The biology of genetic dominance
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Once the proteins are made, the cell typically cannot tell from which gene copy that protein came from. And this is where things get a bit more complicated.
Typically, when a scientist uses the terms recessive versus dominant to refer to a gene, it means that they are talking about variations of a gene also called alleles. Alleles are different sequences of the same gene that affect the function of the protein that they code for. In short, a dominant allele becomes a trait even if just one copy of it is present. A recessive allele does not become a trait unless both copies of the gene, one from mom and one from dad, are present. If one dominant allele and one recessive allele are present, the dominant allele trait will be expressed.
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But you might still be asking yourself why that is, which is totally OK. It actually comes down to the protein level of things. This is especially true for eye color, whereby brown eyes are a dominant trait and blue eyes are a recessive trait. So, when one brown eye allele and one blue eye allele are present together, the individual will have brown eyes. In terms of proteins, that simply means the following: recessive alleles are the result of a loss of function in the protein.
This means that there is a mutation in the allele itself that stops the protein from being expressed. This loss of function could be caused by something as simple as the swapping of an important amino acid or it could be something as complicated as a mutation that stops the coding and subsequently the expression of the protein completely. Now if you are completely thrown for a loop, think of it this way. Brown eyes are brown because of the pigment in them, namely melanin. The brown eye allele codes for the expression of the pigment, melanin.
In the case of a loss of function of the brown eye allele, there is no pigment expression , which means that there is no pigment whatsoever and the result will be a blue eye. So, if you think about this in terms of dominant and recessive and everything we have covered so far, it makes sense that the dominant allele will be expressed even if just one is present. This is because that allele causes the melanin to be made which is visible even if the other allele is recessive as that allele stops the melanin from being made.
Although dominance reversals are predicted to arise under biologically reasonable conditions [ 26 — 30 ], empirical evidence for them is rare, though few studies systematically test for them. In this primer, we review theory and data on dominance reversals and their implications for balancing selection. We then highlight an exciting new study by Grieshop and Arnqvist [ 31 ], which reports evidence for extensive sex differences in dominance for fitness in a seed beetle population exhibiting high levels of SA genetic variation.
The study takes a creative approach to infer sex differences in dominance and provides new support for dominance reversals as important population genetic mechanisms for maintaining genetic variation for fitness. Antagonistic selection—which generates genetic trade-offs between different contexts of selection or fitness—has long been suspected to contribute to the maintenance of genetic variation, yet this suggestion has been met with some debate [ 11 ].
On the one hand, fitness trade-offs are thought to be common because they arise naturally within even the simplest contexts of environmental variability [ 32 ], pleiotropy between traits or life stages [ 33 ], and sex differences in selection [ 34 ]. On the other hand, polymorphisms exhibiting trade-offs are rarely expected to be stably maintained, particularly when selection is weak, unless the alleles affecting the trade-off exhibit dominance reversals [ 11 ].
SA selection represents a special case of the broader debate e.
Consider the following case of a single SA gene with two alleles—a female-beneficial allele A f and a male-beneficial allele A m. In this model, h f , h m , s f , and s m are assumed to be constant, generations do not overlap, and fertilizations are random with respect to the genotypes of breeding adults. Under parallel dominance, sex asymmetries in the strength of selection i.
It is only when selection is very strong i. Otherwise, SA selection removes genetic variation at the gene. Left panel: strong selection.
Why would I be offered a genetic test?
Right panel: weak selection. The grey shaded regions show the expanded parameter space for balancing selection caused by the dominance reversal. This expanded parameter space due to dominance reversal is particularly pronounced when selection is modest to weak right panel. Theoretical curves are based on Eq 1 , and the figure is based on Figs 1 and 3 of Kidwell and colleagues [ 9 ].
Patterns of inheritance
A f , female-beneficial allele; A m , male-beneficial allele; h f , dominance coefficient of the A m allele in females; h m , dominance coefficient of the A f allele in males; SA, sexually antagonistic; s f , the cost to females of being homozygous for the A m allele; s m , the cost to males of being homozygous for the A f allele. Beneficial reversals of dominance result in the deleterious allele of a given sex becoming partially masked within that sex i.
Dominance reversals can lead to a net heterozygote advantage for mean relative fitness see Table 1 , which expands conditions for balancing selection under SA selection. In contexts in which the condition for balancing selection is not met i. This effect arises because SA alleles that are ultimately destined for fixation or loss will, nevertheless, have long persistence times in the population relative to unconditionally beneficial or harmful mutations; long persistence times elevate the contributions of transient SA polymorphisms to standing genetic variation for fitness.
