Dominant and recessive lethal genes in animals. Trait and lethal genes

GENES

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

Recessive genes

A RECESSIVE GENE (i.e., a trait it determines) MAY NOT MANIFEST IN ONE OR MANY GENERATIONS until two identical recessive genes from each parent meet (the sudden manifestation of such a trait in offspring should not be confused with a mutation);
Dogs that have only ONE RECESSIVE GENE - a 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 its paired DOMINANT GENE. Such dogs (carriers of the 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 OWNS, and those further, and it, thus, will remain in the breed. If, by chance or thoughtlessly, TWO CARRIERS OF THIS GENE are paired, they will give part of the offspring with undesirable traits.

Dominant genes

The presence of a dominant gene is always clearly and externally manifested by the corresponding sign. Therefore, dominant genes carrying an undesirable trait are much less dangerous for the breeder than recessive ones, since their presence is always manifested, 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 may be dominant, but still do not appear outwardly unless they are supported by other genes, sometimes even recessive.

Mates do not always give ratios exactly according to the expected average results, and to obtain a reliable result from a given mating, a large litter or more offspring in several litters must be produced.

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, genetics becomes too complex to be understood by the average dog scientist!

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 found in the parental pair. Only then will there be a descendant manifesting the result of the mutation of this gene.

Many exterior changes are caused by mutations. Classic examples of this are square-faced breeds such as the early mastiffs hundreds of years ago, and all short-faced breeds such as Pekingese, Pugs, Bulldogs. Breeds such as Basset, Pekingese and Dachshund suffer from an inherited mutation that causes a deformity known as achondroplasia (abnormal development of the tubular bones of the limbs before birth, resulting in decreased length).

Mutations are natural, but they can also be caused artificially, for example, ionizing radiation (radiation). Medicines and poisons can be another cause and usually cause harmful mutations. Influence the environment can also affect the frequency of mutations. Interestingly, mutations are inherited, i.e. are always reproduced, so that new characteristics or traits can appear constantly.

Lethal genes

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

Semi-lethal genes, such as genes that determine bilateral cryptorchidism, are ultimately lethal to the breed as a result of its extinction. Puppies with "cleft palates", if they have not been operated on, cannot suck and therefore die. Blue-gray with black specks, the color is associated with a semi-lethal gene, and if it is inherited by a descendant from both parents, then this descendant can become blind, deaf or sterile. For this reason, two dogs of this color are never mated. In practice it would be best to consider this color as disqualifying in all breeds.

RELATED TO THE CHARACTER OF DOMINATION

Dominance types. Soon after the rediscovery of Mendel's laws on animals and plants different types it was found that not all traits show complete dominance. Cases of intermediate inheritance, incomplete dominance, overdominance and codominance were 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 domination, but has a trait of an intermediate character. For example, it is known that among sheep, along with normal ears, there are also earless ones. Crossing of earless sheep (aa) with normal-eared (AA), having an ear length of about 10 cm, gives in the first generation offspring (Aa) exclusively with short ears - * - about 5 cm.

Sometimes the trait takes not an average expression, but deviates towards the parent with a dominant trait, then they talk about incomplete dominance. For example, when crossing cows with white spots on the body, white belly and white-bellied bulls with a solid color, offspring with a solid color is obtained, but with small spots on the legs or other parts of the body.

When hybrids of the first generation are over-dominated, heterosis is manifested - the phenomenon of superiority of offspring over parental forms in viability, growth energy, fertility and productivity. Overdominance to a certain extent explains the effect of heterosis observed in the production of three- and four-line hybrids in poultry farming.

When codominating in a hybrid individual, both parental traits are equally manifested. By the type of codominance, most of the antigenic factors of quite numerous systems of blood groups in domestic animals of various species and humans are inherited. Also inherited different types proteins and enzymes: 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, hybrids of the first generation (Aa) differ in phenotype from the parent with a dominant trait (AA). Hence, in the F2 offspring, heterozygous individuals will have their characteristic phenotype. As a result, the segregation by phenotype and genotype will be the same: 1: 2: 1. Thus, when crossing long-eared and earless sheep in Fi, all offspring appear short-eared (Fig. 9). When crossing them together (Aa x Aa) in the second generation, one part of the offspring (AA) will have long ears, two parts (Aa) - short and one part (aa) is born without ear. Τᴀᴋᴎᴍ ᴏϬᴩᴀᴈᴏᴍ, splitting by phenotype in the second generation is influenced by the character of the dominance of the trait.

