Multiple allelism determines phenotypic heterogeneity in human populations. It, in turn, is one of the foundations of the diversity of the gene pool. Multiple allelism is caused by gene mutations that change the sequence in the nitrogenous bases of a DNA molecule in a region that corresponds to a particular gene. These mutations can be harmful, useful or neutral. Harmful transformations provoke hereditary pathologies with which multiple allelism is associated. For example, a mutation is known that changes the structure in one of the hemoglobin protein chains due to the transformation of the glutamic acid code into the valine (amino acid) code in the gene at the terminal site. As a result of this transition, a hereditary pathology such as sickle cell anemia develops. Overdomination is due to the fact that in a heterozygous state there is a stronger manifestation of dominant cells than in a homozygous one. This phenomenon interacts with the effect of heterosis and is associated with such signs as the total life expectancy, vitality, and others. In humans, as in other eukaryotes, multiple allelism is detected in various forms. There is a large number of mendeliruyuschih signs that are determined by various interactions. Allelic genes are different forms inherent in the same gene, located on homologous chromosomes, in identical regions.
When predicting inheritance using Mendelian laws, we can calculate the likelihood of children with one or another modeling trait. To analyze the transition of characters from generation to generation, the genealogical method, which is based on the construction of pedigrees, is the most convenient methodological approach.
It should be said that other genes also influence the phenotypic manifestation of any one gene. As examples of complex gene interaction, patterns in the inheritance of the Rh factor system can be used : Rh minus and Rh plus. In the process of studying in 1939 the blood serum of a patient who gave birth to a dead child and had a husband transfusion compatible with the ABO group in the history of the disease, antibodies were detected. They were called Rh antibodies, and the patient's blood group - Rh negative. Rh-positive blood group is determined by the presence on the surface of red blood cells of a separate group of antigens, the coding of which is carried out by structural genes. They, in turn, carry information about membrane polypeptides.
They contribute to a significant decrease in viability and lethal genes lead to the death of the body. They are combined in two groups. The first includes recessive genes. They provoke the death of the body only in a homozygous state. In the second group are dominant genes. Their effect is possible in a heterozygous state.
The manifestation of lethal genes can be observed at different stages of development of the individual. This is the earliest stages (embryonic mortality), and very late stages (fetal death, provoking spontaneous abortion, the birth of nonviable freaks). In addition to lethal, semi-lethal genes are also known. They do not provoke an early death of the body, but significantly reduce its viability.
Dominant lethal genes are present in much smaller numbers compared to recessive ones. The dominant category is the Merle factor. Carriers of dominant genes, if desired, can be easily removed from breeding, since they have a characteristic phenotype. Part of the lethal genes provokes serious abnormalities, another part is a disorder of physiological processes.