Study summary · research use only
Spermatogenesis does not require the local production of follistatin
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this mouse study, the authors examined whether local follistatin production is required for spermatogenesis. Because follistatin-null mice die soon after birth, fetal testes collected at day 18 of gestation from follistatin-null mice were transplanted to the ear of castrated immunocompromised male mice and analysed 7-8 weeks later. They report that full spermatogenesis developed in the transplanted testes of both wild-type and follistatin-null mice. The authors interpret this as indicating that, if follistatin is needed to modulate spermatogenic development, it is not supplied by local testicular production but by circulating follistatin from the host mouse.
Abstract
It has been proposed that follistatin can modulate the actions of activins and/or other members of the transforming growth factor-beta 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.
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