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Spermatogenesis does not require the local production of follistatin

S-Y Lin1, J R Morrison, M M Matzuk

  • 1Monash Institute of Medical Research, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia.

Reproduction (Cambridge, England)
|September 30, 2006
PubMed

Insights

Follistatin does not appear essential for testicular development. If follistatin modulates spermatogenesis, it relies on circulating sources, not local testicular production, according to this study.

Area of Science:

  • Reproductive biology
  • Endocrinology
  • Developmental biology

Background:

  • Follistatin (FS) is hypothesized to regulate testicular function by modulating activins and other TGF-β superfamily members.
  • Overexpression of follistatin in mice has been linked to disrupted spermatogenesis.
  • Follistatin null mice die perinatally, preventing direct study of its absence on testicular function.

Purpose of the Study:

  • To investigate the role of follistatin in the development and maintenance of spermatogenesis.
  • To determine if local testicular production of follistatin is necessary for normal testicular function.

Main Methods:

  • Fetal testes from follistatin null and wild-type mice were collected at day 18 of gestation.
  • Testicular grafts were transplanted into the ears of castrated, immunocompromised mice (RAG1-/-).
  • Grafts were analyzed after 7-8 weeks to assess spermatogenesis.

Main Results:

  • Full spermatogenesis was observed in transplanted testes from both wild-type and follistatin null mice.
  • This indicates that the absence of follistatin did not prevent the development of spermatogenesis in the grafted testes.
  • The findings suggest that follistatin's role, if any, in spermatogenesis is not dependent on local testicular production.

Conclusions:

  • Follistatin is not essential for the development of spermatogenesis in the studied model.
  • Circulating follistatin from the host environment, rather than local testicular production, may be the source if follistatin modulates spermatogenic development.
  • This study utilized a novel transplantation model to overcome limitations of existing follistatin knockout mouse models.

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