This is genes that cause the death of the organism before it reaches puberty. Lethal Genes are recessive. Here are a few examples of their influence: "cleft lip" and "cleft palate" - a defect in the development of the upper jaw, hemophilia - the lack of blood clotting ability, "fetal resorption" in an outwardly prosperous bitch, etc.

semi-lethal genes, For example genes, which determine bilateral cryptorchidism, eventually become lethal for the breed as a result of its extinction. Puppies with a "cleft palate", if they are not operated on, cannot suckle and therefore die. The gray-blue with black speckling color is associated with a semi-lethal gene, and if it is inherited by a descendant from both parents, then this descendant may become blind, deaf or infertile. For this reason, two dogs of this color are never mated. In practice, it would be best to consider this color disqualifying in all breeds.

Elena Piskareva: There are many known lethal genes in domestic animals, but only lethal genes for cleavage of the hard palate, ataxia, hemophilia A, and taillessness have been described in the dog. These genes, as a rule, are not independent, but linked to others. It is known, for example, that the presence in newborn puppies of a gap between the oral cavity and the nasopharynx - splitting of the hard palate - is much more common in dog breeds with a bulldog bite. Puppies born with such a defect are not able to suckle their mother and die in the first days after whelping. It is convenient to consider the process of manifestation of lethal genes using the example of hemophilia A. In this disease, the ability of blood to clot is lost due to the manifestation of the recessive h gene located on the X sex chromosome. It is designated X, in contrast to the XH chromosome, which carries the dominant H gene. in a male with the h-gene of hemophilia, without this gene (XH, Y), half of the males of the first generation will have a combination of Xh Y, i.e. no clotting factor. Such puppies usually die at the age of 1.5 - 3 months. due to external or internal hemorrhage. If it is possible to keep such a male and mate him with a female carrying the recessive hemophilia h gene, then hemophilic females (Xh Xh) are born, who die no later than the first estrus. The lethal baboon-like gene, which in the homozygous state causes a sharp shortening of the axial skeleton of the dog, is lethal for males, but does not lead to the death of bitches. Lethal genes are known, which, when manifested in the embryonic state, are also dangerous for the life of a pregnant bitch, for example, with hereditary muscle contracture, when the bitch cannot be born.

As F. Hatt points out, there are much more lethal and semi-lethal genes than we know.

Modern genetics has accurate facts about the variability and heredity of various traits. The patterns of inheritance of many traits have been identified, and phenotypic and genetic relationships between them have been established. It became possible to use the methods of genetics in the selection of simple qualitative traits determined by one gene or a gene linkage group to exclude lethals and semi-lethals. It has been established that animals that are homozygous for some genes are not viable and are characterized by reduced viability, disorders of morphogenesis, metabolism, and individual biochemical functions. Such animals, if they live, do not economically justify the cost of feeding and maintenance. The most common monogenic lethal traits in cattle breeding include dwarfism (dominant and recessive), hairlessness, acroteriosis, absence of limbs, paralysis of the hind limbs, muscle contracture, short spine, congenital dropsy, shortening of the lower jaw, ankylosis, porphyria (semi-lethal). Most of them are recessive, i.e., with conventional breeding methods, a harmful genetic load can intensively accumulate in a population. Thus, paralysis of the hind limbs in cattle of the Red Danish breed, first recorded in 1924, became widespread by 1950, in particular, 26% of the bulls recorded in the stud books of two provinces of Denmark turned out to be carriers of this gene. Sublethal defects are more common - hairlessness in Black-and-White cattle, dropsy of the brain in Aishir cattle, etc. Mutations that do not manifest themselves clearly, but have an inhibitory effect on the course of physiological processes, are even more common.

In connection with the widespread use of artificial insemination, the use of breeding bulls has become much more intensive. Many of them produce thousands and tens of thousands of descendants. Under these conditions, the rate of spread of various genotype disorders greatly increases. Many populations can become carriers of recessive lethals and semi-lethals. Therefore, it is very important to identify the carriers of these genes. First of all, it is necessary to study the genetic situation in relation to lethals and semi-lethals in modern herds, to establish an accurate account of calves born with defects.

