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

Author:

Lan Kuo-Chung123ORCID,Cheng Yin-Hua1ORCID,Chang Yun-Chiao1,Wei Kuo-Ting24ORCID,Weng Pei-Ling1,Kang Hong-Yo12456ORCID

Affiliation:

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

2. Center for Menopause and Reproductive Medicine Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833401, Taiwan

3. Department of Obstetrics and Gynecology, Jen-Ai Hospital, Taichung 412224, Taiwan

4. Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Kaohsiung 833401, Taiwan

5. Department of Biological Science, National Sun Yat-sen University, Kaohsiung 804201, Taiwan

6. Division of Endocrinology and Metabolism, Department of Internal Medicine, 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.

Funder

Chang Gung Memorial Hospital

Publisher

MDPI AG

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