TMC7 is required for spermiogenesis and male fertility by regulating TGN-derived vesicles.

Infertility affects 10-12 % of couples worldwide, 50 % of which are male. Abnormal spermatogenesis is among the main causes of male infertility. We were curious about the possible role of transmembrane channel-like protein 7 (TMC7) in spermatogenesis because of its aberrant expression in several male infertility patients. In this study, we found that deletion of Tmc7, which is highly expressed during spermiogenesis, causes a human oligoasthenoteratozoospermia (OAT)-like phenotype in male mice. By histological analysis, TEM, RNA-seq and library-free data-independent acquisition mass spectrometry (DIA-MS) of TMC7-null mouse testes, we found that Tmc7 deletion caused abnormal swelling of trans-Golgi network (TGN) vesicles in elongated spermatids. Further immunofluorescence localization analysis revealed that these vesicles were defined by synaptophysin-like 1 (SYPL1). In addition, TMC7 may act as a potential chloride transport channel to regulate the size of transport vesicles. In conclusion, this study demonstrated that TMC7 is essential for male fertility and may be used as a potential protein for the identification and recognition of OAT. On the other hand, TMC7 may be a potential male contraceptive target. Copyright © 2024 Elsevier B.V. All rights reserved.

Citation

Zheng Lv, Longjie Sun, Xuexue Chen, Peilan Guo, Xiaomei Xie, Xiaohong Yao, Shuang Tian, Chaofan Wang, Yujing Shao, Jiali Liu. TMC7 is required for spermiogenesis and male fertility by regulating TGN-derived vesicles. International journal of biological macromolecules. 2025 Mar;293:139070

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PMID: 39732242

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