn, the product of activity structural gene SG 3 is an inducer 2 for the structural genes SG 4 , SG 5, etc.
In the process of development, repression of genes of earlier stages of development also occurs. In this case, the activity products of structural genes at later stages of ontogeny can serve as a repressor (model 2, Fig. 1)
Some structural genes are activated or repressed by the action products of several genes (Model 3, Fig. 1)
The induction or repression of several structural genes can be caused by the product of the activity of one gene. This model can explain the pleiotropic effect of genes, the influence of sex hormones, etc. (model 4, fig. 1).
Disassemble the diagrams in fig. 1 and draw a model of cascaded embryonic induction.
Designate:
Rice. 1. Genetic regulation of organism development
Work 3. Polytene chromosomes
At each stage of development, only a small part of the genome is involved in the creation of tissue-specific products, and strictly defined stage-specific genes are active at different stages of ontogenesis. For example, when studying polytene (giant) chromosomes formed as a result of multiple replication in the cells of the larvae of a number of dipteran insect species, inactive and active regions of chromosomes are clearly visible. The most active zones of DNA - puffs are untwisted sections of chromosomes, on which mRNA is intensively transcribed for the synthesis of stage-specific proteins. With the development of larvae, previously active DNA regions are spiralized, and puffs are formed in other zones.
1. Study according to fig. 2 section of the polytene chromosome undergoing puffing (according to Grossbach, 1973 from S. Gilbert, 1994), draw fig. 2y.
Rice. 2. Puffing process. Stages of pouffe formation (a-d)
2. Examine the micropreparation under a microscope at high magnification and draw. Designate: 1 - euchromatin; 2 - heterochromatin; 3 - pouf.
Work 4. Cloning. Regulatory capacity of the nuclei
During cell differentiation, selective expression occurs different parts genome and limitation of genetic potencies in differentiated cells. However, all genes are preserved in the nuclei of somatic cells and, under appropriate conditions, they can
can be reactivated and ensure the development of a normal embryo. Cloning is the development of a new organism that is a genetic copy of a somatic cell donor. In sexually reproducing species, cloning occurs when nuclei are transferred from a somatic cell to an enucleated egg. Currently obtained by cloning animals of different classes, including mammals. It turned out that in the process of ontogenesis, the genetic potency of somatic cell nuclei decreases, and the older the donor of somatic nuclei, the lower the percentage of development of cloned individuals. It has been established that the genetic potency of different donor cells is not the same.
Examine the drawing of the transplantation of nuclei taken from somatic cells at different stages of frog development (according to Gerdon, 1965 from E. Deucar, 1978) (Fig. 3).
Rice. 3. Transplantation of nuclei from somatic cells into a frog egg at different stages of development of donor cells
Work 5. Cellular processes during periods of gastrulation and organogenesis
Study the table, pictures in the appendix, slides and preparations for animal embryogenesis. Rewrite the table.
Forms of cellular interactions | Formation of normal structures (examples) | Consequences of violations of intercellular interactions (examples) |
Cellular movements | Movement of cells during gastrulation, neural tube formation, movement of neural crest cells | Violation of the formation of gastrula, neural tube; violation of the formation of facial structures |
electoral reproduction | The laying of the rudiments of individual organs | Absence of an organ or part of it, such as a salivary gland |
selective cell death | Death of epithelial cells at the fusion of palatine buds, nasal processes | Syndactyly, cleft palate, cleft lip, facial |
Cell adhesion | Fusion of the rudiments of facial structures (palatine processes, nasal processes with each other and with the maxillary processes) | Cleft palate, upper lip, face |
Cellular condensation | Formation of mesodermal rudiments of teeth | Missing teeth, extra teeth |
Work 6. Embryonic induction. Tooth development in mammals
(Dewkar E., 1978)
The first rudiment of teeth is laid along the gum crest - a dental plate, a thickened strip of ectoderm. Under the dental plate, a number of mesodermal dental papillae appear, which induce the formation of rudiments of the enamel organ from the ectoderm (when the mesodermal papillae are removed, the rudiments of the enamel organ are not formed). Mutual induction between the enamel organ and the mesodermal dental papilla leads to the formation of cells that form enamel, dentin, and pulp. At the next stage of differentiation, the resulting enamel and dentin mutually influence each other's development.
Rice. 4. Early stages of tooth development in mammals (scheme): a - gum of the lower jaw, top view; b - transverse section of the gums; in-e - stages
tooth development;->- - induction;< ^ - взаимная индукция;
1 - gum ridge; 2 - dental plate; 3 - mesodermal dental papillae; 4 - the rudiment of the enamel organ; 5 - ameloblasts; 6 - rudiment of enamel; 7 - odontoblasts; 8 - rudiment of dentin; 9 - the beginning of the pulp; 10 - enamel; 11 - dentine
Disassemble, draw fig. 4 and label the main structures.
Work 7. Nervous regulation in ontogeny
Nervous regulation begins with the laying of the central nervous system and continues throughout the life of the individual.
The interaction between the CNS centers and the innervated organs is established at the early stages of embryogenesis, and these structures mutually stimulate the development of each other. Peripheral nerves departing from the centers of the central nervous system grow to the rudiments of organs and stimulate their development. The absence of peripheral nerves or their damage (for example, drugs, toxoplasma toxins, etc.) causes a violation of the formation of the structures innervated by them. For example, in Europe, several hundred children were born with no limbs, whose mothers during pregnancy took the sleeping pill thalidomide, which blocks the growth of peripheral nerves.
In the postnatal period, the relationship between the nervous system and the innervated organs is preserved. Birth injuries of the brain and peripheral nerves lead not only to paralysis, but also to muscle atrophy and growth retardation of the corresponding limbs or unilateral hypotrophy of facial structures (with congenital paralysis of the VI-VII nerves). Passive movements of the extremities (special devices have been created for this), massage and physiotherapeutic stimulation of the innervated organs contribute to the restoration of damaged structures of the brain and spinal cord.
With neurofibromatosis (an autosomal dominant type of inheritance), tumors of the peripheral nerves develop. If the disease begins in early childhood, then on the side of the body where tumors develop, hypertrophy of bones and soft tissues occurs. For example, facial dysmorphosis develops (asymmetric, disproportionate development of the structures that form the face, Figure Appendix 5).
It has been established that in early childhood games that promote the movement of the hands, especially small, precise forms of activity, stimulate the development of brain structures, including the development of intelligence.
On fig. Figure 5 shows schemes of experiments on the axolotl to study the role of the peripheral nerve in the development of limbs, as well as the formation of motor centers of the spinal cord in the absence of limbs. Removal of a nerve on the left side of the axolotl embryo resulted in the absence of a limb on the operated side of the body.
The absence of a limb may be due to the action of neurotropic teratogens (toxoplasmosis toxins, thalidomide, etc.) (Fig. 5a).
Removal of the limb rudiment from the axolotl embryo leads to a decrease in the size of the ganglia and horns of the gray matter of the spinal cord on the operated side (Fig. 5b).
Analyze the drawings of experiments to study the relationship between nerve centers and innervated organs.
Rice. 5. The relationship of nerve centers and innervated organs (Dyukar E., 1978, with changes):
a - the influence of the spinal nerves on the development of the limb: 1 - spinal cord; 2 - spinal nerve innervating the limb; 3 - spinal ganglion; 4 - limb; b - the influence of the limb rudiment on the development of segments of the spinal cord (transverse section of the axolotl embryo with the limb rudiment removed: 1 - spinal ganglion; 2 - spinal nerve; 3 - dorsal horns of the gray matter of the spinal cord; 4 - ventral horns of the gray matter of the spinal cord
Work 8. Hormonal regulation of the development of the maxillofacial region
Use the table to study the effect of hormones on the development of the human maxillofacial region.
Work 9. The impact of harmful environmental factors on the embryo
Study the table, disassemble and draw a diagram, give examples of direct and indirect damage to the embryo.
The influence of harmful factors on the fetus
Continuation of the table.
Factors | Main mechanisms of violations | Embryo- and fetopathy |
3. Vitamin deficiency (often without maternal hypovitaminosis): | Metabolic disorders in the fetus | |
Vitamin B 2 | Growth failure, formation of biological oxidation enzymes | Cleft palate, hydrocephalus, heart anomalies, etc. |
Vitamin C | Violation of the processes of oxidation, formation connective tissue, biosynthesis | Possible death of the fetus, miscarriage |
Vitamin E | Violation of fat oxidation leading to the appearance of toxic products | Anomalies of the brain, eyes, skeleton |
4. Excess vitamins: | ||
Vitamin A | Violation of growth, redox processes | Cleft palate, anencephaly |
II. Maternal illnesses |
||
1. Rheumatism | Hypoxia, trophic disorders, dystrophic changes in the placenta | Fetal hypotrophy, functional immaturity, anomalies of organs and systems, mainly cardiovascular. Children often have infectious-allergic diseases and disorders of the nervous system. |
The transport of oxygen to the fetus is disturbed, iron deficiency, morphological changes in the placenta | Fetal death, disorders of the central nervous system, anemia in children |
|
Continuation of the table.
