Data from: Genetic dissection of hybrid male sterility across stages of spermatogenesis

Hybrid sterility is a common form of reproductive isolation between
nascent species. Although hybrid sterility is routinely documented and
genetically dissected in speciation studies, its developmental basis is
rarely examined, especially in generations beyond the F1. To identify
phenotypic and genetic determinants of hybrid male sterility from a
developmental perspective, we characterized testis histology in 312 F2
hybrids generated by intercrossing inbred strains of Mus musculus
domesticus and M. m. musculus, two subspecies of house mice. Hybrids
display a range of histologic abnormalities that indicate defective
spermatogenesis. Among these abnormalities, we quantified decreased testis
size, reductions in spermatocyte and spermatid number, increased apoptosis
of meiosis I spermatocytes, and more multinucleated syncytia.
Collectively, our phenotypic data point to defects in meiosis I as a
primary barrier to reproduction. We identified seven quantitative trait
loci (QTL) controlling five histologic traits. A region of chromosome 17
that contains Prdm9, a gene known to confer F1 hybrid male sterility,
affects multinucleated syncytia and round spermatids, potentially
extending the phenotypic outcomes of this incompatibility. The X
chromosome also plays a key role, with loci affecting multinucleated
syncytia, apoptosis of round spermatids, and round spermatid numbers. We
detected an epistatic interaction between QTL on chromosomes 17 and X for
multinucleated syncytia. Our results refine the developmental basis of a
key reproductive barrier in a classic model system for speciation
genetics.