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

A - gene for long ears; a - gene for hearinglessness

Lethal genes. Change in phenotypic cleavage in a ratio of 3: 1 in the second generation monohybrid crossing is associated with different viability of zygotes F2- Different viability of zygotes should be due to the presence of le-tsuibHbix genes. It is customary to call a gene that causes disturbances in the development of an organism, which leads to its death or deformity, as lethal.

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 puberty are called lethal, more than 50% are sublethal (semi-lethal), and less than 50% are sub-vital. It should be noted that this division is to some extent arbitrary and sometimes has no clear boundaries. An example is sex-linked hairlessness in chickens.
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Almost half of the naked chicks die in the last 2-3 days of incubation. Of the number of hatched chicks, about half die before 6 weeks of age if they are raised at a temperature of 32-35 "C. But if the temperature in brooders is increased by 5.5" C, then much less naked chickens will die. At 4-5 months, naked chickens develop rare plumage and they are already able to tolerate rather low temperatures. Under natural conditions, this mutation is likely to be lethal and will lead to 100% death of birds. The given example shows that the nature of the manifestation of a semi-lethal gene can largely depend on environmental conditions.

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

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

In most cases, lethal genes are recessive and, therefore, can be latent for a long time. A perfectly healthy and phenotypically normal animal must be a carrier of a lethal gene, the effect of which is revealed only when it goes into 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 the death of 25 foals on the 2-4th day after birth from the deformity of the rectum - the absence of the anus (Atresia ani). It turned out that all the stallions and mares from which such abnormal foals were born came from the same stallion. He was heterozygous for the lethal gene (LI). Initially, this stallion, when crossed with normal mares (LL), gave offspring, phenotypically normal, but by genotype half of the offspring were free (LL), and half were heterozygous (LI), carrying a recessive deposit (/) of a lethal gene. With related mating of heterozygous animals (N x N), a part of foals appeared homozygous for the lethal gene (It), with rectal deformities. Οʜᴎ everyone died. (More details about abnormalities in lethal genes will be discussed in the corresponding chapter.)

Unequal viability of zygotes of different genotypes can be associated with dominant or recessive lethal mutations that occur in the gametes of parental individuals. They can be realized at different stages of embryogenesis or in postembryonic period... Naturally, the death of a part of the zygotes affects the nature of splitting.

Impact on cleavage dominant genes recessive lethal

Dominant genes with a recessive lethal effect have a pleiotropic effect; on the one hand, they determine the dominant character of the manifestation of any trait in a heterozygote, on the other hand, they cause the death of individuals in a homozygote, that is, they manifest their lethal effect as a recessive. Such genes are known in many animals - yellow coloration of mice, short-leggedness in chickens, linear scaly in carps, platinum coloration in foxes, shirazi coloration in sheep, and many others. They cause a deviation from a 3: 1 split, converting it to a 2: 1 split. Analysis of cleavages involving dominant genes with a recessive lethal effect is complicated by the fact that on relatively small samples, the splitting of 3: 1 and 2: 1 is not always possible to distinguish, but statistical method testing by the χ 2 criterion does not allow making a choice from hypotheses. For example, if, when crossing yellow mice with each other, a splitting of 65 yellow mice: 32 black ones, two hypotheses are not rejected by the% 2 method: 1 - splitting in the experiment corresponds to a splitting of 3: 1, χ 2 = 3.29, p> 0.05; 2 - splitting in the experiment corresponds to splitting 2: 1, χ 2 = 0.17, p> 0.05.

Only on large samples is 2: 1 splitting distinguishable from 3: 1 splitting... When summarizing the data on the inheritance of yellow color in mice obtained by different researchers, the cleavage when crossing yellow mice among themselves was 2386 yellow: 1235 black - ∑ = 3621, χ 2 = 0.96 at H 0 - 2: 1 (at H 0 - 3: 1 in this case χ 2 = 160!).

It is obvious that different methods of genetic testing, for example, setting analyzing and backcrossing, can contribute to the right decision the question of inheritance. In the above example, these are crosses: yellow from F 1 × black; yellow from F 1 × yellow P. In the first case there should be a splitting of 1: 1, in the second - again 2: 1.

It is more difficult to find out that there is a deviation and it is due to the different viability of the zygotes in the case when the death of a part of the zygotes occurs at the postembryonic stage. In this regard, it is necessary to monitor fertility and mortality in the offspring, if there is an assumption about the presence of lethality. The basis for the assumption of lethality is the impossibility of obtaining a uniform offspring when breeding individuals of a certain phenotype in oneself. Examples of analysis are given in tasks III.2 and III.3.

