Recessiveness

recessiveness

Failure of one of a pair of genes (alleles) present in an individual to express itself in an observable manner because of the greater influence, or dominance, of its opposite-acting partner. Both alleles affect the same inherited characteristic, but the presence of the recessive gene cannot be determined by observation of the organism; that is, though present in the organism's genotype (gene makeup), the recessive trait is not evident in its phenotype (observable characteristics). The term recessive is applied both to the trait in the organism having the alleles of a gene pair in the recessive condition and to the allele whose effect can be masked by another allele of the same gene.

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Recessiveness 

a form of phenotypic gene manifestation. G. Mendel crossed individuals differing in a particular characteristic and found that among first-generation hybrids one of the parental characteristics disappears (recessive), while another is manifested (dominant).

The dominant allele of a gene (A) may be present in the states of homozygosity (AA) or heterozygosity (Aa), while the recessive allele (a) may be manifested only by the absence of the dominant form (—a). Thus, a recessive allele is the suppressed member of an allelic pair of genes. The dominance or recessiveness of an allele is revealed only after the interaction of a specific pair of allelic genes and can be traced by analyzing a gene found in several states (a series of multiple alleles). A rabbit, for example, has a series of four genes that determine the color of its fur: C—solid-colored or agouti; c^ch—chinchilla-colored; c^h—Himalayan-colored; and c—albino. If a rabbit has the Cc^ch genotype, c^ch is the recessive allele, while in c^chc^h and c^chc combinations, c^ch is the dominant allele and is responsible for chinchilla coloration.

The nature of the manifestation of a recessive characteristic can be changed by external conditions. In drosophila, for example, rudimentary wings are a recessive mutation; in a homozygote this mutation results in a sharp reduction in wing size at an optimum temperature (25°C). If the temperature rises to 30°C, the wings enlarge and may attain their normal size; that is, the wing size may be manifested as the dominant characteristic.

The recessive action of a gene may be caused by a slowness or change in the course of a biochemical function. In man, many congenital metabolic disorders are inherited recessively; that is, the clinical symptoms of a disease appear only in homozygotes. The disease is not manifested in heterozygotes because of the functioning of the normal dominant allele. Most recessive lethal mutations are caused by disorders of vital biochemical processes, which result in the death of individuals who are homozygous for this gene. Therefore, in livestock breeding and horticulture it is important to detect individuals carrying recessive lethal and semilethal mutations in order to prevent harmful genes from entering into the selection process.

The effect of inbred depression in the crossing of closely related forms is a result of the conversion of harmful recessive genes into a homozygous state and the manifestation of the action of these genes. In breeding, however, recessive mutations often are a valuable source of new breeds. Thus, recessive mutations are used in the breeding of minks to obtain animals with pelts that are platinum or sapphire in color, which are often valued more highly than the dark brown pelts of wild minks.

The crossing of a hybrid with a parental form that is homozygous for recessive alleles is used in genetic analysis. It is thus possible to detect heterozygosity or homozygosity for the analyzed pairs of genes. Recessive mutations are important factors in the evolutionary process. In 1926 the Soviet geneticist S. S. Chetverikov demonstrated that natural populations contain many diverse recessive mutations in a heterozygous state.

REFERENCES

Lobashev, M. E. Genetika, 2nd ed. Leningrad, 1967.
McKusick, V. Genetika cheloveka. Moscow, 1967. (Translated from English.)

M. M. ASLANIAN