Factors | Main mechanisms of violations | Embryo- and fetopathy |
3. Diabetes | Hormonal changes, hyperglycemia and ketoacidosis, deterioration of uteroplacental circulation, pathological changes in the placenta | Fetal death, premature, immature fruits with increased weight, functional immaturity of the pancreas, lungs, less often - changes in the thyroid gland, kidneys. There are anencephaly, hydronephrosis, and other disorders of the central nervous system |
4. Thyrotoxicosis | Increased secretion of thyroid hormones | Violation of the formation of the central nervous system, the thyroid gland and, less than others, the endocrine glands. Less often - anomalies of the cardiovascular system, musculoskeletal system, etc. |
5. Immunological conflict (according to the Rh factor and the AB0 system; most often incompatible: 0 - A, 0 - B, A - B, B - A, combinations of maternal and fetal blood types) | Rh antibodies cross the placenta. Penetration through the placenta of incomplete isoimmune antibodies A and B, which cause hemolysis of fetal erythrocytes. Released indirect bilirubin is a strong tissue toxin | Hemolytic disease of the fetus and newborn |
III. Intrauterine infections |
||
1. Rubella virus | Infection of the embryo, especially in 1-3 months of development | Anomalies of the heart, brain, organs of hearing, vision and others |
The end of the table.
Factors | Main mechanisms of violations | Embryo- and fetopathy |
2. Influenza virus | Infection of the fetus, intoxication of the mother's body, hyperthermia, impaired uteroplacental circulation | Genital anomalies, cataract, cleft lip |
Toxoplasmosis | Deformities of the brain, eyes, limbs, cleft palate |
|
IV. ionizing radiation | Damage to the embryo by penetrating radiation and toxic products of damaged tissues | Congenital radiation sickness. Most often - paralysis of the nervous system. There may be anomalies of the eyes, blood vessels, lungs, liver, limbs |
V. Influence of chemical compounds, including medicinal substances (more than 600 compounds) | direct effect on the fetus. Violation of the structure and function of the placenta. Pathological changes in the mother's body | Various malformations depending on the substance, dose and time of admission |
Direct toxic effect on the fetus, placenta and mother's body | Hypotrophy, the tendency of children to respiratory diseases |
|
Alcohol | Damage to gametes, generative mutations. Direct toxic effect | Mental retardation, mental illness, heart defects, epilepsy, fetal alcohol damage |
Tetracycline | Direct action on the fetus | Spotted enamel on teeth |
Disassemble and draw a diagram 1. Give examples of developmental disorders of the embryo under the influence of harmful factors directly on the embryo or indirectly through the mother's organism and the placenta.
Scheme 1. Ways of exposure to harmful environmental factors on the embryo
Work 10. Classification and mechanisms of formation of malformations
Study and rewrite.
I. On an etiological basis.
1. Hereditary:
a) generative mutations (hereditary diseases);
b) mutations in the zygote and blastomeres (hereditary diseases, mosaicism).
2. Non-hereditary:
a) violation of the implementation of genetic information (phenocopy);
b) violation of the interaction of cells and tissues; malformations of organs and tissues (teratomas, cysts);
c) somatic mutations (congenital tumors).
3. Multifactorial.
II. By the period of ontogenesis. 1. Tametopathy:
a) hereditary;
b) non-hereditary (overripe gametes).
2. Blastopathies until the fifteenth day:
a) hereditary diseases (mosacism - the embryo consists of cells with a normal and atypical set of chromosomes);
b) non-hereditary (twin deformities, cyclopia 1).
3. Embryopathies before the end of the eighth week: most malformations, malformations caused by the action of teratogens.
4. Fetopathy from nine weeks to delivery: malformations of this group are rare: remnants of early structures (persistence - branchial cysts and fistulas); preservation of the original arrangement of organs; underdevelopment of individual organs or the entire fetus, a deviation in the development of organs.
5. Vices emerging in postnatal period (they occur less frequently than the above defects, due to injuries, diseases, exposure to environmental factors).
1 Cyclopia- there is only one orbit in the skull with one or two eyeballs located in the middle. Often combined with the absence of the cerebral hemispheres.
Annex 1
Genetic control of mammalian development
(according to B.V. Konyukhov, 1976)
Annex 2
Sequential stages of face formation, front view
(after Patten of Morris, Human Anatomy, McGrow-Hill, Company, New York)
a - 4-week-old fetus (3.5 mm); b - 5-week embryo 6.5 mm); c - 5.5-week-old fetus 9 mm); d - 6-week-old fetus (12 mm); e - 7-week-old fetus (19 mm); f - 8-week-old fetus (28 mm);
1 - frontal ledge; 2 - olfactory placode; 3 - nasal fossa; 4 - oral plate; 5 - mouth opening; 6 - maxillary process; 7 - mandibular arch; 8 - hyoid arc; 9 - medial nasal process; 10 - lateral nasal process; 11 - nasolacrimal groove; 12 - hyomandibular fissure; 13 - filtrum area formed by merged medial nasal processes; 14 - outer ear; 15 - auditory tubercles around the hyomandibular fissure; 16 - hyoid bone; 17 - cartilage of the larynx
Appendix 3
Mechanisms of fusion of palatine folds in mammalian embryos
a - frontal incision (in the XY cavity, shown in the inset on the left) through the nasal cavity and oral cavity, in the cheek area before the fusion of the palatine folds: 1 - nasal cavity; 2 - nasal septum; 3 - palatine folds; 4 - the rudiment of the language; 5 - lower jaw; b - the same as on a, after fusion of the palatine folds: 6 - zone of cell death and fusion; c - three successive stages (I-III) of the processes of destruction of the epithelium and fusion of the mesenchyme: 1 - epithelium of the left half of the palate; 2 - epithelium of the right half of the sky; 3 - mesenchyme; 4 - macrophages; 5 - dead cells; 6 - continuous mesenchyme; 7 - preserved epithelium; 6 - zone of selective cell death and adhesion
Appendix 4
The development of the salivary glands in humans
The position of the salivary glands in an 11-week-old human embryo: a-b - the early stage of development of the salivary gland in culture; c-e - diagram explaining the relationship between the processes of branching of the gland and the distribution of extracellular material. The laying of the furrow branching in the developing lobule is accompanied by the contraction of microfilaments in the cells at the top of the lobule and the accumulation of collagen fibers outside the basal plate in the region of the sulcus. As these processes progress, the furrow deepens and the level of glycosaminoglycan synthesis in the cells of this area gradually decreases. 1 - parotid gland; 2 - opening of the excretory duct of the parotid gland; 3 - opening of the excretory duct of the submandibular gland; 4 - bookmark of the sublingual gland; 5 - submandibular gland; 6 - glycosaminoglycans; 7 - collagen fibers
Appendix 5
External manifestations of neurofibromatosis (dysmorphosis of facial structures, age spots on the skin)
Questions for self-study
1. What are the differences between regulatory and mosaic types of development?
2. What is the essence of cell differentiation?
3. How is the regulation of the early stages of embryonic development and when does the genome of the embryo begin to function?
4. What is the effect of genes in early development?
5. How does the genetic potency of cell nuclei change during development?
6. How is genetic regulation of differentiation carried out?
7. What cellular processes occur during cleavage, gastrulation, organogenesis?
8. What are the main forms of cell interaction during periods of organogenesis?
9. What is the essence of embryonic induction and its types?
10. What is the chemical structure of inductors and their mechanism of action?
11. What is the importance of the nervous system in the regulation of ontogenesis?
12. What are the mechanisms of hormonal regulation in ontogeny?
13. What are the possible ways of action of environmental factors that cause violation of embryogenesis?
14. Why are embryopathies characterized by deeper disorders than fetopathy?
15. How is the relationship between the mother's body and the fetus, what are the consequences of its violation?
16. What is the difference between hereditary and non-hereditary congenital diseases?
17. What are phenocopies?
18. Violations of what processes in ontogenesis lead to malformations?
19. What are teratogens, their classification, mechanism of action?
Test tasks
Choose one correct answer.
