ArticleJournal of molecular cell biology2025
Intraflagellar transport-associated CCDC92 is required for spermiogenesis and male fertility in mice.
Article in Journal of molecular cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The New Nexin-Dynein Regulatory Complex Component CCDC153 Is Dispensable for Ciliary Motility and Fertility in Mice.Cytoskeleton (Hoboken, N.J.) · 2026Article
- The Cilia-Associated Protein CCDC89 Is Dispensable for Male Fertility in Mice.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Proteomic composition and mutual assembly of the C2a projection in vertebrate motile cilia.eLife · 2026Article
- Filippi syndrome-associated CKAP2L modulates microtubule dynamics essential for mitosis and ciliary length regulation.Journal of molecular cell biology · 2026Article
- JHY enables the transition from switchable to fixed ciliary waveforms in metazoan evolution.EMBO reports · 2026Article
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Authors and funding
12 authors.
Funding
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.
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