DNA methylation of retrotransposon genes is regulated by Piwi family members MILI and MIWI2 in murine fetal testes

Satomi Kuramochi-Miyagawa, Toshiaki Watanabe, Kengo Gotoh, Yasushi Totoki, Atsushi Toyoda, Masahito Ikawa, Noriko Asada, Kanako Kojima, Yuka Yamaguchi, Takashi W. Ijiri, Kenichiro Hata, En Li, Yoichi Matsuda, Tohru Kimura, Masaru Okabe, Yoshiyuki Sakaki, Hiroyuki Sasaki, Toru Nakano

研究成果: Contribution to journalArticle査読

654 被引用数 (Scopus)

抄録

Silencing of transposable elements occurs during fetal gametogenesis in males via de novo DNA methylation of their regulatory regions. The loss of MILI (miwi-like) and MIWI2 (mouse piwi 2), two mouse homologs of Drosophila Piwi, activates retrotransposon gene expression by impairing DNA methylation in the regulatory regions of the retrotransposons. However, as it is unclear whether the defective DNA methylation in the mutants is due to the impairment of de novo DNA methylation, we analyze DNA methylation and Piwi-interacting small RNA (piRNA) expression in wild-type, MILI-null, and MIWI2-null male fetal germ cells. We reveal that defective DNA methylation of the regulatory regions of the Line-1 (long interspersed nuclear elements) and IAP (intracisternal A particle) retrotransposons in the MILI-null and MIWI2-null male germ cells takes place at the level of de novo methylation. Comprehensive analysis shows that the piRNAs of fetal germ cells are distinct from those previously identified in neonatal and adult germ cells. The expression of piRNAs is reduced under MILI- and MIWI2-null conditions in fetal germ cells, although the extent of the reduction differs significantly between the two mutants. Our data strongly suggest that MILI and MIWI2 play essential roles in establishing de novo DNA methylation of retrotransposons in fetal male germ cells.

本文言語英語
ページ(範囲)908-917
ページ数10
ジャーナルGenes and Development
22
7
DOI
出版ステータス出版済み - 4 1 2008
外部発表はい

All Science Journal Classification (ASJC) codes

  • 遺伝学
  • 発生生物学

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