1. GENETIC REGULATION OF ONTOGENESIS
IN VERTEBRATES IT IS CARRIED OUT BY:
1. Reducing the number of genes in the process of development
2. Gene repression
3. Gene derepression
4. Derepression and repression of genes
2. WHEN CLONING REGULATE THE DEVELOPMENT OF THE EMBRYO
1. Sperm
2. Eggs
3. Sperm and eggs
4. Somatic cell
5. Egg and somatic cell donor
3. NONHEREDITARY DEFECTS
OF THE DENTAL SYSTEM ARE TO:
1. Fetopathy
2. Gametopathies
3. Embryopathies
4. Blastopathies
4. HORMONAL REGULATION OF DEVELOPMENT
IN MAMMALS STARTS IN THE PERIOD:
1. Gastrulation
2. Crushing
3. Histo- and organogenesis
4. Fetal
5. THE DOCTRINE ABOUT THE GEM DEVELOPMENT OF ORGANISMS BY SUCCESSIVE FORMATIONS OF NEW STRUCTURES IS CALLED:
1. Preformism
2. Epigenesis
3. Transformation
4. Vitalism
Choose multiple correct answers.
6. THE LAYING AND DEVELOPMENT OF THE RUGILS OF TEETH IN A HUMAN IS REGULATED:
2. Embryonic induction
3. Nervous system
4. Hormones
5. Environmental factors
7. NON-CLEARING OF THE SECONDARY PALATE IN A HUMAN IS DUE TO DISTURBANCE OF CELLULAR PROCESSES:
1. Selective breeding
2. Thickening of mesodermal cells
3. Selective death
4. Adhesion
5. Move
8. THE STAGE OF DEPENDENT DIFFERENTIATION OF CELLS IS CHARACTERIZED:
1. Increased sensitivity to the action of inductors
2. Decreased sensitivity to the action of inductors
3. Lack of ability to transdifferentiate
4. Ability to transdifferentiate
9. THE GREATEST SENSITIVITY OF THE FETAL ORGANS
TO THE ACTION OF THE TERATOGEN IN THE PERIODS:
1. Bookmarks of the rudiments of organs
2. Bookmarks of new organ structures
3. Organ cell differentiation
4. body growth
Set a match.
10. malformations:
1. Hereditary
2. Non-hereditary
MECHANISMS OF APPEARANCE:
a) Generative mutations
b) Mutations in blastomeres
c) Mutations in the cells of the rudimentary organs
d) Violation of the functions of genes
e) Violation of the laying of organs
Literature
Main
Biology / Ed. V.N. Yarygin. - M.: Higher school, 2001. - Book. 1. - S. 150, 280-282, 294, 295, 297, 298, 317-368, 372, 409-418. Pekhov A.P. Biology and general genetics. - M.: Publishing house of RUDN University, 1993. -
Methodical development
laboratory lesson No. 11 for I-year students.
Topic of the lesson: "Regulation of ontogenesis".
Completed by (a) student (ka) of the 1st year
medical institute
31- _____ groups
FULL NAME._________________________
_________________________
Surgut, 2010
Purpose of the lesson : To study the main mechanisms of regulation of ontogenesis, critical periods of human ontogenesis; the influence of harmful factors on the fetus and the mechanisms of the formation of malformations.
Questions for self-preparation of students:
Regulatory and mosaic type of development, their differences.
What is the essence of cell differentiation?
How is the regulation of the early stages of embryonic development; When does the embryonic genome begin to function?
What is the role of genes in early development?
How does the genetic potency of cell nuclei change during development?
How is genetic regulation of differentiation carried out?
What is the difference between the interaction of cells during the period of crushing, gastrulation, organogenesis?
What is the significance of the contact of blastomeres, what does their separation lead to?
Is it possible for a mammalian embryo to develop from a mixture of cells from two or three embryos?
What are the main forms of cell interaction during periods of organogenesis?
What is the essence of embryonic induction, its types?
What is the chemical structure of inductors and their mechanism of action?
What is the importance of the nervous system in the regulation of ontogeny?
What is the essence of humoral regulation of ontogeny, types of regulators.
What are the mechanisms of hormonal regulation in ontogeny?
What is the significance of morphogenetic fields in embryogenesis?
What are the possible ways of action of environmental factors that cause disruption of embryogenesis?
Why are embryopathies characterized by deeper disorders than fetopathy?
How is the relationship between the mother's body and the fetus carried out, what are the consequences of its violation?
What is the difference between hereditary and non-hereditary congenital disorders?
What are phenocopies?
Violations of what processes in ontogeny lead to malformations?
What are the critical periods of embryogenesis?
What are teratogens; their classification, mechanism of action?
Task for students.
Work 1. Regulation of the development of placental mammals.
Rewrite table. 1.
Table 1
| Periods of ontogeny | Types of regulation |
||||||
| genetic | contact interaction of cells | embryonic induction | morphogenetic fields | nervous | hormonal (fetal hormones) | environmental factors |
|
| Progenesis Embryogenesis: Embryo at the stage of crushing Blastula gastrula Embryo at the stage of organogenesis Embryo during the fetal period ^
Postembryonic period
| + mother's genome | ||||||
^ Work 2. Genetic regulation of organism development.
Genes regulate and control the development of an organism at all stages of ontogeny (Fig. 1).
Rice. 1. Genetic control of development of mammals [Konyukhov BV, 1976].
During oogenesis in the cytoplasm of the egg, maternal RNAs are synthesized and deposited, which carry information about proteins and control the development of the embryo from the zygote to the blastula stage. The genes of the embryo begin to function in vertebrates at different stages of cleavage (for example, in humans at the stage of two blastomeres), and the products of their activity begin to regulate the development of the embryo. Thus, the early stages of development are regulated by maternal and germinal genes. Starting from the gastrula stage in vertebrates, the development of the organism is regulated only by the products of the activity of the embryo's own genes.
The regulation of gene expression during the development of organisms is carried out at all stages of protein synthesis, both by the type of induction and by the type of repression, and control at the transcription level determines the time of functioning and the nature of transcription of a given gene.
Analyze some models of genetic regulation at the level of transcription (Fig. 2). Draw model 1.
Rice. 2. Genetic regulation at the level of transcription.
A - model 1: cascade embryonic induction; b - model 2: repression by the end product; c - model 3: regulation of gene expression by several regulatory genes; d - model 4: regulation of several groups of structural genes by one gene.
Designate:
C, sensory gene;
I, integrator gene;
P, promoter;
SG, structural genes;
O - inductor;
Δ is a repressor.
Model 1. Cascade embryonic induction (Fig. 2a).
Inductor 1 interacts with the sensor gene (C), activating the integrator gene (I), the product of which acts through the promoter (P) on structural genes (SG 1, SG 2 and SG 3). In turn, the product of the activity of SG 3 is an inducer 2 for the structural genes SG 4 , SG 5, etc.
Model 2. Repression by the end product (Fig. 2b).
The activity products of structural genes, in turn, repress the activity of the gene that controls the synthesis of inductor 1.
Model 3. Regulation of gene expression by several regulatory genes (Fig. 2c).
Structural genes are activated or repressed by the action products of several genes.
Model 4. Regulation of several groups of structural genes by one gene (Fig. 2d).
Induction or repression of several structural genes by the product of the activity of one gene. This model can explain the pleiotropic effect of genes, the influence of sex hormones, etc.
^ Work 3. Polytene chromosomes.
Only a small part of the genome is involved in the creation of tissue-specific products. Sites of active mRNA synthesis - puffs - are clearly visible in polytene (giant) chromosomes and are unraveled sections of chromosomes that form a less compact structure.
A. Examine the micropreparation under a microscope at high magnification and draw. Designate: 1 - euchromatin, 2 - heterochromatin, 3 - puff.
B. Examine according to fig. 3 region of the polytene chromosome undergoing poofing (according to Grossbach, 1973, from Gilbert S., 1994). Draw fig. 3, Mr.
Rice. 3. Puffing process.
A-d - stages of pouffe formation;
Rice. 3. The Puffing Process (Continued)
D - poofing in polytene chromosomes in dynamics.
Work 4. Regulatory ability of nuclei. Cloning.
In ontogeny, during cell differentiation, selective expression of different parts of the genome occurs and the genetic potency of differentiated cells is limited. However, all genes are preserved in the nuclei of somatic cells, and under appropriate conditions they can be reactivated and ensure the development of a normal embryo. Cloning is the development of a new organism that is an exact genetic copy of the parent. In sexually reproducing species, cloning occurs when nuclei are transferred from a somatic cell to an enucleated egg. When cloned, a young individual is an exact copy of the donor organism of somatic cell nuclei. Currently obtained by cloning animals of different classes, including mammals. It turned out that in the process of development, the genetic potency of the nuclei of somatic cells decreases, and the older the donor of somatic nuclei, the lower the percentage of development of cloned individuals. In addition, it was found that the genetic potency of different donor cells is not the same.
Examine the drawings on the transplantation of nuclei taken from somatic cells at different stages of frog development (according to Gurdon, 1965, from E. Deucar, 1978) (Fig. 4).
^ Fig. 4. Transplantation of nuclei from somatic cells into frog eggs at different stages of development of donor cells.
Work 5. Interaction of blastomeres during cleavage, (medical Faculty).
