Academic Journal

RhoGDIα regulates spermatogenesis through Rac1/cofilin/F-actin signaling

التفاصيل البيبلوغرافية
العنوان: RhoGDIα regulates spermatogenesis through Rac1/cofilin/F-actin signaling
المؤلفون: Zhu, Haixia, Wen, Zongzhuang, Zhang, Aizhen, Liu, Dongyue, Wang, Hongxiang, Cheng, Yin, Yang, Xing, Xiao, Yu, Li, Jianyuan, Sun, Daqing, Wu, Bin, Gao, Jiangang
المساهمون: National Natural Science Foundation of China, Natural Science Foundation of Shandong Province
المصدر: Communications Biology ; volume 6, issue 1 ; ISSN 2399-3642
بيانات النشر: Springer Science and Business Media LLC
سنة النشر: 2023
الوصف: Spermatogenesis is an extremely complex process, and any obstruction can cause male infertility. RhoGDIα has been identified as a risk of male sterility. In this study, we generate RhoGDIα knockout mice, and find that the males have severely low fertility. The testes from RhoGDIα −/− mice are smaller than that in WT mice. The numbers of spermatogonia and spermatocytes are decreased in RhoGDIα −/− testis. Spermatogenesis is compromised, and spermatocyte meiosis is arrested at zygotene stage in RhoGDIα −/− mice. Acrosome dysplasia is also observed in sperms of the mutant mice. At the molecular level, RhoGDIα deficiency activate the LIMK/cofilin signaling pathway, inhibiting F-actin depolymerization, impairing testis and inducing low fertility in mouse. In addition, the treatment of RhoGDIα −/− mice with Rac1 inhibitor NSC23766 alleviate testis injury and improve sperm quality by inhibiting the LIMK/cofilin/F-actin pathway during spermatogenesis. Together, these findings reveal a previously unrecognized RhoGDIα/Rac1/F-actin-dependent mechanism involved in spermatogenesis and male fertility.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1038/s42003-023-04579-7
الاتاحة: http://dx.doi.org/10.1038/s42003-023-04579-7
https://www.nature.com/articles/s42003-023-04579-7.pdf
https://www.nature.com/articles/s42003-023-04579-7
Rights: https://creativecommons.org/licenses/by/4.0 ; https://creativecommons.org/licenses/by/4.0
رقم الانضمام: edsbas.4A50C993
قاعدة البيانات: BASE
الوصف
DOI:10.1038/s42003-023-04579-7