In cases in which polymorphisms are not stably maintained, dominance reversals extend the persistence times of SA alleles. At first glance, one might expect dominance reversals to be uncommon.
What Is a Recessive Gene? Why Are Some Genes Recessive and Some Genes Dominant?
Why should beneficial effects of SA alleles be dominant, whereas their fitness costs remain recessive? Such a scenario is undoubtedly fortuitous for heterozygous individuals, who secure most of the fitness gains associated with SA alleles without incurring much of their costs. On the other hand, such fortuitousness seems too good to be true without a clear biological mechanism to explain why dominance reversals might arise in the first place.
As we review below, classical theories of genetic dominance provide such a mechanism.
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Indeed, these theories predict that dominance reversals should be particularly common among mutations that trade-off between environments, sexes, or fitness components. The earliest debate over the evolutionary causes of dominance pitted R. Fisher against Sewall Wright, initiating a conceptual split within the field of evolutionary biology and resulting in much personal acrimony between the two theoreticians see [ 37 — 38 ].
Mendelian inheritance patterns
The debate sought to explain the widespread observation that harmful mutations are typically recessive or partially recessive with respect to their fitness costs. Fisher [ 39 ] argued that natural selection should favor the evolution of recessivity—that genetic systems should evolve to strongly mask the expression of harmful mutations. Wright [ 40 ] countered by showing that the strength of selection to modify dominance of a deleterious allele would be on the same order of magnitude as the mutation rate and thus too weak to be of evolutionary consequence.
Wright posited, instead, that the observed dominance relations between deleterious and beneficial alleles could arise if fitness followed a diminishing-return function of gene activity e. The diminishing-return relation between genotype and fitness causes deleterious alleles to be partially recessive with respect to fitness i. A concave relation between gene activity and fitness causes deleterious mutations to be partially recessive to beneficial ones.
Dominant and recessive inheritance of genes - KS3 Biology - BBC Bitesize
In the example, a beneficial allele, A , and deleterious allele, a , have additive effects on gene activity i. The fitness surfaces for females and males in blue and red, respectively are each concave but have different optima. The SA alleles have additive effects on gene activity i. A m , male-beneficial allele; h f , dominance coefficient of the A m allele in females; h m , dominance coefficient of the A f allele in males; SA, sexually antagonistic.
When fitness effects of alleles are context dependent, as is the case for SA alleles e. In this case, mutations that move the trait closer to the optimum in one fitness context are partially dominant within that context. SA alleles need not be rare, and the evolution of dominance, including elaboration of dominance reversals, becomes plausible in cases in which heterozygosity is high [ 30 , 38 ]. What are the typical patterns of dominance for SA alleles?
Although the theory outlined above predicts that beneficial effects should be partially dominant and deleterious effects partially recessive, these predictions are difficult to directly confirm.
Our ignorance reflects two logistical challenges. The first is the great difficulty of identifying and characterizing SA genes [ 23 — 24 ]. The second is the difficulty of evaluating dominance among beneficial mutations in general [ 45 ], including conditionally beneficial mutations that are favorable in some contexts and deleterious in others e. Most of what is known about the dominance of fitness-altering mutations applies to deleterious alleles—by far the most abundant class of mutations. These patterns are consistent with the theoretical predictions outlined in the preceding section see [ 42 , 47 ].
In contrast, we know surprisingly little about the dominance of other classes of mutations. Dominance is common among beneficial alleles that have contributed to adaptive divergence in outcrossing populations [ 48 — 49 ], though these variants are expected to show stronger dominance than new beneficial mutations [ 50 ].
Even less is known about the dominance of mutations involved in fitness trade-offs—a class of conditionally beneficial alleles. Even so, the existence of dominance reversals for fitness-related traits has been known for at least 60 years. For example, F1 crosses between mutant strains of Arabidopsis thaliana grown at different day lengths showed alternating dominance effects for flowering time, a key fitness trait in this species [ 51 ]. More recently, a genome-wide assay of gene expression traits in Drosophila revealed apparent dominance reversals between high and low temperatures for 1, genes [ 52 ], though the fitness consequences of the transcriptional variants are unclear.
Several other examples of dominance reversals are known, all involving major-effect loci.