| First Author | Zhu H | Year | 2023 |
| Journal | Commun Biol | Volume | 6 |
| Issue | 1 | Pages | 214 |
| PubMed ID | 36823181 | Mgi Jnum | J:360949 |
| Mgi Id | MGI:7438507 | Doi | 10.1038/s42003-023-04579-7 |
| Citation | Zhu H, et al. (2023) RhoGDIalpha regulates spermatogenesis through Rac1/cofilin/F-actin signaling. Commun Biol 6(1):214 |
| abstractText | Spermatogenesis is an extremely complex process, and any obstruction can cause male infertility. RhoGDIalpha has been identified as a risk of male sterility. In this study, we generate RhoGDIalpha knockout mice, and find that the males have severely low fertility. The testes from RhoGDIalpha(-/-) mice are smaller than that in WT mice. The numbers of spermatogonia and spermatocytes are decreased in RhoGDIalpha(-/-) testis. Spermatogenesis is compromised, and spermatocyte meiosis is arrested at zygotene stage in RhoGDIalpha(-/-) mice. Acrosome dysplasia is also observed in sperms of the mutant mice. At the molecular level, RhoGDIalpha deficiency activate the LIMK/cofilin signaling pathway, inhibiting F-actin depolymerization, impairing testis and inducing low fertility in mouse. In addition, the treatment of RhoGDIalpha(-/-) 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 RhoGDIalpha/Rac1/F-actin-dependent mechanism involved in spermatogenesis and male fertility. |
