Interaction between Chromodomain Y-like Protein and Androgen Receptor Signaling in Sertoli Cells Accounts for

Kuo-Chung Lan1,2,3, Yin-Hua Cheng1, Yun-Chiao Chang1

  • 1Department of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833401, Taiwan.

Cells
|May 24, 2024
PubMed

Insights

The androgen receptor (AR) and chromodomain Y-like protein (CDYL) form a complex crucial for spermatogenesis. Disruption of this AR-CDYL axis in Sertoli cells may cause male infertility.

Area of Science:

  • Reproductive biology
  • Molecular endocrinology
  • Spermatogenesis research

Background:

  • Spermatogenesis relies on androgen receptor (AR) signaling in Sertoli cells.
  • Pathogenic mechanisms of spermatogenic failure due to AR disruption are not fully understood.

Purpose of the Study:

  • To investigate the role of AR-regulated genes in spermatogenesis.
  • To elucidate the molecular mechanisms underlying AR-mediated Sertoli cell function and spermatogenic failure.

Main Methods:

  • Microarray analysis of AR knockout (ARKO) mouse testes.
  • Co-localization and interaction studies of AR and CDYL in Sertoli cells.
  • Analysis of AR-CDYL complex binding to gene promoter regions.

Main Results:

  • Chromodomain Y-like protein (CDYL) and transition protein 1 (TNP-1) were identified as AR-regulated genes decreased in ARKO mice.
  • AR and CDYL co-localize and interact in Sertoli cells, forming a complex that binds to TNP1 promoters.
  • CDYL functions as an AR co-regulator, and its expression reduction is observed in human azoospermia testes.

Conclusions:

  • The androgen receptor-chromodomain Y-like protein axis is vital for regulating genes essential for spermatogenesis in Sertoli cells.
  • Disruption of the AR-CDYL regulatory axis may contribute to spermatogenic failure and male infertility.
  • Targeting the AR-CDYL signaling pathway offers potential therapeutic strategies for male infertility.

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