Problem No. III.2

In the offspring from the crossing of silver-sable minks with each other in F1, splitting is always observed: silver-sable and brown individuals appear.

In one experiment, in several litters, 93 silver-sable and 43 brown puppies were obtained from crossing of silver-sable individuals with an average litter size of 3.66 puppies. From crossing the silver-sable with brown minks, 39 brown and 41 silver-sable minks were obtained. In crosses between brown minks, only brown I offspring were obtained. The litter size in the last two crosses was 4.9-5.2 puppies.

Explain the splitting, determine the genotypes of the silver-sable and brown minks.

Analysis

Since silver-sable minks, when crossed with each other and with brown ones, always give splitting, they are obviously heterozygous. To determine the number of genes, consider the splitting in the experiment:

H 0 - differences in one gene, splitting 3: 1, χ 2 = 3.2, p> 0.05. The deviation is accidental, the hypothesis is not rejected.

The ratio corresponds well to the 1: 1 cleavage by one gene, χ 2 = 0.05, p> 0.80. The deviation is accidental, the hypothesis is not rejected.

Comparison of data on the fertility of minks in different crosses indicates a partial death of zygotes when crossing silver-sable minks. The death of dominant homozygotes can be assumed. Then the genotype of silver-sable minks is Aa, brown minks are aa, and the cleavage in crossing is not 3: 1, but 2: 1 (χ 2 = 0.17, p> 0.05). For the final approval of this hypothesis, it is necessary to set up an additional crossing between silver-sable individuals to increase the sample and statistically test the hypothesis 2: 1. In some cases, more complex analysis is required.

Problem No. III.3

In crosses of platinum, white-faced and Georgian white foxes with silver-black ones, it was found that platinum, white-faced and Georgian white colors, causing a general weakening of pigmentation and the appearance of various piebald, are not sex-linked. When each of these mutants was crossed with silver-blacks, a 2: 1 cleavage was obtained, with the silver-black color being recessive. Consequently, each of them is controlled by one dominant gene with a recessive lethal effect. The death of some mutants is evidenced by data on the size of the litter: silver-blacks have 4.5 puppies per litter, white-faced 3.5, platinum and Georgian whites - less than 3.5.

In order to establish whether these mutations affect the same gene or different, crosses were set up, the results of which are shown below. The allelism test is inapplicable in this case, since the mutations are dominant:

Explain splitting, determine the genotype of all forms.

Analysis

1. Splits in crosses 1 and 2 correspond to the ratio 1: 1: 1: 1 (χ 2 = 5.83, p> 0.10 for crossing 1, χ 2 = 0.55, p> 0.90 for crossing 2) ... They can be due to several reasons.

1. Since in crosses 1 and 2 there are 4 classes and the ratio is 1: 1: 1: 1, it can be assumed that the studied forms differ in two independently inherited dominant genes with a recessive lethal effect, interacting according to the type of complementarity. Moreover, one of the genes is represented by two different dominant alleles.

2. Splitting 1: 1: 1: 1 can be a consequence of the close linkage of these two genes in the absence of crossing over between them:

(In Punnett lattices, phenotypic radicals are given - genes that manifest their action in the phenotype.)

3. The differences in color are due to three independently inherited dominant genes with a recessive lethal effect. In the first (a) and second (b) crosses, splitting occurs in two different genes.

4. Splitting 1: 1: 1: 1 can be the result of close linkage of three interacting genes in the absence of crossing over.

* (The order of the genes can be different, it is given arbitrarily.)

5. Splitting in a ratio of 1: 1: 1: 1 may be the result of differences in one gene, represented by a series of four alleles, three of which are dominant with a recessive lethal effect, and the fourth is recessive:

In order to make a choice between these hypotheses, a crossing was made - white with silver-black.

If the trait was controlled by two or three genes, then with their independent inheritance, one can expect the appearance of four phenotypic classes:

A similar result should be in the crosses of whites, obtained from platinum or Georgian white foxes, with silver-black ones, but instead of the white-faced, platinum should have appeared, which can be easily verified by writing the appropriate crosses.

The splitting obtained in the test crossing - the appearance of white-faced and Georgian white foxes - can be explained either by the interaction of two (or three) closely linked genes, or by the interaction of three alleles with a monogenic difference between the original forms.

