黒木, 俊介 Osaka University KAKEN研究者をさがす
Maeda, Ryo Osaka University
矢野, 雅司 Tokushima University 徳島大学 教育研究者総覧 KAKEN研究者をさがす
Kitano, Satsuki Kyoto University
Miyachi, Hitoshi Kyoto University
Fukuda, Mikiko Kyoto University
Shinkai, Yoichi RIKEN
立花, 誠 Osaka University|Tokushima University KAKEN研究者をさがす
Histone H3 lysine 9 (H3K9) methylation is dynamically regulated by methyltransferases and demethylases. In spermatogenesis, prospermatogonia differentiate into differentiating or undifferentiated spermatogonia after birth. However, the epigenetic regulation of prospermatogonia to spermatogonia transition is largely unknown. We found that perinatal prospermatogonia have extremely low levels of di-methylated H3K9 (H3K9me2) and that H3K9 demethylases, JMJD1A and JMJD1B, catalyze H3K9me2 demethylation in perinatal prospermatogonia. Depletion of JMJD1A and JMJD1B in the embryonic germline resulted in complete loss of male germ cells after puberty, indicating that H3K9me2 demethylation is essential for male germline maintenance. JMJD1A/JMJD1B-depleted germ cells were unable to differentiate into functional spermatogonia. JMJD1 isozymes contributed to activation of several spermatogonial stem cell maintenance genes through H3K9 demethylation during the prospermatogonia to spermatogonia transition, which we propose is key for spermatogonia development. In summary, JMJD1A/JMJD1B-mediated H3K9me2 demethylation promotes prospermatogonia to differentiate into functional spermatogonia by establishing proper gene expression profiles.
Stem Cell Reports
International Society for Stem Cell Research|Cell Press
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
stemcr_15_2_424.pdf 5.29 MB