Rad9a is Required for Spermatogonia Differentiation in Mice
Overview
Authors
Affiliations
Spermatogenesis in testes requires precise spermatogonia differentiation. Spermatocytes lacking the Rad9a gene are arrested in pachytene prophase, implying a possible role for RAD9A in spermatogonia differentiation. However, numerous RAD9A-positive pachytene spermatocytes are still observed in mouse testes following Rad9a excision using the Stra8-Cre system, and it is unclear whether Rad9a deletion in spermatogonia interrupts differentiation. Here, we generated a mouse model in which Rad9a was specifically deleted in spermatogonial stem cells (SSCs) using Cre recombinase expression driven by the germ cell-specific Vasa promoter. Adult Rad9a-null male mice were infertile as a result of completely blocked spermatogonia differentiation. No early spermatocytes were detected in mutant testicular cords of 9-day-old mice. Mutant spermatogonia were prone to apoptosis, although proliferation rates were unaffected. Rad9a deletion also resulted in malformation of seminiferous tubules, in which cells assembled irregularly into clusters, and malformation led to testicular cord disruption. Our findings suggest that Rad9a is indispensable for spermatogonia differentiation and testicular development in mice.
Dynamic Expression Profile of Follicles at Different Stages in High- and Low-Production Laying Hens.
Yang L, Fan X, Tian K, Yan S, Xu C, Tian Y Genes (Basel). 2024; 15(1).
PMID: 38254930 PMC: 10815237. DOI: 10.3390/genes15010040.
Rad9a is involved in chromatin decondensation and post-zygotic embryo development in mice.
Huang L, Meng T, Ma X, Wang Z, Qi S, Chen Q Cell Death Differ. 2018; 26(5):969-980.
PMID: 30154445 PMC: 6461798. DOI: 10.1038/s41418-018-0181-9.