In the US, the Holstein Friesian Breeding Association keeps a regular record of 10 hereditary defects. Methods for identifying carriers of lethal and semi-lethal genes are close inbreeding and a method for testing bulls intended for use in a breeding network on groups of queens that are heterozygous for lethal and semi-lethal genes.

stages of development, but there are flying that cause death, for example, when pupating a Drosophila larvae). Lethal alleles arise as a result of the so-called. lethal mutations - the lethality of such mutations indicates that this gene is responsible for some vital function.

Lethal alleles are called alleles whose carriers die due to developmental disorders or diseases associated with the operation of this gene. There are all transitions between lethal alleles and alleles that cause hereditary diseases. For example, patients with Huntington's chorea (an autosomal dominant trait) usually die within 15-20 years after the onset of the disease from complications, and some sources suggest that this gene is lethal.

Alleles are called sublethal or semi-lethal, the lethal effect of which is frequent, but not obligatory (that is, transitional between lethal alleles and alleles that cause hereditary diseases), mutations are called conditionally lethal, in which an organism carrying such mutations can live in an extremely narrow range of conditions, for example auxotrophic mutations in microorganisms (inability to grow on nutrient media without certain vital substances due to the loss of the ability to synthesize them) substrate-dependent mutations (inability to use certain substances as a source of carbon and energy) and temperature-dependent mutations (the ability to live only in a narrow temperature range - for example some Drosophila mutants are unable to live at temperatures above 25°C).

Notes

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See what "Lethal genes" are in other dictionaries:

LETHAL GENES- LETHAL GENES, genes (see), causing death in a homozygous state. Along with them, a large number of semi-lethal factors are known, leading very often to the birth of various kinds of unviable freaks, or simply one or another ... ...

Lethal Genes- * lethal genes * lethal genes ...

gene synthesis machine- * machine that synthesizes genes * gene machine automatic DNA synthesizer for obtaining short (usually 15 30 bp long) strands of DNA for use in the polymerase chain reaction. Compound genes * compound genes genes ... Genetics. encyclopedic Dictionary

Lethal factors- * lethal factors * lethal factors Mendelian () units (genes and chromosomal aberrations) that cause the death (lethal outcome) of the organism before it reaches puberty. L. f. classify: a) according to the degree of penetrance (see); b) by ... ... Genetics. encyclopedic Dictionary

LETHAL FACTORS- Mendelian units (genes, chromosomes) that cause the death of the organism before it reaches puberty. Lethal factors are classified: 1. According to the degree of death of organisms: absolute, leading to the death of 100% of individuals; sublethal more ... ... Terms and definitions used in breeding, genetics and reproduction of farm animals

HUMAN- HUMAN. Contents: The origin of man ........... 5 24 Human heredity ........... 530 According to the systematic position in the organic world, man belongs to the animal kingdom (Animalia), to the half-kingdom of multicellular (Metazoa), to ... ... Big Medical Encyclopedia

HEREDITY- HEREDITY, the phenomenon of the transfer to offspring of material factors that determine the development of the characteristics of an organism in specific environmental conditions. The task of studying N. is to establish patterns in the occurrence, properties, transmission and ... ... Big Medical Encyclopedia

GENETICS- (from the Greek genesis origin), usually defined as the physiology of variability and heredity. This is how Bateson defined the content of genetics, who proposed this term in 1906, wanting to emphasize that of the three main elements ... Big Medical Encyclopedia

GENE- (from the Greek gignomai I become), hereditary deposit; the term was introduced by Johannsen with the expectation that it does not contain "any hypothesis", and is opposed by them to the concept of "hereditary trait". Being in… … Big Medical Encyclopedia

This article is about the biological taxon. For the everyday concept, see Mushroom. Mushrooms ... Wikipedia

GENES

Designations in the text: A - dominant gene; a - recessive gene

recessive genes

A RECESSIVE GENE (i.e., a trait determined by it) MAY NOT APPEAR IN ONE OR MANY GENERATIONS until two identical recessive genes from each parent meet (the sudden appearance of such a trait in offspring should not be confused with a mutation);
Dogs that have only ONE RECESSIVE GENE - the determinant of any trait, will not show this trait, since the action of the recessive gene will be masked by the manifestation of the influence of the DOMINANT GENE paired with it. Such dogs (carriers of a recessive gene) can be dangerous for the breed if this gene determines the appearance of an undesirable trait, because they will TRANSFER IT TO THEIR OFFspring, and those further, and thus it will remain in the breed. If you accidentally or thoughtlessly pair TWO CARRIERS OF SUCH GENE, they will give part of the offspring with undesirable traits.

