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Meiosis I progression in spermatogenesis requires a type of testis-specific 20S core proteasome.
Nature Communications ( IF 14.7 ) Pub Date : 2019-07-29 , DOI: 10.1038/s41467-019-11346-y Qianting Zhang 1 , Shu-Yan Ji 2 , Kiran Busayavalasa 1 , Jingchen Shao 1 , Chao Yu 1
Nature Communications ( IF 14.7 ) Pub Date : 2019-07-29 , DOI: 10.1038/s41467-019-11346-y Qianting Zhang 1 , Shu-Yan Ji 2 , Kiran Busayavalasa 1 , Jingchen Shao 1 , Chao Yu 1
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Spermatogenesis is tightly regulated by ubiquitination and proteasomal degradation, especially during spermiogenesis, in which histones are replaced by protamine. However, the functions of proteasomal activity in meiosis I and II remain elusive. Here, we show that PSMA8-associated proteasomes are essential for the degradation of meiotic proteins and the progression of meiosis I during spermatogenesis. PSMA8 is expressed in spermatocytes from the pachytene stage, and assembles a type of testis-specific core proteasome. Deletion of PSMA8 decreases the abundance of proteasome in testes. Meiotic proteins that are normally degraded at late prophase I, such as RAD51 and RPA1, remain stable in PSMA8-deleted spermatocytes. Moreover, PSMA8-null spermatocytes exhibit delayed M-phase entry and are finally arrested at this stage, resulting in male infertility. However, PSMA8 is neither expressed nor required for female meiotic progression. Thus, meiosis I progression in spermatogenesis, particularly entry into and exit from M-phase, requires the proteasomal activity of PSMA8-associated proteasomes.
中文翻译：
减数分裂I在精子发生过程中的进展需要一种特定于睾丸的20S核心蛋白酶体。
精子发生受到泛素化和蛋白酶体降解的严格调控，尤其是在精子发生过程中，组蛋白被鱼精蛋白替代。但是，蛋白酶体活性在减数分裂I和II中的功能仍然难以捉摸。在这里，我们显示与PSMA8相关的蛋白酶体对精子发生过程中减数分裂蛋白的降解和减数分裂I的进行是必不可少的。PSMA8在来自粗线期的精细胞中表达，并组装一种类型的睾丸特异性核心蛋白酶体。PSMA8的缺失降低了睾丸中蛋白酶体的丰度。通常在前阶段I后期降解的减数分裂蛋白（例如RAD51和RPA1）在PSMA8缺失的精母细胞中保持稳定。而且，PSMA8无效的精母细胞表现出延迟的M期进入，并最终在该阶段被阻滞，导致男性不育。然而，女性减数分裂进展既不表达也不要求PSMA8。因此，减数分裂I在精子发生中的进展，特别是进入和退出M期，需要与PSMA8相关的蛋白酶体的蛋白酶体活性。
更新日期：2019-07-29
中文翻译：
减数分裂I在精子发生过程中的进展需要一种特定于睾丸的20S核心蛋白酶体。
精子发生受到泛素化和蛋白酶体降解的严格调控，尤其是在精子发生过程中，组蛋白被鱼精蛋白替代。但是，蛋白酶体活性在减数分裂I和II中的功能仍然难以捉摸。在这里，我们显示与PSMA8相关的蛋白酶体对精子发生过程中减数分裂蛋白的降解和减数分裂I的进行是必不可少的。PSMA8在来自粗线期的精细胞中表达，并组装一种类型的睾丸特异性核心蛋白酶体。PSMA8的缺失降低了睾丸中蛋白酶体的丰度。通常在前阶段I后期降解的减数分裂蛋白（例如RAD51和RPA1）在PSMA8缺失的精母细胞中保持稳定。而且，PSMA8无效的精母细胞表现出延迟的M期进入，并最终在该阶段被阻滞，导致男性不育。然而，女性减数分裂进展既不表达也不要求PSMA8。因此，减数分裂I在精子发生中的进展，特别是进入和退出M期，需要与PSMA8相关的蛋白酶体的蛋白酶体活性。
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