A. Influence of the position of blastomeres on their differentiation. Cell differentiation is influenced by its position in a certain place of the embryo at a certain time. In placental animals, until the completion of the eight-cell stage, different blastomeres do not differ from each other in morphology, biochemistry, and potency. However, compactization (rapprochement and increased contact of blastomeres with the formation of a compact cell ball) leads to the formation of outer and inner cells, which differ sharply in their properties. The outer cells form the trophoblast, while the inner cells form the embryo. Experience in blastomere transplantation shows that the formation of trophoblast or embryonic cells from blastomeres is determined by where the cell is located - on the surface or inside a group of cells.
Study fig. 5, and transplantation of blastomeres in mouse embryos [Mints B., 1970; Hillman et al., 1972].
Rice. 5. Interaction of blastomeres during cleavage.
A - transplantation of blastomeres into mouse embryos; b - connection of blastomeres in mouse embryos: 1 - embryo, 2 - trophoblast; c - mechanisms of formation of identical twins and twin deformities in humans: 1 - internal cells of the blastocyst; 2 - blastocyst cavity; 3 - embryo; 4 - amnion cavity; 5 - chorion cavity; 6 - not completely separated twins.
b. Influence of blastomere contact on the development of the embryo. The formation of identical twins and twin deformities in humans.
While maintaining full contact of blastomeres, one organism develops. Also, one organism develops when the blastomeres of several embryos combine. After a special impact, the blastomeres of several four-celled embryos can join to form a common morula. For example, if the blastomeres of embryos of three different lines with contrasting coloration (white, black, and red) are combined, a morula is formed, from which mice develop with differently colored areas of the skin. This is due to the mixing of blastomeres of the embryos of different lines of mice, some of which went to the formation of the embryo and indicates that the hereditary material of the blastomeres does not mix.
Study fig. 5b - connection of blastomeres in embryos [Gilbert S, 1993].
Loss of contact between blastomeres changes their fate. Separation of embryonic cells in the early stages of development leads to the formation of identical twins, since early blastomeres are totipotent. Incomplete separation of the cells of the embryo leads to the appearance of twin deformities, which can be in different species of invertebrates, vertebrates and humans.
Review slides, tables, drawings with examples of twin deformities in different species of animals and humans.
Study fig. 5, c, which shows the mechanism of formation of identical twins and twin malformations in humans [from: Gilbert S., 1993, revised].
Rice. 5. Continuation.
In about 33% of cases, the separation of blastomeres occurs before the formation of a trophoblast. Twins have their own chorion and amnion.
Separation of blastomeres after trophoblast formation but before amnion formation occurs in about 66% of cases. Twins have their own amniotic membranes, but are in a common chorion.
Separation of blastomeres after amnion formation occurs rarely, in a few percent of cases. Twins share amnion and chorion.
Incomplete separation of embryonic cells. Twins have common parts of the body (twin malformation).
Work 6. Cellular processes during periods of gastrulation and organogenesis.
Study table. 2, fig. 6 and 7, animal embryogenesis slides and slides. Rewrite the table.
Rice. 6. Successive stages of face formation (front view). a - 4-week embryo (3.5 mm.); b - 5-week embryo (6.5 mm); c - 5.5-week-old fetus (9 mm); d - 6-week-old fetus (12 mm); e - 7-week-old fetus (19 mm); f - 8-week-old fetus (28 mm). 1 - frontal ledge; 2 - olfactory placode; 3 - nasal fossa; 4 - oral plate; 5 - mouth opening; 6 - maxillary process; 7 - mandibular arch; 8 - hyoid arc; 9 - medial nasal process; 10 - lateral nasal process; 11 - nasolacrimal groove; 12 - hyomandibular fissure; 13 - filtrum area formed by merged medial nasal processes; 14 - outer ear; 15 - auditory tubercles around the hyomandibular fissure; 16 - hyoid bone; 17 - cartilages of the larynx.
table 2
| Forms of cellular interactions | Formation of normal structures (examples) | Consequences of violations of intercellular interactions (examples) |
| ^ Cellular movements Selective cell reproduction selective cell death Cell adhesion Cellular condensation | The movement of cells during gastrulation, during the formation of the neural tube, during the movement of primary germ cells. The laying of the rudiments of individual organs. Separation of fingers, death of epithelial cells during the fusion of the palatine rudiments, nasal processes. Death of neuroepithelial cells during the formation of the neural tube. The formation of the neural tube from the neural plate, the fusion of the rudiments of facial structures (palatine processes, nasal processes with each other and with the maxillary processes). Formation of limb buds. | Violation of the formation of gastrula, neural tube; violation of the structure, change in the number or absence of gonads. The absence of an organ or its share. Syndactyly, cleft palate, cleft lip, face, spinal hernia. Spinal hernia, cleft palate, upper lip, face. Lack of limbs, extra limbs. |
Rice. 7. Development of the palate in the embryo of a pig [Karlson B., 1983].
A-d - stages of development of the secondary palate (preparation of the roof of the oral cavity, x 5); e, f (transverse sections illustrating before and after lowering the tongue, 1 - upper lip; 2 - median palatine process; 3 - lateral palatine process; 4 - nasal septum; 5 - tongue; 6 - suture of the palate.
Work 7. Embryonic induction.
Disassemble fig. 8, a, b, draw and label the main structures.
Rice. 8. Embryonic induction of the kidney and tooth in mammals, a - development of the kidneys: 1 - pronephros. 2 - mesonephric canal, 3 - mesenchyme of the primary kidney, 4 - primary kidney, 5 - outgrowth of the ureter of the secondary kidney, 6 - mesenchyme of the secondary kidney, 7 - rudiment of the secondary kidney, → induction; b - early stages of tooth development: I - gum of the lower jaw (top view): II - transverse section of the gum; III-VI - stages of tooth development: 1 - gingival crest, 2 - dental plate, 3 - mesodermal dental papillae, 4 - rudiment of the enamel organ, 5 - ameloblasts, 6 - rudiment of enamel, 7 - odontoblasts, 8 - rudiment of dentin, 9 - rudiment of pulp, 10 - enamel, 11 - dentin; → induction; ↔ - mutual induction.
^ Medical Faculty :
A. Embryonic induction causing the development of kidneys in mammals (Fig. 8, a).
The mesonephric (Wolffian) canal induces the formation of the primary kidney. The outgrowth of the ureter from the mesonephric canal induces the formation of a secondary kidney, which in turn supports the growth of the ureter. Metanephrogenic mesenchyme induces branching of the ureter. The branching epithelium of the ureter induces mesenchyme to form renal tubules.
^ Faculty of Dentistry
B. Embryonic induction, which determines the development of the tooth in mammals (Fig. 8, b) [Dyukar E., 1978].
The first rudiment of teeth - the dental plate, a thickened strip of ectoderm along the gum crest, develops independently of the mesoderm. Under the dental plate, a number of mesodermal dental papillae appear, which induce the formation of rudiments of the enamel organ from the ectoderm (when the mesodermal papillae are removed, the rudiments of the enamel organ are not formed). Mutual induction between the enamel organ and the mesodermal dental papilla leads to the formation of cells that form enamel, dentin, and pulp. At the next stage of differentiation, the emerging enamel and dentin mutually influence each other's development.
Work 8. The relationship of the nervous system and the organ innervated by it in ontogenesis.
The interaction between the CNS centers and the innervated organs is established at the early stages of embryogenesis, and these structures mutually stimulate each other's development. The absence of peripheral nerves or their damage (for example, drugs, toxoplasma toxins, etc.) cause a violation of the formation of the structures innervated by them. For example, in Europe, several hundred children were born with no limbs, whose mothers took the sleeping pill thalidomide during pregnancy.
In the postnatal period, the relationship between the nervous system and the innervated organs is preserved. Birth injuries of the brain and peripheral nerves lead not only to paralysis, but also to muscle atrophy and growth retardation of the corresponding limbs or unilateral hypotrophy of facial structures (with congenital paralysis of the VI-VII cranial nerves). Passive movements contribute to the restoration of damaged structures of the brain and spinal cord (special devices have been created for this), massage and physiotherapeutic stimulation of the innervated organs.
With neurofibromatosis (an autosomal dominant type of inheritance), tumors of the peripheral nerves develop. If the disease starts at early childhood, then on the side of the body where tumors develop, hypertrophy of bones and soft tissues occurs. For example, facial dysmorphosis develops (asymmetric, disproportionate development of the structures that form the face).
It has been established that in early childhood games that promote the movement of the hands, especially small, precise forms of activity, stimulate the development of brain structures, including the development of intelligence.
Analyze the schemes of experiments to study the relationship between nerve centers and innervated organs.
Removal of a nerve on the left side of the axolotl embryo resulted in the absence of a limb on the operated side of the body. The absence of a limb may be due to the action of neurotropic teratogens (toxoplasmosis toxins, thalidomide, etc.) (Fig. 9, a).
