Fiche publication
Date publication
janvier 1996
Journal
Genes & development
Auteurs
Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre
,
Dr KASTNER Philippe
,
Dr MARK Manuel
,
Dr KREZEL Wojciech
Tous les auteurs :
Kastner P, Mark M, Leid M, Gansmuller A, Chin W, Grondona JM, Décimo D, Krezel W, Dierich A, Chambon P
Lien Pubmed
Résumé
We have generated mouse lines in which the RXR beta gene was disrupted by homologous recombination. Approximately 50% of the RXR beta homozygous mutants died before or at birth, but those that survived appeared normal except that the males were sterile, owing to oligo-astheno-teratozoospermia. Failure of spermatid release occurred within the germinal epithelium, and the epididymis contained very few spermatozoa that, in addition, exhibited abnormal acrosomes and tails. There was a progressive accumulation of lipids within the mutant Sertoli cells, which were histochemically characterized as unsaturated triglycerides. In old mutant males, progressive degeneration of the germinal epithelium occurred, ending with the formation of acellular lipid-filled tubules. The selective expression of RXR beta in Sertoli cells, together with the timing of appearance of the histological abnormalities, suggests that the primary defect resulting from the mutation resides in these cells.
Mots clés
Animals, Animals, Newborn, Fetal Death, genetics, Gene Expression Regulation, Developmental, Heterozygote, Homozygote, Immunohistochemistry, Infertility, Male, genetics, Lipid Metabolism, Male, Mice, Mice, Transgenic, Mutation, Receptors, Cytoplasmic and Nuclear, genetics, Receptors, Retinoic Acid, analysis, Retinoid X Receptors, Seminiferous Tubules, pathology, Sertoli Cells, metabolism, Spermatogenesis, genetics, Spermatozoa, abnormalities, Transcription Factors, analysis, Transcription, Genetic
Référence
Genes Dev.. 1996 Jan;10(1):80-92
