Roles of MIWI, MILI and PLD6 in small RNA regulation in mouse growing oocytes

Yuka Kabayama, Hidehiro Toh, Ami Katanaya, Takayuki Sakurai, Shinichiro Chuma, Satomi Kuramochi-Miyagawa, Yumiko Saga, Toru Nakano, Hiroyuki Sasaki

研究成果: Contribution to journalArticle査読

27 被引用数 (Scopus)

抄録

The mouse PIWI-interacting RNA (piRNA) pathway produces a class of 26-30-nucleotide (nt) small RNAs and is essential for spermatogenesis and retrotransposon repression. In oocytes, however, its regulation and function are poorly understood. In the present study, we investigated the consequences of loss of piRNA-pathway components in growing oocytes. When MILI (or PIWIL2), a PIWI family member, was depleted by gene knockout, almost all piRNAs disappeared. This severe loss of piRNA was accompanied by an increase in transcripts derived from specific retrotransposons, especially IAPs. MIWI (or PIWIL1) depletion had a smaller effect. In oocytes lacking PLD6 (or ZUCCHINI or MITOPLD), amitochondrial nuclease/phospholipase involved in piRNA biogenesis inmale germ cells, the piRNA level was decreased to 50% compared to wild-type, a phenotype much milder than that in males. Since PLD6 is essential for the creation of the 5- ends of primary piRNAs in males, the presence of mature piRNA in PLD6-depleted oocytes suggests the presence of compensating enzymes. Furthermore, we identified novel 21-23-nt small RNAs, termed spiRNAs, possessing a 10-nt complementarity with piRNAs, which were produced dependent on MILI and independent of DICER. Our study revealed the differences in the biogenesis and function of the piRNA pathway between sexes.

本文言語英語
ページ(範囲)5387-5398
ページ数12
ジャーナルNucleic acids research
45
9
DOI
出版ステータス出版済み - 5 19 2017

All Science Journal Classification (ASJC) codes

  • 遺伝学

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