Removal of the limb rudiment from the axolotl embryo leads to a decrease in the size of the ganglia and horns of the gray matter of the spinal cord on the operated side (Fig. 9b).
Rice. 9. The relationship of nerve centers and innervated organs [Dyukar E., 1978, with changes].
A - the influence of the spinal nerves on the development of the limb: 1 - spinal cord, 2 - spinal nerve innervating the limb, 3 - spinal ganglion, 4 - limb; b - the influence of the limb rudiment on the development of spinal segments (transverse media of the axolotl embryo with the limb rudiment removed: 1 - spinal ganglion, 2 - spinal nerve, 3 - dorsal horns of the gray matter of the spinal cord, 4 - ventral horns of the gray matter of the spinal cord.
Work 9. Hormonal regulation of ontogeny in placental mammals.
Study according to the table. 3 effects of hormones on the development of the body.
Table 3
| Source of Education Hormone | Hormones | Main Effects |
| Hypothalamus Pituitary ^ Pineal gland (pineal gland) thyroid gland pancreas adrenal glands Ovaries: follicles corpus luteum Placenta testicles thymus | Liberians GnRH Somatropic hormone Thyroid Stimulating Hormone(s) Adrenocorticotropic Hormone (ACTH) Gonadotropins: A) follicle stimulating hormone (FSH) B) luteinizing hormone C) prolactin (luteotropic hormone - LTH) Melatonin (synthesized at night) Serotonin (synthesized during the day) thyroxine Insulin Cortisol Estrogens Progesterone Progesterone Chorionic somatomammotropin (placental growth hormone) Testosterone Paramesonephric duct inhibitory factor Dihydrotestosterone thymosin | In early embryogenesis, hypothalamic hormones influence the differentiation and migration of neurons. In late embryogenesis and the postnatal period, they regulate development indirectly by changing the synthesis of pituitary hormones. Enhance the synthesis of adenohypophysis hormones. They inhibit the synthesis of adenohypophysis hormones. Determines the moment of onset of puberty and the nature of sexual behavior. Enhances cell proliferation and protein synthesis. Regulates growth in the postnatal period. Accelerates the growth and differentiation of thyroid cells. Stimulates the growth of the adrenal glands and the production of steroids. They enhance the proliferation of stem cells, the growth of follicles in the ovaries, stimulate the growth of seminiferous tubules and testes, the formation of sex hormones in the gonads. Initiate gametogenesis. Maintains the corpus luteum of pregnancy in an active state. Stimulates breast growth and milk secretion. Regulates daily allowance biological rhythms, puberty and reproductive functions. Serotonin-sensitive neurons regulate behavior, sleep, and thermoregulation processes. Regulation of motor activity of the digestive tract. Increases the intensity of metabolism and protein synthesis; regulates the development of the brain, growth and proportions of the body. Necessary for the normal development of skin derivatives. Initiates differentiation of the mammary gland. Enhances proliferation. It is necessary for the normal development of many organs in the later stages of ontogenesis. Stimulates later stages differentiation of the mammary glands. Stimulate the development of female secondary sexual characteristics; promote proliferation and secretion in uterine epithelial cells; initial changes in the mammary glands. Preservation of pregnancy; further differentiation of the mammary glands. Further proliferation of the uterine epithelium and preservation of pregnancy; further differentiation of the mammary glands. Action similar to growth hormone and pituitary prolactin. Determines the development of the male reproductive tract, testicles, secondary sexual characteristics and hormonal function of the hypothalamus (in embryogenesis), inhibits the development of the mammary glands, regulates body growth. Regression of the paramesonephric Müllerian ducts. Development of the prostate gland, penis, scrotum. Proliferation of T-lymphocytes. |
Work 10. Impact of harmful environmental factors on the embryo.
Examine Table 4, disassemble and draw Scheme 1, give examples of direct and indirect damage to the embryo.
Table 4
| Factors | Main mechanisms of violations | Embryo- and fetopathy |
| I. Maternal malnutrition 1. Starvation and malnutrition 2. Protein deficiency 3. Vitamin deficiency (often without maternal hypovitaminosis): Vitamin A vitamin B2 vitamin C vitamin E folic acid 4. Excess vitamins: Vitamin A vitamin C ^ II. Maternal illnesses
4. Anemia 5. Diabetes 6. Thyrotoxicosis 7. Pathology of the adrenal glands 8. Immunological conflict (according to the Rh factor and the AB0 system; most often incompatible: 0 - A, 0 - B, A - B, B - A, combinations of maternal and fetal blood groups) III. Intrauterine infections 1. Rubella virus 2. Influenza virus 3. Polio virus 4. Viral hepatitis (Botkin's disease) Toxoplasmosis ^ IV. ionizing radiation V. Influence of chemical compounds, including medicinal substances (more than 600 compounds) Alcohol | Violation of the trophism of the embryo. Metabolic disorders in the fetus. Violation of redox processes in the epithelium. Growth failure, formation of biological oxidation enzymes. Violation of the processes of oxidation, formation of connective tissue, biosynthesis. Violation of fat oxidation, leading to the appearance of toxic products. Violation of the synthesis of a number of amino acids, methyl groups. Violation of growth, redox processes. Hypoxia, violation of trophism, dystrophic changes in the placenta. Hypoxia, violation of trophism, dystrophic changes in the placenta. Hypoxia, impaired uteroplacental circulation, morphological and functional disorders of the placenta. Violated oxygen transport to the fetus, iron deficiency, morphological changes in the placenta. Hormonal changes, hyperglycemia and ketoacidosis, deterioration of uteroplacental circulation, pathological changes in the placenta. Increased secretion of thyroid hormones. Deficiency or excess of adrenal hormones. Rh antibodies cross the placenta. Penetration through the placenta of incomplete isoimmune antibodies A and B, which cause hemolysis of fetal erythrocytes. The released indirect bilirubin is a strong tissue toxin. Infection of the embryo, especially in the first three months of development. Infection of the fetus, intoxication of the mother's body, hyperthermia, impaired uteroplacental circulation. The virus crosses the placenta, causing disease. Pathological changes in the maternal organism, changes in the placenta. The defeat of the embryo by penetrating radiation and toxic products of damaged tissues. direct effect on the fetus. Violation of the structure and function of the placenta. Pathological changes in the mother's body. Direct toxic effect on the fetus, placenta and mother's body. Damage to gametes, generative mutations. direct toxic effect. | Fetal hypotrophy, various developmental anomalies, mainly of the central nervous system, stillbirth, weakened, disease-prone children. Defects of the organs of vision and the genitourinary system. Deformity of the extremities, splitting of the hard palate, hydronephrosis, hydrocephalus, heart anomalies, etc. Possible death of the fetus, miscarriage. Anomalies of the brain, eyes, skeleton. Defects of the heart and blood vessels. Cleft palate, anencephaly. The chance of miscarriage increases. Fetal hypotrophy, functional immaturity, anomalies of organs and systems, mainly cardiovascular. Children often have infectious-allergic diseases and disorders of the nervous system. Fetal hypotrophy. Malformations, mainly of the heart and blood vessels. Fetal hypotrophy, disorders of the cardiovascular system. Increased incidence in children. Fetal death, violation of the central nervous system, anemia in children. Fetal death, premature, immature fruits with increased weight, functional immaturity of the pancreas, lungs, less often changes in the thyroid gland, kidneys. Anencephaly, hydronephrosis, and other disorders of the central nervous system occur Violation of the formation of the central nervous system, thyroid gland and, to a lesser extent, other endocrine glands. Less commonly, anomalies of the cardiovascular system, musculoskeletal, sexual, etc. Functional inferiority of the adrenal glands. Hemolytic disease of the fetus and newborn. Anomalies of the heart, brain, organs of hearing, vision, etc. Genital malformations, cataracts, cleft lip. congenital poliomyelitis. Deformities at different stages of development. Congenital viral hepatitis complicated by cirrhosis of the liver; developmental delay. Deformities of the brain, eyes, limbs, "cleft palate", heart defects, diseases of the endocrine organs. Congenital radiation sickness. The most common paralysis of the nervous system. There may be anomalies of the eyes, blood vessels, lungs, liver, genitourinary organs, limbs. Various malformations depending on the substance, dose and time of admission. Hypotrophy, the tendency of children to respiratory diseases. Mental retardation, mental illness, heart defects, epilepsy, fetal alcohol damage. |
Scheme 1. Impact of harmful environmental factors on the embryo.
Job 11. Critical periods in human ontogenesis.
Study and rewrite the table. 5.
