ArticleCell proliferation2026
YKT6 Is Essential for Male Fertility by Promoting Meiosis Progression During Spermatogenesis of Mice.
Article in Cell proliferation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Sex differences in urinary extracellular vesicles originating from the genitourinary system in health and disease.American journal of physiology. Renal physiology · 2026Review
- Integrated multiomics profiling of amniotic fluid exosomes reveals dysregulated lipid and protein signatures in fetal 22q11.2 deletion syndrome.Human genomics · 2026Article
- YKT6 Is Essential for Male Fertility by Promoting Meiosis Progression During Spermatogenesis of Mice.Cell proliferation · 2026Article
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Authors and funding
9 authors.
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Abstract
SNARE proteins are required for membrane fusion events throughout the endomembrane system, and are therefore associated with vesicular transport. Here, we found that the SNARE family member, YKT6, is indispensable for male fertility in mice. Conditional Ykt6 knockout in pre-meiotic and meiotic germ cells leads to complete sterility and meiotic arrest in male mice, which exhibit loss of spermatocytes in seminiferous tubules, but without obvious disruption of chromosomal behaviours during meiosis. We observed that the abundance of syncytia increases along with abnormal morphology of the Golgi apparatus, while lysosomes decrease in Ykt6-cKO testes. Quantitative proteomics and immunofluorescent staining both showed dysregulation of vesicular transport in YKT6-deficient spermatocytes. Additionally, the recombinant mouse proteins, HA::YKT6 and MYC::STX1A, could interact in vitro, further supporting a likely role in mediating transport vesicle fusion with the plasma membrane. Finally, the absence of TEX14 signal within syncytia and enlarged TEX14 rings between spermatocytes together suggest a failure to stabilise intercellular bridges in Ykt6-cKO testes. These results demonstrate that YKT6 is required for male fertility by promoting meiosis progression through vesicular transport regulation during spermatogenesis in mice, expanding our understanding of YKT6 functions, and suggesting a possible strategy for future interventions for male infertility in humans.
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