The THO complex and Piwi independently silence transposons in the Drosophila germline and soma

The piRNA pathway has a conserved function in transposon silencing. In Drosophila female, piRNAs derived from dual-strand clusters dominate the germline, and piRNAs produced from uni-strand cluster dominate the somatic follicle cells that surround the germline. The somatic piRNAs are bound by Piwi, and guide Panoramix dependent repressive H3K9me3 modification of target elements. The THO complex, composed of Hpr1, Tho2, Thoc5, Thoc6 and Thoc7, is required for germline piRNA biogenesis. We show that mutations in thoc7 increase transcription and active H3K4me2 modification of transposons targeted by uni-strand cluster, and transposon transcripts are bound by THO. However, thoc7 mutations do not disrupt uni-strand piRNA production, inhibitory H3K9me3 modification of target elements, or Panoramix dependent silencing of a reporter transgene. Mutations in thoc7 also dominantly enhance defects in germline development and transposon silencing associated with piwi mutations. The THO complex and piRNA pathway thus mediate independent epigenetic transposon silencing mechanisms.