Testis-enriched Socs7 is not essential for spermatogenesis and male fertility in mice.

Abstract

Objectives: As a crucial member of the Suppressor of Cytokine Signaling (SOCS) family, SOCS7 regulates various physiological processes, including insulin resistance, inflammation, and tumor suppression. However, its role in male germ cells remains poorly understood. This study aims to investigate the function of SOCS7 in spermatogenesis and uncover its potential regulatory mechanisms.

Methods: We conducted bioinformatics analyses to examine the expression profile of Socs7 in the testes, generated Socs7-knockout (KO) mice using CRISPR/Cas9 genome editing, and assessed testicular morphology through histological and immunohistochemical staining. Semen quality was evaluated using computer-assisted sperm analysis (CASA), and testicular apoptosis was examined using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay.

Results: Bioinformatics analysis revealed high expression of Socs7 in both human and mouse testes. However, Socs7-KO mice exhibited normal fertility, with no significant differences in testicular morphology, sperm quality, or spermatogenesis compared to wild-type (WT) mice. Additionally, testicular apoptosis in Socs7-KO mice was not significantly altered.

Conclusions: Our study demonstrates that although Socs7 is highly expressed in the testes, its deletion does not impair male fertility or spermatogenesis in mice. These findings provide valuable insights into the role of SOCS7 in male reproduction and help prevent unnecessary duplication of research efforts.