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Does murine spermatogenesis require WNT signalling? A lesson from Gpr177 conditional knockout mouse models.

Su-Ren Chen1, J-X Tang1,2, J-M Cheng1,2

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Depleting Gpr177 in mouse germ cells causes age-dependent testicular atrophy and fertility loss by increasing reactive oxygen species (ROS) and apoptosis. Gpr177 in Sertoli cells does not impact spermatogenesis.

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Area of Science:

  • Reproductive Biology
  • Molecular Endocrinology
  • Cellular Signaling

Background:

  • Wingless-related MMTV integration site (WNT) signaling is crucial in the testes, but its precise role in spermatogenesis is complex.
  • Previous studies using β-catenin mutants yielded inconsistent results due to pathway complexity and overlapping WNT expression.

Purpose of the Study:

  • To investigate the role of Gpr177, essential for WNT secretion, in murine spermatogenesis.
  • To dissect the specific functions of WNT signaling in germ cells versus Sertoli cells.

Main Methods:

  • Conditional depletion of the Gpr177 gene in murine germ cells (Mvh-Cre, Stra8-Cre) and Sertoli cells (Amh-Cre).
  • Assessment of fertility, testicular histology, reactive oxygen species (ROS) levels, and apoptosis (Caspase 3 activity) at 8 weeks and 8 months of age.

Main Results:

  • Germ cell-specific Gpr177 depletion led to late-onset testicular atrophy and fertility decline by 8 months.
  • Sertoli cell-specific Gpr177 depletion showed no impact on spermatogenesis or fertility.
  • Increased ROS levels were observed in Gpr177-deficient germ and Sertoli cells in an age-dependent manner.
  • Caspase 3 activity significantly increased only in germ cells of 8-month-old Gpr177 knockout mice.

Conclusions:

  • GPR177 in Sertoli cells is dispensable for normal spermatogenesis.
  • Loss of GPR177 in germ cells impairs spermatogenesis in an age-dependent manner.
  • This impairment is mediated by elevated ROS levels and subsequent germ cell apoptosis.