Dominant genes

The presence of a dominant gene is always clearly and outwardly manifested by the corresponding feature. Therefore, dominant genes that carry an undesirable trait are much less dangerous for the breeder than recessive ones, since their presence always appears, even if the dominant gene "works" without a partner (ie Aa).

But, apparently, in order to complicate matters, not all genes are absolutely dominant or recessive. In other words, some are more dominant than others, and vice versa. For example, some factors that determine coat color can be dominant, but still not outwardly manifest unless they are supported by other genes, sometimes even recessive ones.

Matings do not always give ratios exactly as expected on average, and to get a reliable result from a given mating, you need to produce a large litter or more offspring in multiple litters.

Some external traits may be "dominant" in some breeds and "recessive" in others. Other traits may be due to multiple genes or semi-genes that are not simple dominants or Mendelian recessives. As a result, the genetics becomes too complex to be understood by the average dog breeder!

Mutations

Mutation is a sudden change in a gene. It manifests itself in the first generation of offspring, if the mutant gene is dominant. But a recessive mutant gene can be secretly inherited for several generations until two carriers of such a gene are selected in the parent pair. Only then will a descendant appear, showing the result of the mutation of this gene.

Many exterior changes are caused by mutations. Classical examples of this are square-faced breeds, such as the early Mastiff hundreds of years ago, and all short-faced breeds, such as Pekingese, Pugs, and Bulldogs. Breeds such as Bassets, Pekingeses and Dachshunds suffer from a genetically fixed mutation that causes a deformity known as achondroplasia (abnormal development of the tubular bones of the limbs before birth, expressed as a decrease in their length).

Mutations are natural, but they can also be caused artificially, for example, by ionizing radiation (radiation). Medicines and poisons can be another cause and cause usually deleterious mutations. Environmental influences can also affect mutation rates. Interestingly, mutations are inherited; are always reproducing, so new characteristics or traits may appear all the time.

Lethal Genes

These are genes that cause the death of an organism before it reaches puberty. Lethal genes are recessive. Here are a few examples of their influence: "cleft lip" and "cleft palate" - a defect in the development of the upper jaw, hemophilia - the lack of blood clotting ability, "fetal resorption" in an outwardly prosperous bitch, etc.

Semi-lethal genes, such as those for bilateral cryptorchidism, eventually become lethal to the breed as a result of its extinction. Puppies with a "cleft palate", if they are not operated on, cannot suckle and therefore die. The gray-blue with black speckling color is associated with a semi-lethal gene, and if it is inherited by a descendant from both parents, then this descendant may become blind, deaf or infertile. For this reason, two dogs of this color are never mated. In practice, it would be best to consider this color disqualifying in all breeds.

© H. Harmar "Dogs and their breeding"

Dozens of anomalies are known in farm animals, the occurrence of which is associated with recessive or dominant gene mutations. These anomalies occur in individual populations with different frequencies, which depends on the rate of the mutation process, the animal breeding system, etc. Knowledge of the specific forms of congenital anomalies in animals of each species, as well as the frequency of their manifestation in individual breeds, is necessary for veterinary specialists to selectively prevent the spread of genetic pathology .

Anomalies in cattle. The biological features of this species of animals are small and relatively late ripening. A cow usually brings one calf, which reaches sexual and physiological maturity only by 1.5 years, so the period between the first calving of mother and daughter is on average 5 years. As a result, the appearance of abnormal offspring in the herd can significantly reduce the level of reproduction and the intensity of breeding selection of livestock. A wide range of congenital shomalia determined by lethal, semi-lethal and subvital genes has been studied in cattle. 46 anomalies are included in the International List of Lethal Defects under code A (Table 43). The relative frequency of individual types of anomalies in each breed or population may be different. In the Kostroma breed, according to our data, the most frequently recorded genetic anomaly of the head is shortening of the jaw (Table 44), in the Yaroslavl breed - syndactyly, in the Kholmogory breed - muscle contractures, in the Black-and-White breed - umbilical hernia. Anomalies of the central nervous system were the most common (21%) in cattle in Germany.