Table 5
| Periods of human ontogenesis | Critical periods | Possible violations development |
| Preimplantation and implantation The period of histo- and organogenesis and the onset of placentation Perinatal period (birth) Neonatal period Adolescent (pubertal) Climacteric | For the whole fetus For different organs and systems do not coincide in time For the whole body and individual organs and systems For the whole body and individual organs and systems For the whole body and individual organs and systems | Embryo death Twin deformities hereditary diseases Malformations and anomalies in the development of various organs and systems, the death of the embryo Trauma, cerebral palsy, dementia, death High probability of overheating, hypothermia, pathology of various organisms and systems, non-specific infections and death The risk of manifestation of non-hereditary diseases, metabolic disorders, adolescent behavioral disorders, mental vulnerability, aggressiveness is increased. Mortality is on the rise The risk of developing somatic and mental illnesses increases, the incidence of tumors increases. Mortality rises |
^ Work 12. Classification and mechanisms of formation of malformations.
Study and rewrite the information on the classification of mechanisms for the formation of malformations.
^ I. On an etiological basis.
1. Hereditary: a) generative mutations (hereditary diseases); b) mutations in the zygote and blastomeres (hereditary diseases, mosaicism).
2. Non-hereditary: a) violation of the implementation of genetic information (phenocopy); b) violation of the interaction of cells and tissues; malformations of organs and tissues (teratomas, cysts); c) somatic mutations (congenital tumors.)
3. Multifactorial.
II. By the period of ontogenesis.
Gametopathies: a) hereditary; b) non-hereditary (overripe gametes).
Blastopathies until the 15th day; a) hereditary diseases (mosaicism - the embryo consists of cells with a normal and atypical set of chromosomes); b) not hereditary (twin deformities, cyclopia, sirenomelia).
Embryopathies before the end of the 8th week: most malformations, malformations caused by the action of teratogens.
Phenopathies from 9 weeks before giving birth. The defects of this group are rare: the remains of embryonic structures (persistence); preservation of the original arrangement of organs, for example, cryptorchidism; underdevelopment of individual organs or the entire fetus, deviations in the development of organs.
^ vices, emerging to postnatal period (they occur less frequently than the above defects, due to injuries or diseases).
Control of the final level of knowledge:
Test tasks
1. Choose one correct answer.
^ THE DOCTRINE OF THE GEM DEVELOPMENT OF ORGANISMS BY SUCCESSIVE FORMATIONS OF NEW STRUCTURES IS CALLED:
Preformism.
Epigenesis.
Transformism.
Vitalism.
2. Choose one correct answer.
^ GENETIC REGULATION OF ONTOGENESIS IN VERTEBRATES IS CARRIED OUT BY:
1. Reducing the number of genes in the process of development.
2. Repression of genes.
3. Gene derepression.
4. Derepression and repression of genes.
3. Choose one correct answer.
^
WHEN CLONED, THE GENES REGULATE THE DEVELOPMENT OF THE FETAL:
Sperm.
Oocytes.
Spermatozoa and eggs.
somatic cell.
4. Choose one correct answer.
^ Identical twins are formed as a result;
Segregation of embryonic cells at the gastrula stage.
Separation of embryonic cells at the stage of differentiation of the germ layers.
Complete divergence of blastomeres.
Incomplete divergence of blastomeres.
^
DURING THE FORMATION OF A NEURAL TUBE IS OCCURRED:
Selective cell proliferation.
Thickening of mesodermal cells.
selective cell death.
cell adhesion.
6. Choose one correct answer.
^
EMBRYO INDUCTION BEGINS TO REGULATE THE DEVELOPMENT OF VERTEBRATES IN THE PERIOD:
Crushing.
early gastrulation.
Neurulation.
Organogenesis.
7. Choose multiple correct answers.
^ THE STAGE OF DEPENDENT DIFFERENTIATION OF CELLS IS CHARACTERIZED:
Increased sensitivity to the action of inductors.
Decreased sensitivity to the action of inductors.
Lack of ability to transdifferentiate.
The ability to transdifferentiate.
^
HORMONAL REGULATION OF DEVELOPMENT IN MAMMALS STARTS IN THE PERIOD:
Gastrulation.
Crushing.
Histo- and organogenesis.
Fetal.
9. Choose multiple correct answers.
^
THE GREATEST SENSITIVITY OF THE FETAL ORGANS TO THE ACTION OF A TERATOGEN DURING THE PERIODS:
Bookmarks of the rudiments of organs.
Bookmarks of new organ structures.
Organ cell differentiation.
Organ growth.
10. Match.
^ DEVELOPMENTAL FAULTS: MECHANISMS OF APPEARANCE:
Hereditary. a) generative mutations;
Non-hereditary. b) mutations in blastomeres;
D) violation of the functions of genes;
D) violation of the laying of organs.
Terms:
Adhesion, biological death, adulthood, humoral regulation of ontogenesis, definitive structures of organs, pre-reproductive period, embryo, embryonic membranes, critical period of development, critical periods of embryogenesis, larval development, development of a sexually mature organism, reproductive period, post-reproductive period, puberty, direct development , indirect development (development with metamorphosis), sirenomelia, aging, cyclopia, juvenile period, embryonic induction.
Main literature
1. Biology / Ed. V.N. Yarygin. - M.: Higher school, 2001. - Book. 1. - S. 150, 280-282, 294-295, 297-298, 317-368, 372, 409-418.
2. Pekhov A.P. Biology and general genetics. - M.: Publishing House of RUDN University, 1993. - S. 166, 201-219.
additional literature
1. Gazaryan K.G., Belousov M.V. Biology of individual development of animals. - M.: Higher school, 1983.
2. Gilbert S. Developed biology. - M.: Mir, 19^9.3, v. 1; 1994, v. 2; 1995, v. 3.
1) Levels of regulation of ontogenesis
The expression of all genes is regulated at different levels:
1. Regulation on gene level happens in different ways
1.1. DNA modification (for example, replacing cytosine or guanine with methylcytosine or methylguanine; base methylation reduces gene activity). 1.2. An increase in the volume of DNA in a cell by differential amplification of DNA (for example, multiple copying of rRNA genes) or due to the formation of polytene chromosomes.1.3. Programmed quantitative changes in DNA (for example, a change in the orientation of the promoter). 1.4. DNA splicing (for example, excision of sections of genes encoding antibodies). 1.5. Chromatin diminution is an irreversible loss of a part of the genetic material in the somatic cells of some organisms (ciliates, roundworms, cyclops). 1.6. Changes in the activity of whole chromosomes (for example, inactivation of one of the two X chromosomes in female mammals). 1.7. Modification of DNA sequences using mobile genetic elements, such as transposons.
2. Regulation on transcription level– by regulation of mRNA transcription. The intensive functioning of individual genes or their blocks corresponds to certain stages of development and differentiation. Transcriptional regulators in animals are often steroid hormones.
3. Regulation on splicing level(post-transcriptional modification of mRNA) - provides the possibility of formation various types mature, functionally active mRNA. RNA processing is regulated by ribozymes (catalysts of ribonucleic nature) and maturase enzymes. Some human genetic diseases (phenylketonuria, some hemoglobinopathies) are caused by splicing disorders.
4. Regulation on translation level- due to different activities of different types of mRNA.
5. Regulation on the level of post-translational modification of proteins- regulated by post-translational modification of proteins (phosphorylation, acetylation, cleavage of the original polypeptide chain into smaller fragments, etc.).
The considered examples testify to the variety of ways of implementing genetic information by regulating the activity of the genes themselves or their products. However, it should be noted that regulation at the level of transcription is most economical for the cell, since it prevents the formation of the corresponding mRNAs and proteins when the cell does not need them. At the same time, regulation at the transcriptional level proceeds relatively slowly, whereas, for example, activation of proteins by cleavage of precursor molecules, although uneconomical, occurs very quickly.
2) Genes that regulate the course of ontogenesis
The course of ontogenesis is determined by gene-regulatory networks (cascades). They involve signal proteins and other substances (“morphogens”; secreted by the cell into the surrounding intercellular space), receptors, transcription factors, and small regulatory RNAs. Enhancers (TF binding sites) in the regulatory regions of regulatory genes are an important component of the “genetic program of development”. It depends on the enhancers which switches (and therefore, where and when) the given gene will be turned on.
In all animals, a special family of genes, the HOX genes, is responsible for marking the embryo along the anterior-posterior axis. First found in Drosophila, then in all animals.
The discovery of similar Hox genes in different types of animals made us take a fresh look at the morphogenesis of animals and its transformations in the course of evolution. It became clear that by changing one gene or the time (or place) of its inclusion, it is possible to transform, create, remove or transfer to another place an entire organ at once, while maintaining the general plan of the structure. Hox genes in Drosophila, humans, and many other animals are located in the chromosome in a strict order, in the same order in which differentiation of the main parts of the body of a bilaterally symmetrical animal occurs. First, the genes responsible for the structure of the organs on the head begin to work in the early embryo, then on the chest, then the genes begin to shape the tail.
