PUBLICATION

New insights into the role of mTORC1 in male fertility in zebrafish

Authors
Chen, Y., Tang, H., Wang, L., Wei, T., Liu, X., Lin, H.
ID
ZDB-PUB-191102-15
Date
2019
Source
General and comparative endocrinology   286: 113306 (Journal)
Registered Authors
Keywords
LH, Sertoli cell, mTORC1, sperm maturation, zebrafish
MeSH Terms
  • Animals
  • Fertility/genetics*
  • Male
  • Mechanistic Target of Rapamycin Complex 1/metabolism*
  • Sertoli Cells/metabolism
  • Sperm Motility/genetics*
  • Zebrafish
PubMed
31669651 Full text @ Gen. Comp. Endocrinol.
Abstract
Mechanistic target of rapamycin complex 1 (mTORC1) plays crucial roles in male fertility. In mammals, deregulation of mTORC1 led to disordered spermatogonia proliferation and spermatogenesis, which eventually caused infertility in males. However, its roles in male fertility of non-mammalian species remain unclarified. In the present study, it was found that treatment of rapamycin, an mTORC1 inhibitor, resulted in infertility with decreased milt production and sperm motility in zebrafish. However, it is surprising to find that spermatogenesis was normal in these fish. All types of germ cells were found and the proliferation of spermatogonia and spermatocyte were normal. These results suggested that maturation of sperm may be impaired in males treated with rapamycin. Increased apoptosis was found surrounding the lumen containing spermatozoa, implicating a loss of Sertoli cells in testes treated with rapamycin. Moreover, LH/hCG mediated up-regulation of steroidogenic genes was abolished. The expression of npr and ar induced by LH/hCG was also blocked, which further suppressed the signaling of progestin and androgen. Collectively, mTORC1 maintains male fertility via different mechanisms in fish and mammals. mTORC1 is dispensable for spermatogenesis in zebrafish, but possibly supports the maintenance of Sertoli cells and mediates the signaling of hormones, which are crucial for sperm maturation.
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Human Disease / Model
Sequence Targeting Reagents
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