The second place in the frequency of registration (14%) was occupied by a complex anomaly - a combination of umbilical hernias with splitting of the abdomen and the fetus as a whole. The frequency of anomalies, or the percentage of abnormal offspring to its total number, within specific populations can also be very different and, according to average estimates, do not exceed 1%. However, this indicator depends on the completeness and accuracy of registration of anomalies. So, in Germany, after organizing a clear accounting, they concluded that the frequency of anomalies increased several times. The question is different: are all anomalies amenable to visual observation? Obviously not all. Thus, in the Kostroma rock, the average frequency of all forms of anomalies over a 12-year period was 1.15%. The frequency of total mortality of offspring (aborted, stillborn, abnormal, dead without visible defects of calves) in this farm was 10.2%. A certain proportion of this mortality is also associated with gene mutations that cause not morphological defects, but metabolic disorders and other anomalies, the detection of which is possible only by special methods.

Breeders can play a special role in the spread of genetic anomalies both in cattle and in animals of other species. Hundreds and thousands of offspring can be obtained from each manufacturer during artificial insemination per year. So, 100 thousand calves were received from one bull abroad. If such a producer turns out to be a carrier of a gene mutation, then it will quickly spread in the breed. Here are some examples from the numerous facts described in the literature. As a result of the intensive use of the bull Prince Adolf, brought to Sweden, and subsequent spontaneous inbreeding for him, the frequency of hairlessness in individual Swedish herds was over 5%. The same situation occurred in Sweden after the import of the bull Gallus, which turned out to be a heterozygous carrier of the gene that causes the absence of limbs.

In the offspring of individual bulls of the Black-and-White breed and Charolais in the USA and Germany, cases of the birth of dwarf calves were recorded with a frequency of 23.3 and 22.2%, respectively. In the former In Czechoslovakia, when examining the descendants of 166 sires, it was found that 43 of them were carriers of lethal genes. In one bull, a carrier of the dominant cleft lip anomaly, the defect appeared among 44% of bulls and 71% of heifers from his offspring.

In the Kostroma breed, we analyzed the distribution of shortening of the lower jaw and pug-likeness through the bull Burkhan, who himself had defective calves in the offspring; his sons, grandchildren, great-grandchildren, female descendants also gave abnormal offspring (Fig. 57). Most of the calves are from inbreeding and mating of parents with a normal phenotype in the presence of a common ancestor. Therefore, we can conclude that the type of inheritance of this anomaly is recessive. It can be seen from the figure that the largest number of defective calves was registered in the offspring of the bull Zheton 3501 (the grandson of the bull Burkhan) when it was used in a commercial economy, where some of the cows had the same recessive gene in the genotype.

anomalies in pigs. The International List of Lethal Defects in Pigs includes 18 genetic anomalies. Most of them are due to autosomal recessive genes (Table 45). Genetic anomalies can occupy a significant place in the pathology of pigs. Let's look at a few such examples. In Spain, a study of 23,449 piglets out of 2,399 litters from Duroc, Yorkshire, Hampshire and White Chester boars showed 6.21; 6.02; 9.66; 2^62% abnormal litters.

According to Olivier (1979), 7 genetic anomalies of the skin, 17 of the skeleton, 3 of the eyes, 13 of the neuromuscular, 6 of the blood, 6 of the hormonal-metabolic, 5 of the digestive system, and 9 of the genitourinary were described in pigs. The main anomalies were cryptorchidism, hernias, pseudohermaphroditism, etc. The author of the study believes that these anomalies are the result of the action of one gene at different stages of embryo formation.

In Denmark, 6669 dead piglets from 2936 litters were examined for two years to determine the nature and frequency of occurrence of congenital anomalies. Various anomalies were detected in 1.4% of piglets born, or 6.2% of the dead before weaning. Pathological anatomical examination of 25.9% of abnormal pigs revealed underdevelopment of valves, non-closure of the anus, subaortic stenosis, ectopia of the heart and other defects of the cardiovascular system. In 23.4% of piglets, various developmental disorders of the motor system were found. Anomalies of the central nervous system were found in 5.9% of piglets, among them a bifurcated brain and dropsy of the brain. Infection of the rectum, small intestines or their incomplete development was found in 30% of piglets, and various hernias and ascites - in 6.8%. Cleft lip, cleft palate, rhinocephalitis and other anomalies of the facial part of the head were found in 6.1%; hermaphroditism, non-closure of the ureter, dropsy of the kidneys and urethra - in 1.7% of piglets. These anomalies were manifested in the offspring of individual producers during inbreeding, which indicates the hereditary nature of their occurrence.

