Stage-specific disruption of X chromosome expression during spermatogenesis in sterile house mouse hybrids.
Stage-specific disruption of X chromosome expression during spermatogenesis in sterile house mouse hybrids.
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DOI：
10.1093/g3journal/jkab407
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发表时间：
2022-02-04
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影响因子：
--
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杂种不育是一种复杂的表型，可能是由于精子发生在多个发育阶段的破坏。在这里，我们解开了两个建议的杂交雄性不育机制的家鼠，小家鼠和M。M. musculus，通过比较模式的基因表达不育F1杂种从一个互惠的交叉。我们发现，来自两个交叉方向的杂交雄性小鼠在减数分裂I前期显示出破坏的X染色体表达，这与减数分裂性染色体失活（MSCI）和Prdm 9相关不育的丧失一致，但在M. M. X染色体与以前的研究一致。在减数分裂后的发育过程中，X染色体上的基因表达仅在一个交叉方向上被破坏，这表明在这个后期阶段的错误表达是基因型特异性的，而不是在两个正反交中观察到的MSCI破坏的简单下游后果。相反，减数分裂后表达的破坏可能取决于早期破坏的MSCI的大小，或特定X连锁基因或基因网络的破坏。或者，只有一个潜在的赤字的Sly拷贝，Y-连锁扩增子基因家族的杂交种，表现出在减数分裂后细胞的过度表达，与先前提出的模型之间的拮抗性协同进化的X-和Y-连锁扩增子基因的破坏在精子发生后期的表达。这两种调控机制的相对贡献及其对不育表型的影响有待进一步研究。我们的研究结果进一步支持了这一假设，即家鼠的X连锁杂交不育具有可变的遗传基础，基因型特异性基因调控的破坏有助于X染色体在不同发育阶段的过度表达。总的来说，这些发现强调了精子发生过程中X染色体表观遗传调控的关键作用，并表明这些过程在杂交后代中容易受到破坏。
Hybrid sterility is a complex phenotype that can result from the breakdown of spermatogenesis at multiple developmental stages. Here, we disentangle two proposed hybrid male sterility mechanisms in the house mice, Mus musculus domesticus and M. m. musculus, by comparing patterns of gene expression in sterile F1 hybrids from a reciprocal cross. We found that hybrid males from both cross directions showed disrupted X chromosome expression during prophase of meiosis I consistent with a loss of meiotic sex chromosome inactivation (MSCI) and Prdm9-associated sterility, but that the degree of disruption was greater in mice with an M. m. musculus X chromosome consistent with previous studies. During postmeiotic development, gene expression on the X chromosome was only disrupted in one cross direction, suggesting that misexpression at this later stage was genotype-specific and not a simple downstream consequence of MSCI disruption which was observed in both reciprocal crosses. Instead, disrupted postmeiotic expression may depend on the magnitude of earlier disrupted MSCI, or the disruption of particular X-linked genes or gene networks. Alternatively, only hybrids with a potential deficit of Sly copies, a Y-linked ampliconic gene family, showed overexpression in postmeiotic cells, consistent with a previously proposed model of antagonistic coevolution between the X- and Y-linked ampliconic genes contributing to disrupted expression late in spermatogenesis. The relative contributions of these two regulatory mechanisms and their impact on sterility phenotypes await further study. Our results further support the hypothesis that X-linked hybrid sterility in house mice has a variable genetic basis, and that genotype-specific disruption of gene regulation contributes to overexpression of the X chromosome at different stages of development. Overall, these findings underscore the critical role of epigenetic regulation of the X chromosome during spermatogenesis and suggest that these processes are prone to disruption in hybrids.
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影响因子：
4.5
作者：
Cocquet J;Ellis PJ;Mahadevaiah SK;Affara NA;Vaiman D;Burgoyne PS
通讯作者：
Burgoyne PS
影响因子：
3.3
作者：
Campbell, Polly;Good, Jeffrey M.;Nachman, Michael W.
通讯作者：
Nachman, Michael W.
影响因子：
3.3
作者：
Dufkova, Petra;Macholan, Milos;Pialek, Jaroslav
通讯作者：
Pialek, Jaroslav
影响因子：
3.3
作者：
Alibert, P;FelClair, F;Auffray, JC
通讯作者：
Auffray, JC
DOI：
10.1111/j.2517-6161.1995.tb02031.x
发表时间：
1995-01-01
影响因子：
5.8
作者：
BENJAMINI, Y;HOCHBERG, Y
通讯作者：
HOCHBERG, Y