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在分离失真减数分裂驱动系统中，不同的精子发生表型是精子消除的基础。

Distinct spermiogenic phenotypes underlie sperm elimination in the Segregation Distorter meiotic drive system.

机构信息

Laboratoire de Biologie et Modélisation de la Cellule, CNRS UMR 5239, École Normale Supérieure de Lyon, University of Lyon, Lyon, France.

University of Rochester Medical Center, Department of Biomedical Genetics, Rochester, New York, United States of America.

出版信息

PLoS Genet. 2021 Jul 6;17(7):e1009662. doi: 10.1371/journal.pgen.1009662. eCollection 2021 Jul.

DOI:10.1371/journal.pgen.1009662
PMID:34228705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8284685/
Abstract

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.

摘要

分离歪曲因子（SD）是果蝇中一种雄性减数分裂驱动系统。杂合子雄性携带自私的 SD 染色体很少传递同源的 SD+染色体。众所周知，扭曲是由 SD 染色体上的主要扭曲基因座及其靶标——一种称为 Rsp 的卫星 DNA 之间的相互作用引起的。然而，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，我们展示了不同基因型但具有相似强烈扭曲程度的 SD/SD+雄性具有不同的精子发生表型。在某些基因型中，SD+精母细胞在去除组蛋白后不能完全掺入鱼精蛋白，并在精子发生的个体化阶段退化。相比之下，在其他 SD/SD+基因型中，鱼精蛋白的掺入似乎较少受到干扰，但精母细胞核异常致密，成熟精子核最终在精囊中释放。我们对不同 SD+染色体的分析表明，精子发生缺陷的严重程度与 Rsp 卫星的拷贝数有关。我们提出，当 Rsp 拷贝数非常高（>2000）时，精母细胞核致密缺陷达到一个触发检查点的阈值，该检查点控制精子染色质质量，在个体化过程中消除异常精母细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/8b440bd05f7c/pgen.1009662.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/dab0059b7030/pgen.1009662.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/6fb48e80d9e0/pgen.1009662.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/4e6bcbccb20b/pgen.1009662.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/cea87c00a4f3/pgen.1009662.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/18de3b7ce377/pgen.1009662.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/2efc16fad9d9/pgen.1009662.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/74c6361e2bed/pgen.1009662.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/5281fd982fad/pgen.1009662.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/8b440bd05f7c/pgen.1009662.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/dab0059b7030/pgen.1009662.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/6fb48e80d9e0/pgen.1009662.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/4e6bcbccb20b/pgen.1009662.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/cea87c00a4f3/pgen.1009662.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/18de3b7ce377/pgen.1009662.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/2efc16fad9d9/pgen.1009662.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/74c6361e2bed/pgen.1009662.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/5281fd982fad/pgen.1009662.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38e5/8284685/8b440bd05f7c/pgen.1009662.g009.jpg

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