The Hox gene family is divided into 14 classes. These 14 classes are believed to have arisen by duplication of one or a few original genes, the replicas then mutated and acquired new functions. Coelenterates and ctenophores have only 4 classes of Hox genes. The putative common ancestor of bilaterally symmetric animals must have had at least 8 of them. Mammals have all 14 classes. The principle of operation of these genes is the same. All of them are transcription factors, that is, their function is to "turn on" or "turn off" other genes. As a result of the work of Hox genes, a cascade of reactions is launched, leading to the appearance of the necessary proteins in the cell. Later it turned out that in some animals they are not located at all as correctly as in humans and Drosophila. In addition to the Hawks genes, there are many other developmental regulators. Most are pleiotropic. Pleiotropy is the multiplicity of functions and phenotypic manifestations. One and the same gene-regulator (TF) can regulate several completely different processes at different stages of embryonic development. These are “professional switches”, which, in principle, do not care what to switch (if the regulated gene had the right enhancer). Therefore, in the course of evolution, new “subroutines” can easily fall under their control. This is how new signs appear.
So, the course of ontogenesis is regulated by: chronogens, genes of spatial organization (see the manual on genetics)
3) The principle of the work of genes in ontogenesis
It is important to note that the process of building an individual of each species begins right from the first division. Therefore, we can say that the development of an individual occurs according to the strictest program of cell-by-cell construction, during which the step-by-step implementation of genetic information occurs, starting from the first division. The genome reflects precisely the strict cellular sequence of construction of any individual: from the first cell division to the complete formation of an individual, from the first cell to the second, from it to the 3rd, to the 4th, to the 5th .... to the “last”. It is this sequence of construction that is contained in the so-called. “the non-coding part of the genome, called by evolutionists the “garbage part” of the genome. A study of the works of Corresponding Member L.I. an individual that goes through a strictly sequential cell construction, when an embryo is first formed as an initial substrate from stem cells, then it is segmented and the rudiments (“kidneys”) of the main parts of the body are formed with their further development into semi-finished products, and further, into complete organs. Moreover, the entire program (algorithm) of such construction is recorded in the genome together with information about all the traits of the individual. Therefore, it can be argued that the construction program is actually information about all organs, members and systems! This is a single and inseparable information. There is no separate information in the genome about the construction plan (program) and separately about “hereditary traits”, i.e. on the composition and structure of bodies and members.
New and important in describing the structure of the genome and the process of ontogeny, I consider the following points to be noted. The entire life program of an individual, implemented by the genome, seems to be conveniently divided into 3 major stages:
1st - formation, construction of an individual until the moment of birth (the first and main part of the ontogeny program);
2nd - growth of an individual to maturity (the second important part of the ontogeny program);
3rd - aging and death.
It seems that all of them have their own characteristics and differ greatly in the mechanisms of software implementation.
The 1st period, the core of ontogenesis, is the most difficult programmatically, because it is necessary to build, form in the most closely interconnected, closely intertwined and interdependent all organs, members and systems of different protein content. And its essence is the control of cell-by-cell construction, control of cell division, when each cell has its “destiny” determined: whether it divides or not, and in the 2nd case, which somatic protein will fill it.
At the 2nd stage, in fact, it is not necessary to select protein, because. we are talking about the growth of an already formed individual, and it is only necessary to ensure strict proportionality of the growth of all members and organs of an already formed and formed protein structure (maybe with the exception of only reproductive system). For this, the genome probably contains sections of programs for the growth of all organs and members, as a continuation of the programs for their construction. Apparently, they are all built according to similar algorithms for a proportional increase in size and volume and are a continuation of organ construction programs. These are also very complex programs, incl. and proportional growth programs for toroidal structures such as hollow bones, blood vessels, and other structures of great complexity. At the same time, it is known that a large role in the growth process is played by growth hormone, the pituitary hormone, which largely determines the duration of growth and the final “size” of the individual.
At the 3rd stage, only the process of cell renewal takes place, by replacing them with “new” ones, but of worse quality, probably due to a deterioration in the quality of all processes of expression and cell division, transcription, translation and mitosis in general, caused, as it is considered today, by a constant decrease in length of telomeric ends of chromosomes. Moreover, each protein somatic tissue has a strictly defined renewal frequency, how often it will renew its cells. Brain cells, muscles of the heart, liver and some others are practically not updated.
General principles work of the program for managing the formation, construction of an individual in ontogenesis. It seems that the ontogeny program is based on the implementation of 3 main principles:
The 1st principle - “every cell has its own place”, is the principle of construction itself: the fate of each cell is predetermined and implemented through the standard procedure “division - non-division - specialization”. This information is sequentially read from a certain area (areas) of the genome and is implemented using the epigenetic mechanism: in the initial position, all genes of the genome are closed by methyl groups and, in accordance with the genome reading program, they are sequentially removed and the desired gene, next in the order of cell construction, is activated by the acetylation group histones. Further, this gene is again closed by a methyl group. It is possible that these "closing groups" on the nails and hair do not exist, and they grow constantly.
2nd principle, the principle of control and increase in the reliability of the correctness of construction: certain control Hox-genes (DNA sections) allow construction where necessary, in the area of \u200b\u200bits own responsibility, and prohibit construction where it is not necessary (so that teeth appear in the mouth and did not appear in any other place, the eyes in the previously prepared eye sockets of the head, and not on the arm, etc.).
3rd principle, the principle of combining programs: because most organs of both humans and animals are very complex, complex in nature and include the simultaneous formation of the bone skeleton, and blood vessels, and lymph, and various muscle tissues, skin tissues, nerves, tendons, neurons, hairline and much more, then all these individual programs are actually integrated into the corresponding cluster, and, as it were, nested, superimposed on each other. Implementation of the first principle. Because all organs and members constituting single organism individuals have a very complex, ornate, but quite definite, strictly specific look and shape, then by controlling the process of cell division it is easy to achieve almost any planned shape. This is achieved precisely by the fact that not all the cells that have appeared divide, i.e. there is a process of controlling the direction of division, and, accordingly, the direction of the construction of the organ, the formation of its shape. And the fate of each cell, from those just formed at the mitosis phase, in accordance with the general construction plan, is predetermined by the program: whether this cell will be subjected to differentiation, by expression in it of the corresponding protein-coding gene, or this cell will enter the phase of mitosis and will be subjected to further division. It is for this that interphase exists in the process of mitosis with stage G1 and critical point R. It is through the corresponding volume of trigger protein synthesis that the further fate of the cell at point R1 is determined. Those. the amount of this protein determines the further fate of the cell and, thus, the shape of the created organ or member. If a given cell does not divide, but is subject to specialization, then the content of the cell, i.e. the kind of protein in that specialized cell is known in advance from the purpose of that organ or member.
This successive-parallel process, this program for the realization of the fate of each cell, is actually the program of ontogenesis. Therefore, if a little trigger protein is formed in this cell, then this is the signal to start the process of specialization of this cell, and not to divide it. For further specialization, it is necessary to indicate to this cell what it should be in terms of protein content, i.e. which protein (or a group of proteins in case of alternative splicing) to activate in it exactly in accordance with the general plan and the general construction program. Obviously, in the process of reading the genome, the amount of the trigger protein is determined by the general program of construction (ontogenesis) and is encoded by a special DNA control sequence. It can be safely assumed that this information is contained in the "non-coding" part of the genome in the zone of dispersed (i.e. scattered) repetitive DNA sequences located between genes: their "long" (Line) repeats give the command to produce a trigger protein in large quantities (R is greater than the R threshold), and as a result, the cell goes into the division stage. If a short (Sine) sequence follows, then the trigger protein is produced below the threshold and the cell enters the specialization phase. The total number of dispersed DNA sequences in the genome is about 2 million, which is of the same order as the number of fetal cells before childbirth (about 200 million). order of formation of the shape of the organ. At the same time, the process of activation of these DNA repeats, most quickly, is carried out sequentially and formally using epigenetic markers: the removal of repressive methyl groups and the addition of activation groups - histone acetylation. Therefore, these, the so-called. "non-coding regions of DNA" are coding! They do not encode somatic proteins and amino acids, but regulatory proteins and amino acids.
