Speaker
Description
Reproductive isolation is central to speciation, and hybrid sterility in Mus musculus subspecies provides a powerful model to study its genetic basis. A key player in this process is the HstX2 locus on the X chromosome, which in tandem with the only known hybrid sterility gene in vertebrates PRDM9, intriguingly regulates both meiotic recombination rate variation and hybrid male sterility, two interconnected processes that shape genome evolution and reproductive barriers. This system follows classical models of hybrid sterility: 1. Dobzhansky-Muller Incompatibilities (DMIs): Independent evolution of genetic elements in different subspecies leads to incompatibilities in hybrids, triggering sterility through genetic conflict. 2. Haldane’s Rule & Dominance Theory: Hybrid sterility disproportionately affects the heterogametic sex (XY males in mammals), as recessive incompatibilities on the X chromosome are fully expressed. 3. The Large-X Effect & Faster-X Hypothesis: The X chromosome evolves rapidly, accumulating genetic changes that drive hybrid sterility and recombination divergence. At the core of HstX2 is a cluster of microRNAs, the SpermiRs, which evolve through copy number variation and single nucleotide polymorphisms. These genetic changes modulate hybrid sterility in a dosage-dependent manner and modulate recombination rate by differential interaction with target proteins respectively, suggesting a shared regulatory mechanism between these two evolutionary forces. By dissecting the evolution of this locus across Mus musculus subspecies, we gain insight into how genetic conflict, epigenetic regulation, and recombination dynamics interact to drive postzygotic isolation.