Very convincing evidence of the hereditary nature of cryptorchidism in pigs was obtained by Fridin and Newman. According to them, in Canada, one-, two-sided cryptorchidism is observed annually in 1-2% of all boars entering the market. The authors crossed cryptorchids with their mothers and full sisters. The offspring from such crosses were mated with each other. As a result of such selection and selection, the frequency of cryptorchidism in experimental animals of the Yorkshire breed increased to an average of 42.9%, and especially when two sires were used. When examining piglets in the United States in one year, about 400 thousand animals were found with scrotal hernia.

Observations show that testicular hypoplasia is often the cause of impaired fertility in boars. The frequency of this anomaly, according to researchers from Germany, was 19.6%. 30 such boars were left for reproduction

Wa, each of them covered from 4 to 40 queens (439 heads in total), but only four of them gave birth. The analysis showed that pathological forms of spermatozoa in these boars are 80-100%. All 30 abnormal animals had common ancestors, which indicates the hereditary nature of testicular hypoplasia and defects in spermiogenesis.

The presence of crater teats in pigs is one of the serious defects, since piglets do not receive milk from them. According to the Bavarian Institute for Animal Husbandry (Germany), the frequency of this anomaly in German Landraces was 6.6%. As noted by P. N. Kudryavtsev et al. (MVA), the number of pigs with inactive crater nipples has increased in recent years. The number of such teats ranges from 1 to 8. Piglets that get crater teats die.

Crater is a trait caused by a single autosomal recessive gene. This was experimentally verified by P. N. Kudryavtsev et al. After preliminary selection of boars and gilts-carriers of anomalies (Kchkch), normal but heterozygous individuals (Kchkch), giving birth to piglets with cratering, and normal homozygous pigs (KchKch), the authors crossed between these groups of animals. In the first variant, 27 normal homozygous queens were crossed with 15 boars. All 258 offspring were normal. In the second variant, where one of the parents was homozygous (KchKch) and the other heterozygous (KchKch), all piglets were also normal. In the third variant, 13 heterozygous boars were crossed with 16 heterozygous queens. Of the 168 piglets born, 39 (23.2%) had crater teats. And finally, in the fourth variant, one of the parents was homozygous, and the other was heterozygous. 170 piglets were obtained from them, of which 86 (50.5%) were with normal teats and 84 (49.5%) with cratered ones. The results of this experiment prove the recessive type of inheritance of teat crater in pigs.

Anomalies in sheep. About 90 congenital anomalies have been described in sheep. According to Dennis and Leipold, most of the known genetic defects in sheep are due to monogenic autosomal recessive inheritance (Table 46). Most often, this type of animal has craniofacial defects, especially agnathia, as well as curvature of the forelimbs, microagnathia, hermaphroditism, cryptorchidism, hypospadiasis, prognathia, anus atresia, microtia, entropia, torticollis, polythelia, arthrogryposis. The analysis showed that 55.4% of the defects were related to the musculoskeletal system, 12.7 - to the digestive system, 9.7 - to the cardiovascular, 7.1 - to the urogenital, 6 - to the central nervous system, 3. 5 - to anomalies of the ligaments, 3.2 - to the abdominal, 1.5% - to the endocrine system. Although the frequency of individual defects is low, the cumulative contribution of all anomalies can be detrimental to farms. In New Zealand, a country with developed sheep breeding, the frequency of lethal defects was about 1% of dead lambs. In the USA, lethal defects in the first 2 weeks of life were observed in 11.4% of lambs.

The average embryonic mortality in sheep is 20%. This indicates that many unidentifiable lethal genes may be active during this period.

Individual genetic anomalies in sheep can be widespread. Thus, in Bulgaria, in the herds of Merino sheep, a high mortality of lambs was observed in the early postnatal period. It occurred as a result of the fact that the lambs did not receive milk due to defects in the udder of their mothers: from hypoplasia with small remnants of glandular tissue to its complete absence. The frequency of this hereditary anomaly in different herds ranged from 6 to 40%.