4) Totipotency
TOTIPOTENCY The ability of individual cells in the process of realizing the genetic information contained in them not only to differentiate, but also to develop into a whole organism. Fertilized eggs of plants and animals are totipotent. Somatic cells of animals are characterized by tissue specificity from the early stages of embryonic development, and therefore they do not have totipotency. However, stem cells in renewing animal tissues within the same tissue type can develop in different directions. For example, mammalian hematopoietic stem cells give rise to erythrocytes and leukocytes. Plant somatic cells are able to fully realize their developmental potential with the formation of a whole organism. Specialized cells of various organs (leaf, root, flower) are capable of reproduction in an artificial environment outside the body. When creating an optimal ratio of phytohormones in a nutrient medium, cultivated cells can form shoots or turn into germ-like structures as a result of somatic embryogenesis, which then develop into a whole organism. The ability of plant somatic cells to exhibit totipotency depends on the genotype. The totipotency of somatic cells underlies their use in genetic and cell engineering. Homeotic mutations in Drosophila. Once segmentation is complete, homeotic genes come into play, a large class of genes that control the development of a body part from a specific segment. As a result of a homeotic mutation, some other part of the body develops from this segment. Among the homeotic genes, the best known are Bithorax-Complex (BX-C) and Antennapedia-Complex (Ant-C). In Drosophila, larvae and adults have pronounced segments: one head, three thoracic and eight abdominal. Each adult segment contains a set of differentiated morphological structures. The mesothoracic segment bears a pair of wings and a pair of legs, the metathoracic segment bears a pair of legs and a pair of halters - special club-shaped formations that help maintain balance in flight. There is a group of genes responsible for the formation of halters and abdominal segments. One of the genes influencing these processes is BX-C. Without this gene, the embryo develops to a certain stage and then dies. If this organism remained alive, then it would have 10 pairs of wings and 10 pairs of legs. The function of the BX-C gene is to inactivate the genes that form the legs and wings in all subsequent segments after the second thoracic segment. BX-C Complex Contains three different genes: Ubx, Abd-A and Abd-B. Each of them controls the formation of a certain group of segments. Mutations of these genes cause all subsequent segments to form like one of the previous ones. If all three genes are deleted, only the first thoracic (T1) and ninth abdominal (A9) segments controlled by other genes develop normally, all other segments (TK and all abdominal) develop as T2. If the Ubx gene is preserved, but Abd-A and Abd-B are damaged, all thoracic segments develop normally, and all abdominal segments are represented by the very first - A1. When the Abd-B gene is damaged, all the thoracic segments develop normally, then the abdominal segments Al, A2 and A3, and all the rest are formed as the A4 segment.
5) Mechanisms working in the process of ontogenesis(see Yarygin's textbook pp. 328-347)
6) Teratogens
Teratogenic effect (from the Greek τερατος "monster, freak, deformity") - a violation of embryonic development under the influence of teratogenic factors - some physical, chemical (including drugs) and biological agents (for example, viruses) with the occurrence of morphological abnormalities and malformations . Teratogenic factors include drugs, drugs, and many other substances. The following features of the influence of teratogenic factors are distinguished
The effect of teratogenic factors is dose-dependent. In different biological species, the dose-dependence of the teratogenic effect may vary. For each teratogenic factor, there is a certain threshold dose of teratogenic effect. Usually it is 1-3 orders of magnitude lower than the lethal one. Differences in teratogenic effects in different biological species, as well as in different representatives of the same species, are associated with the characteristics of absorption, metabolism, and the ability of a substance to spread in the body and cross the placenta.
Sensitivity to various teratogenic factors during fetal development may vary. The following periods of intrauterine development of a person are distinguished. Teratogens are a class of chemicals or physical influences, which have a teratogenic property expressed to varying degrees. These are, first of all, some medicines, drugs, alcohol, tobacco and marijuana smoking, cocaine, hormones, xenobiotics in general. environment(accumulated in huge quantities in the course of technological progress, especially over the last 1-1.5 centuries, chemical substances alien to the ancient biological structures of living beings), the negative effect of many of them on a developing organism is not known enough. See Thalidomide. Teratogenic, presumably, are some products of dysmetabolism that occur during diseases of the pregnant mother. Those substances that do not cause gross physical abnormalities, but are able to have a negative impact on behavioral, emotional or cognitive processes, and there are apparently much more such substances than teratogens themselves, are called behavioral or psychological teratogenic factors. Teratogens are also ionizing radiation that can cause mutations in the process of gametogenesis, electromagnetic radiation, mechanical factors (for example, tight corsets, with which women try to hide their pregnancy).
7) Types of malformations in humans
CNS malformations are polygenic diseases.
Exogenous factors include diabetes, deficiency folic acid, maternal intake of valproic acid, hyperthermia. Malformations of the central nervous system are also observed in monogenic diseases, for example, in Meckel-Gruber syndrome and Roberts syndrome, aneuploidy (trisomy on the 18th and 13th chromosomes), triploidy, and in translocations that give unbalanced gametes. Malformations of the central nervous system are also found in Goldenhar syndromes and OEIS (by the first letters of the following words: Omphalocele - hernia of the umbilical cord, Exstrophy of bladder - exstrophy Bladder, Imperforate anus - atresia anus, Sacral abnormalities - malformations of the sacrum).
The main congenital malformations of the CNS include anencephaly, vertebral fissure, encephalocele, exencephaly, and cleft of the spinal canal and skull. They form as a result of neural tube rupture. About 80% of CNS malformations are hydrocephalus. Often it is combined with other malformations of the central nervous system. Congenital heart defects: Congenital heart defects are often combined with other malformations. Concomitant gross malformations are present in every fourth child with congenital heart disease. In children with congenital heart defects, the prevalence of other malformations is 10 times higher.
The prevalence of congenital heart defects in newborns is 0.5-1%. 15% of deaths in children under the age of one year are due to congenital heart defects. Reasons: Genetic factors. Chromosomal abnormalities, predominantly trisomies. Monogenic diseases with autosomal dominant and recessive inheritance linked to the X chromosome. 2% of all congenital heart defects are associated with environmental factors. These include, in particular, the rubella virus, as well as drugs such as alcohol, trimethadione and lithium carbonate.
The genetic risk depends on the concomitant malformations and the cause of the disease. If a man suffers from congenital clubfoot (without concomitant defects), the risk of disease of siblings and children is about 3%. If a woman is sick, the risk for siblings is about 5% and for children it is 3%.
A diaphragmatic hernia is formed as a result of the movement of the abdominal organs (stomach, small intestine, less often the liver) into the chest cavity through a congenital defect of the diaphragm. Congenital hip dislocation is one of the most common malformations. Women are observed 6 times more often than men. With a breech presentation, the risk of this malformation increases by 10-15 times. If a woman is sick, the risk for siblings is 3-4%, and for sisters - 10%. If a man is sick, the risk is slightly higher. If the defect was observed in both parents and children, the genetic risk increases to 10-15%.
Gastrointestinal malformations: Pyloric stenosis, Duodenal atresia
(Considered a polygenic disease, although autosomal recessive inheritance has been described), Hirschsprung disease (congenital agangliosis of the colon).
8) Embryonic induction
Embryonic induction (from Latin mductio - guidance, excitation) - the influence of one embryonic germ (inductor) on the development (differentiation) of another; underlies organogenesis. Manifested at all stages of embryonic development. For example, in the blastula, the cells of the site of the future dorsal lip are inducers and affect the development of other parts of the embryo, in particular, the notochord.
The notochord, together with the mesoderm adjacent to it (the so-called chordomesoderm), in turn induces the laying of the nervous system; the part of the brain from which the retina of the eye is formed affects the adjacent part of the ectoderm, causing its differentiation into the cornea, etc.
Embryonic induction is carried out with direct contact and interaction of groups of cells with each other (surface interaction) or by transferring an inducing action through chemical substances that have the properties of low molecular weight proteins. The action of inductors, as a rule, is devoid of species specificity. The phenomenon of embryonic induction was discovered in 1901 by the German embryologist H. Spemann. Embryonic induction is only one of the mechanisms of ontogeny. Many developmental phenomena require other mechanisms. The section of the dorsal lip of the blastopore, which, when transplanted, causes the formation of mesoderm and neuroectoderm in a new place, was called the "Spemann organizer." (See Yarygin's textbook, pp. 347-353)
8) Persistence- this is a defect of the embryonic stage of development, consisting in the remainder of the embryonic structures after birth.
Atresia- this is a malformation, consisting in the absence of a hole in the organ.
Stenosis- this is a congenital or acquired abnormal narrowing of the lumen of any hollow organ (esophagus, intestines, blood vessel)
hypoplasia- these are developmental anomalies, consisting in the underdevelopment of a tissue, organ, part of the body or the whole organism.
Amplification(lat. amplificatio - amplification, increase), in molecular biology - the process of formation of additional copies of sections of chromosomal DNA, usually containing certain genes or segments of structural heterochromatin. Amplification may be a response of cells to a selective effect (for example, under the action of methotrexate). Amplification is one of the mechanisms for the activation of oncogenes during tumor development, for example, the N-myc oncogene during the development of neuroblastoma (the most common form of dense tissue cancer in children). Amplification is also the accumulation of copies of a specific nucleotide sequence during PCR - polymerase chain reaction.
In addition, see pp. 361-364 (Yarygin).
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