SummaryMutation in CFAP43 leads to severe asthenozoospermia and multiple morphological abnormalities of the sperm flagellum (MMAF) in both human and mouse. Previous studies have shown that disruption of intra-manchette transport (IMT) caused failure of flagellum assembly and sperm head shaping. In a previous study, therefore, we postulated that disruption of IMT may contribute to the failure of sperm flagellum formation and result in MMAF, however the mechanisms underlying these defects are still poorly understood. Cfap43-deficient mice were studied here to reveal the cellular mechanisms of abnormal sperm head morphology and MMAF. Depletion of Cfap43 led to abnormal spermiogenesis and caused MMAF, sperm head abnormality and oligozoospermia. Furthermore, both abnormal manchette and disorganized ectoplasmic specialization (ES) could be observed at the elongated spermatids in Cfap43-deficient mice. Therefore, our findings demonstrated that, in mice, CFAP43-mediated IMT is essential for sperm head shaping and sperm flagellum formation.

中文翻译：

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精子头部整形和鞭毛形成需要 CFAP43 介导的细胞内运输

摘要突变CFAP43导致人和小鼠严重的弱精子症和精子鞭毛 (MMAF) 的多种形态异常。先前的研究表明，内腔运输 (IMT) 的中断导致鞭毛组装和精子头部成形失败。因此，在之前的一项研究中，我们假设 IMT 的破坏可能导致精子鞭毛形成失败并导致 MMAF，但这些缺陷背后的机制仍然知之甚少。Cfap43此处研究了缺陷型小鼠以揭示异常精子头部形态和 MMAF 的细胞机制。耗竭Cfap43导致精子发生异常并引起MMAF、精子头部异常和少精子症。此外，在拉长的精子细胞中可以观察到异常的小细胞和杂乱无章的外质特化（ES）。Cfap43- 缺陷小鼠。因此，我们的研究结果表明，在小鼠中，CFAP43 介导的 IMT 对于精子头部塑造和精子鞭毛形成至关重要。