![]() The resulting high rate of molecular evolution in mitonuclear genes increases the likelihood of genetic incompatibilities as closely related species adapt to different environments. The rapid evolution of mitochondrial DNA requires compensatory changes in the nuclear genes to ensure proper functioning. However, this small collection of genes interacts with thousands of genes in the nuclear genome. The mitochondria – also known as the powerhouses of the cell – only contain 13 protein-coding genes. These genetic incompatibilities can arise between countless interacting genes, but one specific situation concerns mitonuclear genes. Over evolutionary time, numerous of these incompatibilities may arise, each possibly contributing to hybrid sterility or unviability. Alleles a and b have never “met” each other and it is possible that allele a has a deleterious effect that becomes apparent when allele b is present, or vice versa. When these populations meet and interbreed, this will result in the genotype AaBb. ![]() ![]() In the other population, another mutation (B -> b) appears and goes to fixation, resulting in AAbb, which is also fertile and viable. In one population, a mutation (A -> a) appears and goes to fixation, resulting in aaBB, which is fertile and viable. Here is the short version:Ĭonsider two allopatric populations diverging independently, with the same ancestral genotype AABB in both populations. During the 19s, Theodosius Dobzhansky and Herman Muller developed a theoretical model to explain the evolution of these incompatibilities. These developmental issues can mostly be traced back to genetic incompatibilities: mismatches between certain genetic variants. Exploring the interactions between mitochondria, sex chromosomes and beak color. ![]()
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