Data from: Misregulation of spermatogenesis genes in Drosophila hybrids is lineage-specific and driven by the combined effects of sterility and fast male regulatory divergence.

Hybrid male sterility is a common outcome of crosses between different
species. Gene expression studies have found that a number of
spermatogenesis genes are differentially expressed in sterile hybrid
males, compared with parental species. Late-stage sperm development genes
are particularly likely to be misexpressed, with fewer early-stage genes
affected. Thus, a link has been posited between misexpression and
sterility. A more recent alternative explanation for hybrid gene
misexpression has been that it is independent of sterility and driven by
divergent evolution of male-specific regulatory elements between species
(faster male hypothesis). The faster male hypothesis predicts that
misregulation of spermatogenesis genes should be independent of sterility
and approximately the same in both hybrids, whereas sterility should only
affect gene expression in sterile hybrids. To test the faster male
hypothesis vs. the effect of sterility on gene misexpression, we analyse
spermatogenesis gene expression in different species pairs of the
Drosophila phylogeny, where hybrid male sterility occurs in only one
direction of the interspecies cross (i.e. unidirectional sterility). We
find significant differences among genes in misexpression with effects
that are lineage-specific and caused by sterility or fast male regulatory
divergence.