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The quality of a gene having more than one phenotypic effect.



the multiple effect of a gene; the capacity of one hereditary factor—a gene—to affect simultaneously several different characters of an organism.

In the early development of Mendelism, when no radical distinction was made between the genotype and the phenotype, the idea of the single effect of the gene (“one gene, one character”) predominated. However, the relationship between the gene and a character has turned out to be much more complex. G. Mendel discovered that a single hereditary factor in pea plants can determine various characters: the red color of the flowers, the gray color of the seed pods, and the pink spot at the base of the leaves. It was subsequently shown that the manifestations of a gene can be diverse and that practically all genes that have been carefully studied are capable of pleiotropy, that is, each gene acts on the entire system of the developing organism and each hereditary character is determined by many genes (actually by the entire genotype). For example, the genes that determine the coat color of the house mouse also influence the body size, and the gene that influences eye pigmentation in the Mediterranean flour moth has another ten morphological and physiological manifestations.

Pleiotropy often extends to characters that have evolutionary significance, such as fertility, longevity, and the ability to survive under extreme environmental conditions. In Drosophila, many mutations that have been studied influence viability. The gene for white eyes also influences the color and shape of internal organs and decreases fertility and longevity. The significance of pleiotropy in evolution was emphasized as early as 1926 by S. S. Chetverikov: “The idea of the multiple effect of the gene (pleiotropy), introduced by Morgan, is extremely important for an understanding of the way natural selection is effected. This leads us to view the genotypic environment as a complex of genes that act internally and genetically on the manifestation of each gene in its character.”

Inasmuch as it is presumed that each gene, as a rule, has a single primary biochemical action, pleiotropy is explained by a hierarchical superstructure of secondary and tertiary gene interactions that lead to a broad spectrum of phenotypic characters that are not obviously related to each other. Pleiotropy is evidence of the interrelationship of cellular metabolism and the biochemical mechanisms of ontogeny. It also attests to the presence, between the primary action of a gene and its phenotypic manifestation, of many intermediate links, upon which other genes and environmental factors may exert influence.


Malinovskii, A. A. “Rol’ geneticheskikh i fenogeneticheskikh iavlenii ν evoliutsii vida,” part 1. Izvestiia AN SSSR: Seriia biologicheskaia, 1939, issue 4.
Lobashev, M. E. Genetika, 2nd ed. Moscow, 1967.
Chetverikov, S. S. “O nekotorykh momentakh evoliutsionnogo protsessa s tochki zreniia sovremennoi genetiki.” In Klassiki sovetskoi genetiki Leningrad, 1968. Pages 133–70.
Serebrovskii, A. S. Nekotorye problemy organicheskoi Evoliutsii, ch. 4. Moscow, 1973.
References in periodicals archive ?
Revisiting the antagonistic pleiotropy theory of aging: TOR-driven program and quasi-program.
Compensatory selection, comparable to antagonistic pleiotropy, could explain the maintenance of polymorphism in a population of red deer (Pemberton et al.
The antagonistic pleiotropy simulations in MR take an infinite sites approach by assuming that each mutation occurs at a distinct genetic locus.
Therefore, large-scale QTL mapping might be a quite frustrating approximation to test for balancing selection due to antagonistic pleiotropy.
The trade-off hypothesis implies that loci responsible for genetic variation in fitness in the two habitats show antagonistic pleiotropy such that alleles improving fitness in one habitat reduce fitness in the other habitat [ILLUSTRATION FOR FIGURE 1A OMITTED].
Since the basic hypothesis underlying many analyses of the evolution of life-history traits is that a great deal of genetic variation in natural populations might be maintained by antagonistic pleiotropy (e.
Several mechanisms could, in theory, maintain variation for quantitative traits: mutation-drift balance of selectively neutral alleles (Lynch and Hill 1986), overdominance (Robertson 1956), mutation-selection balance (Barton and Turelli 1989), antagonistic pleiotropy (Rose and Charlesworth 1981), and environmental heterogeneity (Gillespie and Turelli 1989).
Early one- and two-locus models of ecological specialization, based on antagonistic pleiotropy, invoked trade-offs in performance in different environments, and predicted that performance in different environments should be negatively correlated (Maynard Smith 1966; Felsenstein 1981; Rausher 1984; Diehl and Bush 1989).
Mutations affecting life-history traits include the following classes: (1) deleterious mutations of large effect, generally showing widespread pleiotropy; (2) mildly detrimental mutations; [TABULAR DATA FOR TABLE 4 OMITTED] and (3) mutations showing antagonistic pleiotropy.
Antagonistic pleiotropy can contribute to polymorphism through heterozygote superiority, particularly when deleterious effects are recessive (Rose 1985).
Alternatively, antagonistic pleiotropy and negative genetic correlations will result from genetic variation in resource allocation (Riska 1986; van Noordwijk and de Jong 1986; Houle 1991).
In some quantitative genetic studies, failure to find significant evidence for antagonistic pleiotropy may be attributable to low statistical power due to modest sample size.