In sheep, cryptorchidism was often observed, which was combined with such a secondary sexual characteristic as polledness. Polled rams have low fecundity. Through strict breeding selection, it was possible to create a type of polled rams with normal fertility, however, abnormal individuals are also found among them.

anomalies in birds. Birds, primarily chickens, are the most studied in relation to the genetics of anomalies. The International List of Lethal Defects includes 45 anomalies in chickens, 6 in turkeys and 3 in ducks. The most common anomalies of the beak (parrot beak, crossed beak). Their frequency, according to William et al., is 1.1% loss during the incubation of eggs of White Leghorn and Rhode Island hens. Beak anomalies are also common in ducks.

Max Gibbon and Sheikelferd described an anomaly when crossing white leghorns with butterkamps and bantams and then breeding "in themselves" - polydactyly. In addition to it, syndactyly and feathered legs were observed in chickens. The frequency of the syndrome was 16.8%. When crossing an abnormal F2 rooster with phenotype-normal chickens, splitting was observed - half of the normal and half of the abnormal individuals (1: 1). It has been established that this complex of traits is controlled by a single autosomal gene that has a semi-lethal effect, since the embryonic and postembryonic survival rate of abnormal chickens is very low.

Anomalies in horses. Of the hereditary anomalies in horses, 10 are included in the International List of Lethal Defects. Among them, 3 anomalies of the skeleton, 2 - of the reproductive system, 2 - of the kidneys and muscles, one anomaly of the intestines, nervous system, organs of vision.

In horses of heavy draft breeds, atresia of the colon is more common. The distribution of this anomaly was noted in the offspring of the stallion Superba of the Percheron breed. It has also been described in foals of a thoroughbred riding breed of Ostfriz origin. Imperfect epitheliogenesis was registered in heavy draft breeds. In foals of the Oldenburg breed in Germany, ataxia, called Oldenburg, was found. It spread in line 9. One of the most frequently recorded anomalies in horses is an umbilical hernia. It occurs in light and heavy breeds.

Some other genetic and hereditary-environmental anomalies are known in horses. So, in the USA, in horses of several breeds, the appearance of foals with a kind of white spotting, called "overo", is observed. When crossing horses of the "overo" type, foals with pink skin are born, in which hypoplasia of the intestinal tract and isoerythrolysis are observed, as well as colic, leading to death.

In England, in horses of a double-blooded riding breed, animals with impaired coordination of movements - “wobble disease” were registered and studied. A genetic predisposition to this anomaly has been established.

The heritability of extremity dermatoses in horses has been proven. Defects with a hereditary predisposition are often found chronic deforming inflammation of the hock joint - spar, the so-called "crutch leg" in foals, as well as chronic aseptic inflammation of the coronal block of hooves, observed mainly in race and running horses.

RELATED TO CHARACTER DOMINATION

Dominance types. Soon after the rediscovery of Mendel's laws on animals and plants of various species, it was found that not all traits show complete dominance. Cases of intermediate inheritance, incomplete dominance, overdominance and codominance have been identified.

With intermediate inheritance, the offspring in the first generation retains uniformity, but it does not completely resemble any of the parents, as it was with complete dominance, but has a sign of an intermediate character. For example, it is known that among sheep, along with normal ears, there are also earless ones. Crossing earless sheep (aa) with normal-eared sheep (AA), having an ear length of about 10 cm, gives in the first generation offspring (Aa) exclusively with short ears - * - about 5 cm.

Sometimes a trait does not take on an average expression, but deviates towards the parent with a dominant trait, then one speaks of incomplete dominance. For example, when cows with white spots on the body, white belly and limbs are crossed with bulls with a solid color, offspring are obtained with a solid color, but with small spots on the legs or other parts of the body.

With overdominance in hybrids of the first generation, heterosis manifests itself - the phenomenon of superiority of offspring over parental forms in terms of viability, growth energy, fertility and productivity. Overdominance to a certain extent explains the effect of heterosis observed when obtaining three- and four-line hybrids in poultry farming.

When codominating in a hybrid individual, both parental traits are equally manifested. According to the type of codominance, most of the antigenic factors of quite numerous blood group systems are inherited in domestic animals of various species and humans. Different types of proteins and enzymes are also inherited: hemoglobin, amylase, etc.

