Satyaki P R V, Cuykendall Tawny N, Wei Kevin H-C, Brideau Nicholas J, Kwak Hojoong, Aruna S, Ferree Patrick M, Ji Shuqing, Barbash Daniel A
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York, United States of America.
PLoS Genet. 2014 Mar 20;10(3):e1004240. doi: 10.1371/journal.pgen.1004240. eCollection 2014 Mar.
Hybrid incompatibilities (HIs) cause reproductive isolation between species and thus contribute to speciation. Several HI genes encode adaptively evolving proteins that localize to or interact with heterochromatin, suggesting that HIs may result from co-evolution with rapidly evolving heterochromatic DNA. Little is known, however, about the intraspecific function of these HI genes, the specific sequences they interact with, or the evolutionary forces that drive their divergence. The genes Hmr and Lhr genetically interact to cause hybrid lethality between Drosophila melanogaster and D. simulans, yet mutations in both genes are viable. Here, we report that Hmr and Lhr encode proteins that form a heterochromatic complex with Heterochromatin Protein 1 (HP1a). Using RNA-Seq analyses we discovered that Hmr and Lhr are required to repress transcripts from satellite DNAs and many families of transposable elements (TEs). By comparing Hmr and Lhr function between D. melanogaster and D. simulans we identify several satellite DNAs and TEs that are differentially regulated between the species. Hmr and Lhr mutations also cause massive overexpression of telomeric TEs and significant telomere lengthening. Hmr and Lhr therefore regulate three types of heterochromatic sequences that are responsible for the significant differences in genome size and structure between D. melanogaster and D. simulans and have high potential to cause genetic conflicts with host fitness. We further find that many TEs are overexpressed in hybrids but that those specifically mis-expressed in lethal hybrids do not closely correlate with Hmr function. Our results therefore argue that adaptive divergence of heterochromatin proteins in response to repetitive DNAs is an important underlying force driving the evolution of hybrid incompatibility genes, but that hybrid lethality likely results from novel epistatic genetic interactions that are distinct to the hybrid background.
杂种不相容性（HIs）导致物种间的生殖隔离，从而促进物种形成。几个杂种不相容基因编码适应性进化的蛋白质，这些蛋白质定位于异染色质或与异染色质相互作用，这表明杂种不相容性可能是由与快速进化的异染色质DNA共同进化导致的。然而，对于这些杂种不相容基因的种内功能、它们相互作用的特定序列，或者驱动它们分化的进化力量，我们所知甚少。基因Hmr和Lhr在遗传上相互作用，导致黑腹果蝇和拟果蝇之间出现杂种致死现象，但这两个基因的突变都是可行的。在这里，我们报告Hmr和Lhr编码的蛋白质与异染色质蛋白1（HP1a）形成异染色质复合物。通过RNA测序分析，我们发现Hmr和Lhr是抑制卫星DNA和许多转座元件（TEs）家族转录本所必需的。通过比较黑腹果蝇和拟果蝇之间Hmr和Lhr的功能，我们鉴定出了几个在这两个物种间受到不同调控的卫星DNA和TEs。Hmr和Lhr突变还会导致端粒TEs大量过表达以及端粒显著延长。因此，Hmr和Lhr调节三种类型的异染色质序列，这些序列导致了黑腹果蝇和拟果蝇在基因组大小和结构上的显著差异，并且极有可能与宿主适应性产生遗传冲突。我们进一步发现，许多TEs在杂种中过表达，但在致死杂种中特异性错误表达的那些TEs与Hmr功能并没有密切关联。因此，我们的结果表明，异染色质蛋白针对重复DNA的适应性分化是驱动杂种不相容基因进化的一个重要潜在力量，但杂种致死现象可能是由杂种背景特有的新上位遗传相互作用导致的。
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