Abstract
Postzygotic reproductive isolation is the reduction of fertility or viability in hybrids between genetically diverged populations. One example of reproductive isolation, hybrid male sterility, may be caused by genetic incompatibility between diverged genetic factors in two distinct populations. Genetic factors involved in hybrid male sterility are disproportionately located on the X chromosome. Recent studies showing the evolutionary divergence in gene regulatory networks or epigenetic effects suggest that the genetic incompatibilities occur at much broader levels than had previously been thought (e.g., incompatibility of protein-protein interactions). The latest studies suggest that evolutionary divergence of transcriptional regulation causes genetic incompatibilities in hybrid animals, and that such incompatibilities preferentially involve X-linked genes. In this review, we focus on recent progress in understanding hybrid sterility in mice, including our studies, and we discuss the evolutionary significance of regulatory divergence for speciation.
Highlights
Decreased reproductive fitness in interspecific or intersubspecific hybrid animals is referred to as hybrid sterility, and is widely observed in natural populations and laboratory crosses
Hybrid sterility partially or completely impedes genetic exchange between evolutionarily diverged populations, and the cessation of gene flow accelerates the genetic divergence between the populations
Hybrid sterility may be caused by genetic incompatibilities between evolutionarily diverged interacting genes, which are known as “DobzhanskyMuller incompatibilities” (Bateson, 1909; Dobzhansky, 1936; Muller, 1942)
Summary
Decreased reproductive fitness in interspecific or intersubspecific hybrid animals is referred to as hybrid sterility, and is widely observed in natural populations and laboratory crosses. Hybrid sterility may be caused by genetic incompatibilities between evolutionarily diverged interacting genes (or genomic factors), which are known as “DobzhanskyMuller incompatibilities” (Bateson, 1909; Dobzhansky, 1936; Muller, 1942). Male-biased X-linked genes tend to be expressed during the premeiotic phase (Wang et al, 2001; Khil et al, 2004), whereas those expressed during meiotic and postmeiotic phases are driven out onto the autosomes by retrotransposition (Khil et al, 2004, 2005; Sin et al, 2012). We address why the X chromosome has a disproportionately large effect on hybrid sterility by showing that, compared with autosomes, the X chromosome has unusual biological characteristics which influence its gene content.
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