Bounds to parapatric speciation: A Dobzhansky–Muller incompatibility model involving autosomes,X chromosomes,and mitochondria

We investigate the conditions for the origin and maintenance of postzygotic isolation barriers, so called (Bateson‐)Dobzhansky–Muller incompatibilities or DMIs, among populations that are connected by gene flow. Specifically, we compare the relative stability of pairwise DMIs among autosomes, X chromosomes, and mitochondrial genes. In an analytical approach based on a continent‐island framework, we determine how the maximum permissible migration rates depend on the genomic architecture of the DMI, on sex bias in migration rates, and on sex‐dependence of allelic and epistatic effects, such as dosage compensation. Our results show that X‐linkage of DMIs can enlarge the migration bounds relative to autosomal DMIs or autosome‐mitochondrial DMIs, in particular in the presence of dosage compensation. The effect is further strengthened with male‐biased migration. This mechanism might contribute to a higher density of DMIs on the X chromosome (large X‐effect) that has been observed in several species clades. Furthermore, our results agree with empirical findings of higher introgression rates of autosomal compared to X‐linked loci.