Additive genetic effects
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Additive genetic effects occur when two or more genes source a single contribution to the final phenotype, or when alleles of a single gene (in heterozygotes) combine so that their combined effects equal the sum of their individual effects.[1][2] Non-additive genetic effects involve dominance (of alleles at a single locus) or epistasis (of alleles at different loci).
Additive genetic effects pertain to the cumulative influence of individual genes on a phenotype or trait; the term "additive" implies that the effects of individual alleles, or gene variants, can be summed up to produce the total genetic effect on a trait. These effects are crucial in several fields, including evolutionary biology, medicine, and agriculture.
Despite potential gene interactions within and between loci, empirical studies have consistently shown that additive variance often accounts for a substantial part of the total genetic variance, typically over half, and sometimes close to 100%. Even under the standard model of neutral mutation, a high proportion of additive variance can be expected irrespective of the extent of dominance or epistasis at individual loci.[3]
While epistasis may have significant effects on individual genes, it has minimal effect on quantitative traits, which are typically determined by many genes.[4]
The advent of biobank-scale datasets has made it possible to obtain more precise estimates of the contribution of non-additive genetic effects. Dominance heritability contributes minimally to complex trait variation,[3][5] at about 0.13% of the additive heritability in one study.[6]
Although epistasis may have relevance in comprehending genetic architecture, such as function or human disease, this does not necessarily mean that loci exhibiting it will contribute significantly to genetic variance. Epistasis, similar to dominance, appears not to be important in complex traits.[7]
See also
References
- ^ Rieger, R.; Michaelis, A.; Green, M.M. (1968), A glossary of genetics and cytogenetics: Classical and molecular, New York: Springer-Verlag, ISBN 9780387076683
- ^ "Medical Definition of Additive genetic effects".
- ^ a b Zhu, Zhihong; Bakshi, Andrew; Vinkhuyzen, Anna A.E.; Hemani, Gibran; Lee, Sang Hong; Nolte, Ilja M.; van Vliet-Ostaptchouk, Jana V.; Snieder, Harold; Esko, Tonu; Milani, Lili; Mägi, Reedik; Metspalu, Andres; Hill, William G.; Weir, Bruce S.; Goddard, Michael E. (2015). "Dominance Genetic Variation Contributes Little to the Missing Heritability for Human Complex Traits". The American Journal of Human Genetics. 96 (3): 377–385. doi:10.1016/j.ajhg.2015.01.001. ISSN 0002-9297. PMC 4375616. PMID 25683123.
- ^ Crow, James F. (2010-04-27). "On epistasis: why it is unimportant in polygenic directional selection". Philosophical Transactions of the Royal Society B: Biological Sciences. 365 (1544): 1241–1244. doi:10.1098/rstb.2009.0275. ISSN 0962-8436. PMC 2871814. PMID 20308099.
- ^ Hivert, Valentin; Sidorenko, Julia; Rohart, Florian; Goddard, Michael E.; Yang, Jian; Wray, Naomi R.; Yengo, Loic; Visscher, Peter M. (2021). "Estimation of non-additive genetic variance in human complex traits from a large sample of unrelated individuals". The American Journal of Human Genetics. 108 (5): 786–798. doi:10.1016/j.ajhg.2021.02.014. PMC 8205999. PMID 33811805.
- ^ Pazokitoroudi, Ali; Chiu, Alec M.; Burch, Kathryn S.; Pasaniuc, Bogdan; Sankararaman, Sriram (2021). "Quantifying the contribution of dominance deviation effects to complex trait variation in biobank-scale data". The American Journal of Human Genetics. 108 (5): 799–808. doi:10.1016/j.ajhg.2021.03.018. ISSN 0002-9297. PMC 8206203. PMID 33811807.
- ^ Mäki-Tanila, Asko; Hill, William G (2014-07-01). "Influence of Gene Interaction on Complex Trait Variation with Multilocus Models". Genetics. 198 (1): 355–367. doi:10.1534/genetics.114.165282. ISSN 1943-2631. PMC 4174947. PMID 24990992.
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