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ORIGINAL RESEARCH article

Front. Cell Dev. Biol.
Sec. Cellular Biochemistry
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1481659
This article is part of the Research Topic Advances on Molecular Mechanisms Regulating Reproduction - From Gametogenesis to Fertilization View all articles

Tle6 Deficiency in Male Mice Led to Abnormal Sperm Morphology and Reduced Sperm Motility

Provisionally accepted
Kousuke Kazama Kousuke Kazama 1,2Yuki Miyagoshi Yuki Miyagoshi 1Hirofumi Nishizono Hirofumi Nishizono 1*
  • 1 Medical Research Institute, Kanazawa Medical University, Uchinada, Japan
  • 2 Faculty of Life and Environmental Science, University of Yamanashi, Kofu, Yamanashi, Japan

The final, formatted version of the article will be published soon.

    Infertility affects over 15% of the global population, and genetic mutations are a substantial cause of infertility. Recent studies have focused on the subcortical maternal complex and its role in early embryonic development. TLE6, a core protein in the subcortical maternal complex, is crucial for female fertility; however, its role in male germ cells remains poorly understood. In this study, we generated a novel Tle6 knockout mouse model using CRISPR-Cas9 to examine the impact of Tle6 mutations on male fertility. Tle6 knockout males exhibited a reduced total sperm count compared to wild-type mice, with a marked decrease in highly motile sperm. Histological observation of Tle6 +/- mouse testes showed no apparent structural changes, though impaired sperm maturation was observed. Immunofluorescence staining showed that TLE6 localizes to the midpiece of sperm. It was also confirmed that the expression of Tle6 is reduced in Tle6 +/-male mice. In addition, Tle6 +/-mice exhibited a significant increase in serum testosterone levels compared to wild-type mice. Changes in the expression of genes related to sperm function were also observed in the testes of Tle6 knockout mice. These findings suggest that TLE6 is involved in sperm production and function, and that mutations in TLE6 may impair the production of functional sperm in humans, potentially leading to infertility.

    Keywords: Transducin-like enhancer of split 6, subcortical maternal complex, Infertility, Male germ cell, sperm

    Received: 16 Aug 2024; Accepted: 15 Oct 2024.

    Copyright: © 2024 Kazama, Miyagoshi and Nishizono. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Hirofumi Nishizono, Medical Research Institute, Kanazawa Medical University, Uchinada, 920-0293, Japan

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