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Spermatogenesis does not require the local production of follistatin

Monash Institute of Medical Research, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia and ¹ Departments of Pathology, Molecular and Cellular Biology and Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA

Correspondence should be addressed to D M de Kretser; Email: david.de.kretser{at}med.monash.edu.au

It has been proposed that follistatin can modulate the actions of activins and/or other members of the transforming growth factor-ß superfamily of proteins on testicular function, since mice overexpressing follistatin showed spermatogenic disruption. However, since mice with targeted disruption of the follistatin gene die soon after birth, it is not feasible to determine the effect of the absence of follistatin on testicular function using this model. To further understand the role of follistatin on the development and maintenance of spermatogenesis, fetal testes, collected by Caesarean section at day 18 of gestation from follistatin null mice, were transplanted to the external ear of castrated recombination activating gene 1 immunocompromised male mice. The testicular grafts were then analysed 7–8 weeks after transplantation and showed that full spermatogenesis developed in both the testes of wild-type and follistatin null mice. This study indicates that, if follistatin is required to modulate spermatogenic development, it is not supplied by local testicular production but by circulating follistatin from the host mouse.