Splitting according to the phenotype 3:1 in the second generation of monohybrid crossing is observed with the complete dominance of the trait.

With intermediate inheritance, incomplete dominance and codominance, as a result of the different nature of the interaction of allelic genes, first-generation hybrids (Aa) differ in phenotype from the parent with a dominant trait (AA). Hence, in the F2 offspring, heterozygous individuals will have their own phenotype. As a result, the splitting by phenotype and genotype will be the same: 1:2:1. So, when crossing long-eared and earless sheep in Fi, all descendants appear short-eared (Fig. 9). When they are crossed with each other (Aa x Aa) in the second generation, one part of the offspring (AA) will have long ears, two parts (Aa) will have short ears, and one part (aa) will be born without ears. Τᴀᴋᴎᴍ ᴏϬᴩᴀᴈᴏᴍ, phenotypic splitting in the second generation is influenced by the nature of the trait dominance.

Rice. 9. Scheme of inheritance of earlessness in sheep:

A - gene for long ears; a - earlessness gene

lethal genes. A change in phenotypic splitting in a ratio of 3:1 in the second generation of monohybrid crossing may be associated with different viability of F2 zygotes. Different viability of zygotes should be due to the presence of the let-tsuibHbix genes. A lethal gene is a gene that causes disturbances in the development of an organism, which leads to its death or deformity.

The study of congenital anomalies has shown that with different lethal genes, the death of individuals is different and can occur at different stages of development.

According to the classification proposed by Rosenbauer (1969), genes that cause the death of 100% of individuals before they reach sexual maturity are called lethal, more than 50% are sublethal (semi-lethal), and less than 50% are subvital. It should be noted that this division is to some extent conditional and sometimes does not have clear boundaries. An example is sex-linked hairiness in chickens.
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Almost half of the naked chicks die in the last 2-3 days of incubation. Of the hatched, about half of the chicks die before 6 weeks of age, if they are grown at a temperature of 32-35 "C. But if the temperature in the brooders is increased by 5.5 "C, then significantly fewer naked chickens will die. At 4-5 months, naked chickens grow sparse plumage and they are already able to tolerate fairly low temperatures. Under natural conditions, this mutation is likely to be lethal and lead to 100% death of birds. This example shows that the nature of the manifestation of a semi-lethal gene can largely depend on environmental conditions.

Lethal genes are either dominant or recessive. Among the first lethal factors, an allele was discovered that causes the yellow color of mice. The yellow gene is dominant (Y). Its recessive allele (y) in the homozygous state causes the appearance of black color. Crossing yellow mice among themselves gave in the offspring two parts of individuals of yellow and one part of black, i.e., a splitting of 2: 1 was obtained, and not 3: 1, as followed from Mendel's rule. It turned out that all adult mice are heterozygous (Yy). When crossing with each other, they should have given one part of homozygous offspring for yellow color (YY), but it dies even in the embryonic period, two parts of heterozygotes (Yy) will be yellow and one part of homozygotes for a recessive trait (yy) will be black. The crossover scheme looks like this:

In the same way, the gray color of wool is inherited in Karakul sheep (Sokolsky, Malich, etc.), platinum color in foxes, the distribution of scales in linear carps, etc.

Lethal genes in most cases are recessive and therefore can be latent for a long time. A completely healthy and phenotypically normal animal should be a carrier of a lethal gene, the effect of which is detected only upon transition to a homozygous state. Lethal genes most often pass into the homozygous state during related mating. In the practice of animal husbandry, when breeding horses, there was a case of death of 25 foals on the 2nd-4th day after birth from rectal deformity - the absence of an anus (Atresia ani). It turned out that all the stallions and mares from which such abnormal foals were born descended from the same stallion. He was heterozygous for the lethal gene (LI). Initially, this stallion, when crossed with normal mares (LL), gave offspring that were normal in phenotype, but in terms of genotype, half of the offspring were prosperous (LL), and half were heterozygous (LI), carrying a recessive deposit (/) of the lethal gene. In related mating of heterozygous animals (N x N), a part of foals appeared, homozygous for the lethal gene (It), with a deformity of the rectum. Οʜᴎ all died. (More details about anomalies in lethal genes will be discussed in the corresponding chapter.)