山东师范大学宋婷团队在研究中取得进展。他们发现了鞭毛内转运相关的CCDC92是小鼠精子发生和雄性生育所必需的。2025年8月5日出版的《分子细胞生物学报》杂志发表了这项成果。

在本研究中，研究组发现小鼠CCDC92缺乏导致精子头和鞭毛的严重异常，导致雄性不育。睾丸Ccdc92基因敲除精子的超微结构分析显示严重变形的manchette结构。manchette缺陷损害了精子核的延伸和顶体的锚定，导致了畸形的棒状核和顶体的分离。在分子上，CCDC92与鞭毛内运输（IFT）复合物组分相互作用，并精子细胞发育过程中与IFT蛋白共定位。定量蛋白质组学进一步揭示了CCDC92对轴突微管内蛋白的鞭毛分布的要求。他们的发现证明了CCDC92在调节精子形成中的重要作用，并为男性不育的病理提供了新的见解。

据了解，圆形精细胞向流线型精细胞的分化涉及一系列显著的形态变化，如精子头的形成和鞭毛的形成。然而，精子形成的潜在机制尚不清楚。

附：英文原文

Title: Intraflagellar transport-associated CCDC92 is required for spermiogenesis and male fertility in mice

Author: Lu, Yue, Zi, Xirui, Lyu, Qian, Li, Qingchao, Yin, Hanxiao, Wang, Yinghao, Chen, Qijun, Kang, Bingkun, Nai, Shanshan, Zhou, Jun, Zhao, Huijie, Song, Ting

Issue&Volume: 2025-08-05

Abstract: The differentiation of a round spermatid into a streamlined sperm cell involves a series of remarkable morphological changes, such as sperm head shaping and flagellum formation. However, the underlying mechanism of spermatid shaping remains unclear. In this study, we find that CCDC92 deficiency in mice leads to severe abnormalities of the sperm head and flagellum and causes male infertility. Ultrastructural analyses of testicular elongating Ccdc92 knockout spermatids reveal severely deformed manchette structures. The manchette defects impair the subsequent sperm nucleus elongation and acrosome anchoring, resulting in misshapen rod-like nuclei and detached acrosomes. Molecularly, CCDC92 interacts with intraflagellar transport (IFT) complex components and colocalizes with IFT proteins at the manchette in developing spermatids. Quantitative proteomics further reveals the requirement of CCDC92 for proper flagellar distribution of axonemal microtubule inner proteins. Our findings demonstrate an essential role of CCDC92 in regulating spermatid shaping and provide novel insights into the pathology of male infertility.

DOI: 10.1093/jmcb/mjaf022

Source: https://academic.oup.com/jmcb/advance-article/doi/10.1093/jmcb/mjaf022/8222501?searchresult=1