I. INTRODUCTION
Genetic dominance describes the relationship between the phenotype and the genotype at a diploid locus in heterozygotes. An allelic variant may behave as dominant when a single copy is sufficient for full phenotypic expression, co‐dominant when the effects of the two alleles are equally apparent, or recessive when a single copy of the allele has no detectable phenotypic effect. These interactions depend on the partner allele in the heterozygous genotype: a dominant allele in one genotype may be recessive when paired with another allelic variant. The dominance relationship among alleles also depends on the focal character: for instance, a pleiotropic allele can cause a dominant effect for one trait but a recessive effect for another trait. Starting from Mendel’s observations on peas, it has been repeatedly documented that strict additivity is the exception rather than the rule for many traits. However, we know shockingly little about the actual distribution of dominance coefficients for new mutations (Manna, Martin & Lenormand, 2011), and even less for segregating variants in natural populations (Eyre‐Walker & Keightley, 2007). This lack of empirical data prevents estimating the extent to which mutations are visible to natural selection and therefore severely limits the power of population genomic approaches to predict the adaptive potential of species.
Understanding the biological phenomenon of dominance has been a topic of intense and continued interest, both from the population genetics and the functional biology communities. Nevertheless, these two scientific communities have approached this question in different ways. The evolution of dominance is thus an excellent case study of the sometimes conflictual, yet fruitful interactions between these disciplines. The population genetics community has explored the conditions under which natural selection acts on dominance interactions at the level of organismal fitness. These generic models largely neglected the molecular processes underlying these interactions. By contrast, the functional biology community provided detailed mechanistic models focusing on the genotype‐to‐phenotype map, detailing the molecular processes involved. However, by focusing on the organismal level, they largely ignored the complexity of predicting the evolutionary fate of mutations within populations. In particular, intragenomic conflicts among regulatory elements can lead to counter‐intuitive evolutionary outcomes and were initially ignored. Recent theoretical models have moved towards more integrative approaches, and are now considering the diversity of molecular processes by which gene expression can be linked to fitness through explicit phenotypes. These models are bridging the gap between the two research fields, revealing that just as gene expression and integrated phenotypes are evolvable properties, so are dominance interactions.
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To embrace the complexity of dominance relationships and of their evolution, here we provide definitions for the dominance‐related terms used in different fields (Table 1) and specifically review the range of mechanisms that have been proposed to cause variation of dominance at three different levels (Fig. 1). First, at the fitness level, i.e. when dominance relationships result from contrasted evolutionary fates of alleles with a dominance assumed to be fixed. This process was initially formulated by Haldane (1927), and we review recent empirical examples consistent with this phenomenon. Second, at the level of phenotypic integration, whereby differences between homozygotes and heterozygotes translate into different levels of biochemical activity being integrated over successive cellular and developmental processes, ultimately resulting in different organismal phenotypes. This aspect is akin to the ‘physiological’ model proposed by Wright (1934). We review recent studies providing detailed molecular explanations for how dominance could arise as the consequence of such processes, beyond the classical case of enzymes. Third, at the level of allelic expression, through the qualitative modification of gene regulatory networks. This aspect is akin to the controversial model of ‘dominance modifiers’ proposed by (Fisher, 1928), for which recent studies have now provided compelling evidence in specific biological situations.
Altogether, in this review, we argue that recent advances in theoretical modelling of the evolution of gene expression, along with the uncovering of molecular mechanisms involved in dominance, now provide a more comprehensive, less‐polarized view of the evolutionary biology of genetic dominance.
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