Defects in the
                    <i>H3t</i>
                    Gene Cause an Increase in Leydig Cells With Impaired Spermatogenesis in Mice

Qianmei Wu, Miho Ito, Takeru Fujii, Kaori Tanaka, Kohta Nakatani, Yoshihiro Izumi, Takeshi Bamba, Takashi Baba, Kazumitsu Maehara, Kosuke Tomimatsu, Tatsuya Takemoto, Yasuyuki Ohkawa, Akihito Harada

doi:10.1111/gtc.13182

<jats:title>ABSTRACT</jats:title> <jats:p> Abnormalities in spermatogenesis, a fundamental component of male reproductive function, can cause male infertility. Somatic cells constituting the testis microenvironment are essential for controlling normal spermatogenesis. Although testicular somatic cells are thought to sense and respond to germ cells to ensure proper spermatogenesis, the details of this signaling mechanism are unknown. Here, we investigated somatic cell dynamics in testicular tissue lacking spermatogenesis using the mice with deletion of the testis‐specific histone H3 variant gene <jats:italic>H3t</jats:italic> . Testicular tissue sections of H3t <jats:sup>Δ/Δ</jats:sup> mice exhibited an increased interstitial area compared with those of wild‐type mice, which was primarily attributed to an increase in Leydig cell numbers. Furthermore, this increase in Leydig cells led to increased testosterone synthesis, which occurred alongside cellular senescence‐associated β‐galactosidase activity. These findings suggest that Leydig cells monitor the progress of spermatogenesis and possess a mechanism to promote functional germ cell formation. </jats:p>

Defects in the <i>H3t</i> Gene Cause an Increase in Leydig Cells With Impaired Spermatogenesis in Mice

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