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Spermatogenesis and Sertoli Cell Activity in Mice Lacking Sertoli Cell Receptors for Follicle-Stimulating Hormone and Androgen

Department of Human Anatomy and Genetics (M.H.A., H.M.C.), University of Oxford, Oxford OX1 3QX, United Kingdom; Division of Cell Sciences (P.J.B., A.M., P.J.O.), University of Glasgow Veterinary School, Glasgow G61 1QH, United Kingdom; Laboratory for Experimental Medicine and Endocrinology (G.V., K.D.G.), Catholic University of Leuven, B-3000 Leuven, Belgium; Unité Mixte de Recherche 6175 (F.G.), Institut National de la Recherche Agronomique, Centre National de Recherche Scientifique, Université de Tours, 37380 Nouzilly, France

Address all correspondence and requests for reprints to: P. J. O'Shaughnessy, Division of Cell Sciences, University of Glasgow Veterinary School, Bearsden Road, Glasgow G61 1QH, United Kingdom. E-mail: p.j.oshaughnessy{at}vet.gla.ac.uk.

Spermatogenesis in the adult male depends on the action of FSH and androgen. Ablation of either hormone has deleterious effects on Sertoli cell function and the progression of germ cells through spermatogenesis. In this study we generated mice lacking both FSH receptors (FSHRKO) and androgen receptors on the Sertoli cell (SCARKO) to examine how FSH and androgen combine to regulate Sertoli cell function and spermatogenesis. Sertoli cell number in FSHRKO-SCARKO mice was reduced by about 50% but was not significantly different from FSHRKO mice. In contrast, total germ cell number in FSHRKO-SCARKO mice was reduced to 2% of control mice (and 20% of SCARKO mice) due to a failure to progress beyond early meiosis. Measurement of Sertoli cell-specific transcript levels showed that about a third were independent of hormonal action on the Sertoli cell, whereas others were predominantly androgen dependent or showed redundant control by FSH and androgen. Results show that FSH and androgen act through redundant, additive, and synergistic regulation of spermatogenesis and Sertoli cell activity. In addition, the Sertoli cell retains a significant capacity for activity, which is independent of direct hormonal regulation.