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Abstract：
Postzygotic reproductive barriers such as sterility and lethality of hybrids are important for establishing and maintaining reproductive isolation between species. Identifying the causal loci and discerning how they interfere with the development of hybrids is essential for understanding how hybrid incompatibilities (HIs) evolve, but little is known about the mechanisms of how HI genes cause hybrid dysfunctions. A previously discovered Drosophila melanogaster locus called Zhr causes lethality in F1 daughters from crosses between Drosophila simulans females and D. melanogaster males. Zhr maps to a heterochromatic region of the D. melanogaster X that contains 359-bp satellite repeats, suggesting either that Zhr is a rare protein-coding gene embedded within heterochromatin, or is a locus consisting of the noncoding repetitive DNA that forms heterochromatin. The latter possibility raises the question of how heterochromatic DNA can induce lethality in hybrids. Here we show that hybrid females die because of widespread mitotic defects induced by lagging chromatin at the time during early embryogenesis when heterochromatin is first established. The lagging chromatin is confined solely to the paternally inherited D. melanogaster X chromatids, and consists predominantly of DNA from the 359-bp satellite block. We further found that a rearranged X chromosome carrying a deletion of the entire 359-bp satellite block segregated normally, while a translocation of the 359-bp satellite block to the Y chromosome resulted in defective Y segregation in males, strongly suggesting that the 359-bp satellite block specifically and directly inhibits chromatid separation. In hybrids produced from wild-type parents, the 359-bp satellite block was highly stretched and abnormally enriched with Topoisomerase II throughout mitosis. The 359-bp satellite block is not present in D. simulans, suggesting that lethality is caused by the absence or divergence of factors in the D. simulans maternal cytoplasm that are required for heterochromatin formation of this species-specific satellite block. These findings demonstrate how divergence of noncoding repetitive sequences between species can directly cause reproductive isolation by altering chromosome segregation.
摘要：
杂交后的生殖障碍，例如杂种的不育和致死性，对于建立和维持物种之间的生殖隔离很重要。确定因果基因座并辨别它们如何干扰杂种的发展对于理解杂种不相容性（HIs）如何演变至关重要，但对HI基因如何引起杂种功能障碍的机制知之甚少。先前发现的果蝇基因座Zhr会导致来自果蝇雌性和D.melanogaster雄性的杂交的F1女儿的致死性。Zhr映射到D.melanogasterX的异色区域，该区域包含359bp的卫星重复序列，这表明Zhr是一种嵌入异染色质中的罕见蛋白质编码基因，或者是由形成异染色质的非编码重复DNA组成的基因座。后一种可能性提出了异色DNA如何在杂种中诱导致死性的问题。在这里，我们表明杂种雌性死亡是由于在首次建立异染色质的早期胚胎发生过程中染色质滞后引起的广泛有丝分裂缺陷。滞后染色质仅限于父系遗传的D.melanogasterX染色单体，主要由359bp卫星块的DNA组成。我们进一步发现，携带整个359bp卫星块缺失的重排X染色体正常分离，而359-bp的卫星块易位到Y染色体导致男性的Y分离缺陷，强烈表明359bp的卫星块特异性和直接抑制染色单体分离。在由野生型亲本产生的杂种中，在整个有丝分裂过程中，359bp的卫星块高度拉伸并异常富含拓扑异构酶II。在D.simulans中不存在359bp的卫星块，这表明致命性是由D.simulans母体细胞质中缺乏或发散的因子引起的，这些因子是这种物种特异性卫星块的异染色质形成所必需的。这些发现证明了物种之间非编码重复序列的差异如何通过改变染色体分离直接导致生殖分离。
