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Retinoids and spermatogenesis: Lessons from mutant mice lacking the plasma retinol binding protein
Author(s) -
Ghyselinck Norbert B.,
Vernet Nadège,
Dennefeld Christine,
Giese Norbert,
Nau Heinz,
Chambon Pierre,
Viville Stéphane,
Mark Manuel
Publication year - 2006
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20795
Subject(s) - biology , spermatid , sertoli cell , spermatogenesis , retinoic acid , endocrinology , medicine , spermiogenesis , microbiology and biotechnology , context (archaeology) , mutant , genetics , gene , paleontology
Using Rbp4 ‐null mice as models, we have established for the first time the kinetics of the spermatogenetic alterations during vitamin A deficiency (VAD). Our data demonstrate that the VAD‐induced testicular degeneration arises through the normal maturation of germ cells in a context of spermatogonia differentiation arrest. They indicate that retinoic acid (RA) appears dispensable for the transition of premeiotic to meiotic spermatocytes, meiosis, and spermiogenesis. They confirm that RA plays critical roles in controlling spermatogonia differentiation, spermatid adhesion to Sertoli cells, and spermiation, and suggest that the VAD‐induced arrest of spermatogonia differentiation results from simultaneous blocks in RA‐dependent events mediated by RA receptor γ (RARγ) in spermatogonia and by RARα in Sertoli cells. They also provide evidence that expression of major RA‐metabolizing enzymes is increased in mouse Sertoli cells upon VAD and that vitamin A‐deficient A spermatogonia differ from their RA‐sufficient counterparts by the expression of the Stra8 gene. Developmental Dynamics 235:1608–1622, 2006. © 2006 Wiley‐Liss, Inc.