Developmentally regulated piRNA clusters implicate MILI in transposon control

被引：795

作者：

Aravin, Alexei A. ^{[1
]}

Sachidanandam, Ravi ^{[1
]}

Girard, Angelique ^{[1
]}

Fejes-Toth, Katalin ^{[1
]}

Hannon, Gregory J. ^{[1
]}

机构：

[1] Cold Spring Harbor Lab, Howard Hughes Med Inst, Watson Sch Biol Sci, Cold Spring Harbor, NY 11724 USA

来源：

SCIENCE | 2007年 / 316卷 / 5825期

关键词：

D O I：

10.1126/science.1142612

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Nearly half of the mammalian genome is composed of repeated sequences. In Drosophila, Piwi proteins exert control over transposons. However, mammalian Piwi proteins, MIWI and MILI, partner with Piwi-interacting RNAs (piRNAs) that are depleted of repeat sequences, which raises questions about a role for mammalian Piwi's in transposon control. A search for murine small RNAs that might program Piwi proteins for transposon suppression revealed developmentally regulated piRNA loci, some of which resemble transposon master control loci of Drosophila. We also find evidence of an adaptive amplification loop in which MILI catalyzes the formation of piRNA 5' ends. Mili mutants derepress LINE-1 (L1) and intracisternal A particle and lose DNA methylation of L1 elements, demonstrating an evolutionarily conserved role for PIWI proteins in transposon suppression.

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页码：744 / 747

页数：4

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