A sharp decrease in the viability of white foxes, noted in the experiment, speaks in favor of the action of allelic mutations, since in this case, in terms of genotype, white foxes are compounds for two dominant mutations of one gene, both with a recessive lethal effect. It is difficult to expect a decrease in viability when two different genes interact (complementarity). Therefore, it was concluded that white, white-faced, Georgian white, platinum and silver-black colors in foxes are controlled by a series of alleles of one gene, three of which are dominant with a recessive lethal effect. Fox genotypes: white A 1 / A 2, A 1 / A 3, A 2 / A 3; white-faced A 1 / a; platinum A 3 / a; Georgian white A 2 / a; silver-black a / a (according to Belyaev et al., 1973).

It should be emphasized that with multiple allelism in the case of heterozygosity of the initial forms, the maximum number of phenotypic classes in the cleavage may not be 3, but 4, as in the case described above. In a population, the number of possible genotypes with multiple allelism increases many times over; it can be determined by the formula: 1 / 2n (n + 1), where n is the number of alleles. For example, if there are 7 alleles of any locus, the number of possible genotypes in the population will be 28: 1/2 × 7 × 8 = 28.

Effect of recessive lethal mutations on cleavage

Recessive autosomal and sex-linked fly, causing the death of homozygotes in crosses of heterozygotes by flying, they can affect the cleavage by genes linked to lethalc heterozygote. To identify the fly, different test crosses are usually placed. An example of the analysis of flying is the problem No. III.4.

Task number III.4

In the Drosophila line from line no. 100, containing inversions, half of the females had a gray color, and half had a yellow body coloration, and the yellow females were sterile. All males of this line were yellow in color. The ratio of females to males was different from normal, it looks more like a 2♀♀: 1♂♂ split. It was suggested that the lack of males in line No. 100 is probably associated with the presence of gray females flying in the X chromosome, which are obviously heterozygous — splitting into gray and yellow females occurs in the line. To establish the genetic structure of this line and test the assumption of the presence of a fly in the X chromosome of females, crosses were set, the results of which are presented below.

Reciprocal crosses

Gray females from F 1 were individually crossed with yellow males from line no. 100.

Analysis

Based on the analysis performed, we will write down the schemes of all crosses.

The proposed hypotheses explain all the results well enough. However, the question of the reason for the sterility of yellow females in line No. 100 remains unclear. We invite the reader to consider this question and offer some hypothesis to explain it.

Have plants many recessive mutations associated with a lack or absence of chlorophyll, which leads either to a decrease in the viability of plants, or to their death at different stages of development. This is the reason for deviations in splitting, and also makes it necessary to take into account splits not only on seedlings, but also at later stages of development in order to determine the proportion of plant death and the nature of the inheritance of the trait. So, in corn, the gene is homozygous wd (white deficiency) have white seedlings (splitting on seedlings 3/4 green: 1/4 white). However, after 1-3 weeks, all white plants die off after using the seed nutrient reserves and in the later stages of plant development, splitting disappears - 3 green: 0 white. Similar mutations are known in peas, barley, rye, wheat, etc.

Other mutations cause the death of only a part of individuals at a certain stage of development, which leads to a decrease in the proportion of recessives in cleavage and a change in the ratio of phenotypes - 4: 1, 5: 1, etc. These ratios vary, since, as a rule, the viability of such mutants in highly dependent on conditions.

In man reduced viability and mortality due to the action of recessive mutations manifests itself in different periods of embryogenesis and at different stages of development. The reasons for the decrease in viability and lethal effect can be associated with both gene mutations and chromosomal abnormalities. Cytogenetic analysis of abortive embryos makes it possible to establish the cause of the death of many of them. On average, more than 42% of spontaneous abortions occur due to chromosome aberrations at all stages of pregnancy: a significant part of newborns with chromosomal aberrations die during the first and subsequent years of life.

Among the gene lethal mutations leading to intrauterine death or death in infancy, one can name recessive mutations that cause thalassemia, sickle cell anemia, cystic fibrosis, congenital ichthyosis, anencephaly (no brain), phenylketonuria, etc.

Cytogenetic and biochemical methods of analysis, study of the structure and activity of enzymes in health and disease, as well as in heterozygous carriers are widely used to study lethal or reducing the viability of mutations in humans; chromatography, different types of electrophoresis.

