ArticleJournal of cellular and molecular medicine2024
CCDC157 is essential for sperm differentiation and shows oligoasthenoteratozoospermia-related mutations in men.
Article in Journal of cellular and molecular medicine, 2024. 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, 9 citations in OpenAlex.
- Loss-of-function mutations in Ccdc113 cause male infertility in both humans and mice.Asian journal of andrology · 2026Article
- Article
- Of mice and men: translating mouse knockout models of human male infertility.Reproduction (Cambridge, England) · 2025Review
- Loss of Cep135 causes oligoasthenoteratozoospermia and male infertility in mice.Cellular and molecular life sciences : CMLS · 2025Article
- CCDC157 is essential for sperm differentiation and shows oligoasthenoteratozoospermia-related mutations in men.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Oligoasthenoteratospermia (OAT), characterized by abnormally low sperm count, poor sperm motility, and abnormally high number of deformed spermatozoa, is an important cause of male infertility. Its genetic basis in many affected individuals remains unknown. Here, we found that CCDC157 variants are associated with OAT. In two cohorts, a 21-bp (g.30768132_30768152del21) and/or 24-bp (g.30772543_30772566del24) deletion of CCDC157 were identified in five sporadic OAT patients, and 2 cases within one pedigree. In a mouse model, loss of Ccdc157 led to male sterility with OAT-like phenotypes. Electron microscopy revealed misstructured acrosome and abnormal head-tail coupling apparatus in the sperm of Ccdc157-null mice. Comparative transcriptome analysis showed that the Ccdc157 mutation alters the expressions of genes involved in cell migration/motility and Golgi components. Abnormal Golgi apparatus and decreased expressions of genes involved in acrosome formation and lipid metabolism were detected in Ccdc157-deprived mouse germ cells. Interestingly, we attempted to treat infertile patients and Ccdc157 mutant mice with a Chinese medicine, Huangjin Zanyu, which improved the fertility in one patient and most mice that carried the heterozygous mutation in CCDC157. Healthy offspring were produced. Our study reveals CCDC157 is essential for sperm maturation and may serve as a marker for diagnosis of OAT.
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