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Updated: Jun 25, 2025

Isolation of Sertoli Cells and Peritubular Cells from Rat Testes
Published on: February 8, 2016
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.
Abstract:
Spermatogenesis is a highly regulated process dependent on androgen receptor (AR) signaling in Sertoli cells. However, the pathogenic mechanisms of spermatogenic failure, by which loss of AR impairs downstream target genes to affect Sertoli cell function, remain incompletely understood. By using microarray analysis, we identified several AR-regulated genes involved in the maturation of spermatogenesis, including chromodomain Y-like protein (CDYL) and transition proteins 1 (TNP-1), that were significantly decreased in ARKO mouse testes. AR and CDYL were found to co-localize and interact in Sertoli cells. The AR-CDYL complex bound to the promoter regions of TNP1 and modulated their transcriptional activity. CDYL acts as a co-regulator of AR transactivation, and its expression is decreased in the Sertoli cells of human testes from patients with azoospermia. The androgen receptor-chromodomain Y-like protein axis plays a crucial role in regulating a network of genes essential for spermatogenesis in Sertoli cells. Disruption of this AR-CDYL regulatory axis may contribute to spermatogenic failure. These findings provide insights into novel molecular mechanisms targeting the AR-CDYL signaling pathway, which may have implications for developing new therapeutic strategies for male infertility.
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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