Androgen receptor in Sertoli cells is not required for testosterone-induced suppression of spermatogenesis, but contributes to Sertoli cell organization in Utp14b jsd mice.

ABSTRACT: Testosterone acting through the androgen receptor (AR) maintains the arrest of spermatogonial differentiation in juvenile spermatogonial depletion (jsd mutation in the Utp14b gene) mutant adult male mice. It is not known which of the somatic cell types expressing AR mediates this inhibition. To determine whether Sertoli cells are responsible, we selectively eliminated AR in Sertoli cells in jsd mice containing a floxed-Ar gene and an anti-Müllerian hormone-Cre transgene. In these Sertoli AR-knockout (SCARKO)-jsd mice, spermatogonial differentiation did not recover. However, the normal organization of Sertoli cell nuclei was drastically disrupted in SCARKO-jsd mice compared with SCARKO or jsd mice. In addition, the extent of ectoplasmic specializations was reduced; tight junctions were not

SUBMITTER: Wang G 

PROVIDER: S-EPMC2797546 | biostudies-literature | 2009 May-Jun

REPOSITORIES: biostudies-literature