Haprin-deficient spermatozoa are incapable of in vitro fertilization
Haprin-deficient spermatozoa are incapable of in vitro fertilization
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DOI：
10.1002/mrd.23344
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发表时间：
2020-04-20
影响因子：
2.5
通讯作者：
Tanaka, Hiromitsu
中科院分区：
文献类型：
--
作者：
Aoki, Yusuke;Tsujimura, Akira;Tanaka, Hiromitsu
Haprin (TRIM36) 是一种泛素蛋白连接酶，可介导靶蛋白的泛素化和随后的蛋白酶体降解。它在小鼠和人类的睾丸中表达，被认为参与精子发生、顶体反应和受精。然而，人们对 Haprin 的功能作用知之甚少。本研究的目的是调查 Haprin 在生育方面的生理作用。产生了纯合的 harin 缺陷小鼠，并对这些小鼠及其精子进行了分析，以检测形态和生育相关的异常。在这些模型中，观察到正常的精子发生，但与野生型小鼠相比，haprin缺陷型小鼠的精子形态和活力较差，精子质量下降。有趣的是，haprin缺陷的小鼠表现出正常的体内生育能力，但在标准体外受精条件下不能使卵母细胞受精。总之，本研究证明 Haprin 缺乏会导致精子形态异常，表明 Haprin 参与精子发生。
Haprin (TRIM36) is a ubiquitin-protein ligase that mediates ubiquitination and subsequent proteasomal degradation of target proteins. It is expressed in the testes in both mice and humans and is thought to be involved in spermiogenesis, the acrosome reaction, and fertilization. However, the functional role of Haprin is poorly understood. The aim of this study was to investigate the physiological role of Haprin in fertility. Homozygous haprin-deficient mice were generated and these mice, and their spermatozoa, were analyzed to detect morphological and fertility-related abnormalities. In these models, normal spermatogenesis was observed but sperm quality was reduced with haprin-deficient mice having poorer sperm morphology and motility than wild-type mice. Interestingly, haprin-deficient mice showed normal in vivo fertility but could not fertilize oocytes under standard in vitro fertilization conditions. In conclusion, this study demonstrated that Haprin deficiency causes morphological abnormalities in spermatozoa, indicating that Haprin is involved in spermiogenesis.