The TDRD9-MIWI2 complex is essential for piRNA-mediated retrotransposon silencing in the mouse male germline - PubMed (original) (raw)
doi: 10.1016/j.devcel.2009.10.012.
Takashi Tanaka, Mihoko Hosokawa, Michael Reuter, Alexander Stark, Yuzuru Kato, Gen Kondoh, Katsuya Okawa, Takeshi Chujo, Tsutomu Suzuki, Kenichiro Hata, Sandra L Martin, Toshiaki Noce, Satomi Kuramochi-Miyagawa, Toru Nakano, Hiroyuki Sasaki, Ramesh S Pillai, Norio Nakatsuji, Shinichiro Chuma
Affiliations
- PMID: 20059948
- DOI: 10.1016/j.devcel.2009.10.012
Free article
The TDRD9-MIWI2 complex is essential for piRNA-mediated retrotransposon silencing in the mouse male germline
Masanobu Shoji et al. Dev Cell. 2009 Dec.
Free article
Abstract
Host-defense mechanisms against transposable elements are critical to protect the genome information. Here we show that tudor-domain containing 9 (Tdrd9) is essential for silencing Line-1 retrotransposon in the mouse male germline. Tdrd9 encodes an ATPase/DExH-type helicase, and its mutation causes male sterility showing meiotic failure. In Tdrd9 mutants, Line-1 was highly activated and piwi-interacting small RNAs (piRNAs) corresponding to Line-1 were increased, suggesting that feedforward amplification operates in the mutant. In fetal testes, Tdrd9 mutation causes Line-1 desilencing and an aberrant piRNA profile in prospermatogonia, followed by cognate DNA demethylation. TDRD9 complexes with MIWI2 with distinct compartmentalization in processing bodies, and this TDRD9-MIWI2 localization is regulated by MILI and TDRD1 residing at intermitochondrial cement. Our results identify TDRD9 as a functional partner of MIWI2 and indicate that the tudor-piwi association is a conserved feature, while two separate axes, TDRD9-MIWI2 and TDRD1-MILI, cooperate nonredundantly in the piwi-small RNA pathway in the mouse male germline.
2009 Elsevier Inc. All rights reserved.
Comment in
- Defending the genome in tudor style.
van der Heijden GW, Bortvin A. van der Heijden GW, et al. Dev Cell. 2009 Dec;17(6):745-6. doi: 10.1016/j.devcel.2009.11.007. Dev Cell. 2009. PMID: 20059942
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