Segregation Distorter (SD) is a male meiotic drive system in Drosophila melanogaster. Males heterozygous for a selfish SD chromosome rarely transmit the homologous SD+ chromosome. It is well established that distortion results from an interaction between Sd, the primary distorting locus on the SD chromosome and its target, a satellite DNA called Rsp, on the SD+ chromosome. However, the molecular and cellular mechanisms leading to post-meiotic SD+ sperm elimination remain unclear. Here we show that SD/SD+ males of different genotypes but with similarly strong degrees of distortion have distinct spermiogenic phenotypes. In some genotypes, SD+ spermatids fail to fully incorporate protamines after the removal of histones, and degenerate during the individualization stage of spermiogenesis. In contrast, in other SD/SD+ genotypes, protamine incorporation appears less disturbed, yet spermatid nuclei are abnormally compacted, and mature sperm nuclei are eventually released in the seminal vesicle. Our analyses of different SD+ chromosomes suggest that the severity of the spermiogenic defects associates with the copy number of the Rsp satellite. We propose that when Rsp copy number is very high (> 2000), spermatid nuclear compaction defects reach a threshold that triggers a checkpoint controlling sperm chromatin quality to eliminate abnormal spermatids during individualization.

中文翻译：

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分离畸变减数分裂驱动系统中精子消除的基础是不同的生精表型

分离畸变仪（SD）是果蝇中的雄性减数分裂驱动系统。自私SD染色体杂合的雄性很少传播同源SD +染色体。众所周知，畸变是由SD染色体上的主要畸变基因位点Sd与SD +染色体上的靶标（称为Rsp的卫星DNA）之间的相互作用引起的。但是，导致减数分裂后SD +精子消除的分子和细胞机制仍不清楚。在这里，我们显示不同基因型但畸变程度相似的SD / SD +雄性具有不同的生精表型。在某些基因型中，SD +精子细胞在去除组蛋白后无法完全掺入鱼精蛋白，并在精子发生的个体化阶段退化。相反，在其他SD / SD +基因型中，鱼精蛋白的掺入似乎较少受到干扰，但精子核被异常压紧，最终精子中释放出成熟的精子核。我们对不同SD +染色体的分析表明，生精缺陷的严重程度与Rsp卫星的拷贝数有关。我们建议，当Rsp拷贝数很高（> 2000）时，精子核致密化缺陷会达到一个阈值，该阈值会触发一个检查点来控制精子染色质的质量，从而消除个体化过程中的异常精子。