MVH in piRNA processing and gene silencing of retrotransposons

被引:215
作者
Kuramochi-Miyagawa, Satomi [1 ,2 ,3 ]
Watanabe, Toshiaki [4 ]
Gotoh, Kengo [1 ]
Takamatsu, Kana [2 ]
Chuma, Shinichiro [5 ,6 ]
Kojima-Kita, Kanako [1 ]
Shiromoto, Yusuke [2 ]
Asada, Noriko [2 ]
Toyoda, Atsushi
Fujiyama, Asao
Totoki, Yasushi [7 ]
Shibata, Tatsuhiro [7 ]
Kimura, Tohru [2 ]
Nakatsuji, Norio [5 ,6 ]
Noce, Toshiaki
Sasaki, Hiroyuki [4 ]
Nakano, Toru [1 ,2 ]
机构
[1] Osaka Univ, Grad Sch Frontier Biosci, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Grad Sch Med Sci, Suita, Osaka 5650871, Japan
[3] Japan Sci & Technol Agcy, PRESTO, Kawaguchi, Saitama 3320012, Japan
[4] Res Org Informat & Syst, Natl Inst Genet, Dept Integrated Genet, Div Human Genet, Mishima, Shizuoka 4118540, Japan
[5] Kyoto Univ, Inst Frontier Med Sci, Kyoto 6068507, Japan
[6] Kyoto Univ, Grad Sch Med, Kyoto 6068507, Japan
[7] Natl Canc Ctr, Res Inst, Canc Genom Project, Tokyo 1040045, Japan
基金
日本学术振兴会;
关键词
Spermatogenesis; MVH; small RNA; piRNA; retrotransposon; epigenetic regulation; SMALL RNAS; ARGININE METHYLATION; DNA METHYLATION; TUDOR DOMAIN; PIWI; HOMOLOG; PROTEIN; MILI; GERMLINE; VASA;
D O I
10.1101/gad.1902110
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
VASA is an evolutionarily conserved RNA helicase essential for germ cell development. The mouse PIWI family proteins MILI and MIWI2 are involved in production of Piwi-interacting RNAs (piRNAs) in fetal male germ cells through a ping-pong amplification cycle. Expression of retrotransposons is elevated in MILI- and MIWI2-deficient male germ cells due to defective de novo DNA methylation, which is presumably caused by impaired piRNA expression. Here, we report that essentially the same abnormalities are observed in MVH (mouse VASA homolog)-deficient mice. Comprehensive analysis of piRNAs in MVH-deficient fetal male germ cells showed that MVH plays crucial roles in the early phase of the ping-pong amplification cycle.
引用
收藏
页码:887 / 892
页数:6
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