Overdominance

Overdominance is a rare condition in genetics where the phenotype of the heterozygote lies outside the phenotypical range of both homozygous parents. Overdominance can also be described as heterozygote advantage regulated by a single genomic locus, wherein heterozygous individuals have a higher fitness than homozygous individuals. However, not all cases of the heterozygote advantage are considered overdominance, as they may be regulated by multiple genomic regions.[1] Overdominance has been hypothesized as an underlying cause for heterosis (increased fitness of hybrid offspring).[2][3]

Sickle cell anemia overdominance

Examples

Sickle cell anemia

An example of overdominance in humans is that of the sickle cell anemia. This condition is determined by a single polymorphism. Possessors of the deleterious allele have lower life expectancy, with homozygotes rarely reaching 50 years of age. However, this allele also yields some resistance to malaria. Thus in regions where malaria exerts or has exerted a strong selective pressure, sickle cell anemia has been selected for its conferred partial resistance to the disease. While homozygotes will have either no protection from malaria or a dramatic propensity to sickle cell anemia, heterozygotes have fewer physiological effects and a partial resistance to malaria.[4]

Salmonoid major histocompatibility complex

Major histocompatibility complex (MHC) genes exhibit extensive variation, generally attributed to the notion of heterozygous individuals identifying a wider range of peptides than homozygous individuals. In arctic char population in Finland, fish heterozygous for MHC alleles had fewer cysts, grew larger, and had a better chance at survival, all indicating a higher fitness of the heterozygotes.[5]

Gymnadenia rhellicani colour polymorphism

In Gymnadenia rhellicani, flower pigmentation is controlled by changes to amino acids 612 and 663 in GrMYB1, which plays a role in anthocyanin pigment production. Red flowers, heterozygous with black and white alleles, maintain a reproductive fitness advantage over white and black varieties presumably because they attract both bee and fly pollinator populations. Since the emergence of the white allele, the frequency of the red phenotype has been increasing in wild populations in multiple regions of the alps.[6]

Polar overdominance

Polar overdominance is a type of overdominance where either only the paternal or maternal allele is being synthesized in the offspring. An example of this was illustrated by a famous ram named Solid Gold and his offspring. This ram was known for its callipyge phenotype (pronounced muscular features and hindquarters) caused by a mutated allele, but only 15% of its offspring received these same traits. Solid Gold’s offspring only expressed the same callipyge phenotype if they inherited the mutated allele from Solid Gold and a wildtype allele from their mother, which would result in a Cpat/Nmat genotype. Offspring with genotypes such as: Cpat/Cmat, Npat/Nmat, and Npat/Cmat did not express the callipyge phenotype.[7]  

Gillespie model

Population Geneticist John H. Gillespie established the following model:[8]

Genotype: A1A1 A1A2 A2A2
Relative fitness: 1 1-hs 1-s

Where h is the heterozygote effect and s is the recessive allele effect. Thus given a value for s (i.e.: 0<s<1), h can yield the following information:

h=0 A1 dominant, A2 recessive
h=1 A2 dominant, A1 recessive
0<h<1 incomplete dominance
h<0 overdominance
h>1 Underdominance

For the case of sickle cell anemia the situation corresponds to the case h<0 in the Gillespie Model.

See also

References
  1. Charlesworth, Deborah; Willis, John H. (November 2009). "The genetics of inbreeding depression". Nature Reviews Genetics. 10 (11): 783–796. doi:10.1038/nrg2664. ISSN 1471-0056. PMID 19834483. S2CID 771357.
  2. Parsons, P. A.; Bodmer, W. F. (April 1961). "The Evolution of Overdominance: Natural Selection and Heterozygote Advantage". Nature. 190 (4770): 7–12. Bibcode:1961Natur.190....7P. doi:10.1038/190007a0. ISSN 0028-0836. PMID 13733020. S2CID 4223238.
  3. Timberlake, W.E. (2013), "Heterosis", Brenner's Encyclopedia of Genetics, Elsevier, pp. 451–453, doi:10.1016/b978-0-12-374984-0.00705-1, ISBN 978-0-08-096156-9, retrieved 2022-11-04
  4. Aidoo, Michael; Terlouw, Dianne J; Kolczak, Margarette S; McElroy, Peter D; ter Kuile, Feiko O; Kariuki, Simon; Nahlen, Bernard L; Lal, Altaf A; Udhayakumar, Venkatachalam (April 2002). "Protective effects of the sickle cell gene against malaria morbidity and mortality". The Lancet. 359 (9314): 1311–1312. doi:10.1016/S0140-6736(02)08273-9. PMID 11965279. S2CID 37952036.
  5. Kekäläinen, Jukka; Vallunen, J. Albert; Primmer, Craig R.; Rättyä, Jouni; Taskinen, Jouni (2009-09-07). "Signals of major histocompatibility complex overdominance in a wild salmonid population". Proceedings of the Royal Society B: Biological Sciences. 276 (1670): 3133–3140. doi:10.1098/rspb.2009.0727. PMC 2817134. PMID 19515657.
  6. Kellenberger, Roman T.; Byers, Kelsey J. R. P.; De Brito Francisco, Rita M.; Staedler, Yannick M.; LaFountain, Amy M.; Schönenberger, Jürg; Schiestl, Florian P.; Schlüter, Philipp M. (2019-01-08). "Emergence of a floral colour polymorphism by pollinator-mediated overdominance". Nature Communications. 10 (1): 63. Bibcode:2019NatCo..10...63K. doi:10.1038/s41467-018-07936-x. ISSN 2041-1723. PMC 6325131. PMID 30622247.
  7. Oczkowicz, M. (2009-01-23). "Polar overdominance – a putative molecular mechanism and the new examples in mammals". Journal of Animal and Feed Sciences. 18 (1): 17–27. doi:10.22358/jafs/66362/2009. ISSN 1230-1388.
  8. Gillespie 2004

References
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