The change in phenotype splitting in the ratio of 3: 1 in the second generation of monohybrid crossing is associated with different viability of F2 zygotes. The different viability of zygotes may be due to the presence of lethal genes. Lethal is a gene that causes disorders 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 maturity are called lethal, more than 50% are sub-lethal (semi-lethal), and less than 50% are sub-vital. However, it should be noted that this division is to some extent arbitrary and sometimes has no clear boundaries. An example is sex-linked hairlessness in chickens. Almost half of the naked chicks die in the last 2-3 days of incubation. Of the number of hatched chicks, about half die before 6 weeks of age if they are raised at a temperature of 32-35 "C. But if the temperature in brooders is increased by 5.5 ° C, then much less naked chickens will die. For 5 months naked chickens develop rare plumage and they are already able to tolerate rather low temperatures.

Under natural conditions, this mutation is likely to be lethal and will lead to 100% death of birds. The given example shows that the nature of the manifestation of a semi-lethal gene can largely depend on environmental conditions.

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

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

In most cases, lethal genes are recessive and therefore can be latent for a long time.

A perfectly healthy and phenotypically normal animal can be a carrier of a lethal gene, the effect of which is detected only when it goes into a homozygous state. In the homozygous state, lethal genes most often pass during related mating. In the practice of animal husbandry, when breeding horses, there was a case of the death of 25 foals on the 2-4th day after birth from the deformity of the rectum - the absence of the anus (Atresia ani). It turned out that all the stallions and mares from which such abnormal foals were born came from the same stallion. He was heterozygous for the lethal gene (LI). Initially, this stallion, when crossed with normal mares (LL), gave offspring, phenotype normal, but by genotype half of the offspring were free (LL), and half were heterozygous (LI), carrying a recessive inclinations (0 lethal gene. When related mating of heterozygous animals (N x N), some foals appeared homozygous for the lethal gene (II), with rectal deformities.

Dominant and recessive genes

Imagine two homologous chromosomes. One of them is maternal, the other is paternal. Copies of genes located on the same sections of the DNA of such chromosomes are called allelic or simply alleles. (Greek. alios is another). These copies can be the same, that is, completely identical. Then they say that the cell or organism containing them is homozygous for a given pair of alleles (Greek. homos - equal, same and zygote - paired). Sometimes, for brevity, such a cell or organism is simply called a homozygote. If the allelic genes differ slightly from each other, then the cells or organisms containing them are called heterozygous (Greek. heteros is another).

It is very easy to understand this situation. Imagine that your dad and mom independently typed the same short note using a typewriter, and you are holding both sheets of paper with the resulting texts in your hands. Texts are allelic genes. If the parents typed neatly and without errors, both options will be exactly the same up to the last character. This means that you are homozygous for these texts. If the texts differ due to typos and inaccuracies, their owner should be considered heterozygous. It's simple.

An organism or cell can be homozygous for some genes and heterozygous for others. Here, too, everything is clear. If you have more than one pair of sheets with a specific text, but many such pairs, each of which contains its own text, then some texts will completely coincide, while others will differ.

Now imagine that you have in your hands again two sheets of paper with texts. One text is printed perfectly, without a single mistake. The second one is exactly the same, but with a gross typo in one word or even with a missing phrase. In this situation, such a modified text can be called mutant, that is, changed (lat. mutatio - change, transformation). The situation is the same with genes. It is generally accepted that there are "normal", "correct" genes. Geneticists call them wild-type genes. Against their exemplary background, any altered genes can be called mutant.

The word "normal" is written in quotation marks in the previous paragraph for a reason. In the process of evolution, during the copying of genes, which occurs during any cell division, small changes slowly, gradually and constantly accumulate. They also occur during the formation of gametes and, thereby, are passed on to subsequent generations. In the same way, with repeated successive rewriting by hand of a long text, new and new inaccuracies and distortions will inevitably appear in it. Historians studying ancient literature are well aware of this. Therefore, it is sometimes difficult to say which variant of a gene is "normal" and completely correct. However, when a blatant gross lapse arises, it is quite obvious against the background of the original text. With this in mind, we can talk about normal and mutant genes.

How does a mutant gene behave when paired with a normal one? If the effect of a mutation is manifested in a phenotype, that is, the consequences of the presence of a mutant gene in heterozygotes can be recorded as a result of any measurements or observations, then such a mutant gene is called dominant. (lat. dominus is the master). He kind of "suppresses" the normal gene. As you remember, the word “dominant” in Russian means “dominant”, “dominant”, “standing out above all”. For example, the military say: "This height dominates the entire area." If, together with a wild-type gene, a mutant gene does not manifest its action in any way, the latter is called recessive. (lat. cessatio - inaction).

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