RT Journal Article
SR Electronic
T1 Repetitive DNA promotes RNAi-mediated heterochromatin formation via an anti-silencing factor in fission yeast
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2022.07.04.498379
DO 10.1101/2022.07.04.498379
A1 Takahiro Asanuma
A1 Soichi Inagaki
A1 Tetsuji Kakutani
A1 Hiroyuki Aburatani
A1 Yota Murakami
YR 2022
UL http://biorxiv.org/content/early/2022/07/04/2022.07.04.498379.abstract
AB In most eukaryotes, constitutive heterochromatin defined by H3K9me2/me3 is enriched on repetitive DNA, such as the satellite repeats of pericentromeres1. Furthermore, repetitive transgenes often cause the formation of silent heterochromatin in diverse model organisms2. Although these facts suggest that the repetition itself promotes heterochromatin formation, the mechanism by which this occurs is still unclear3–7. Here, using Schizosaccharomyces pombe, we show that tandemly repeated reporter genes promote RNA interference (RNAi)-mediated heterochromatin formation in cooperation with an anti-silencing factor. The repeated gene itself does not cause heterochromatin formation; however, once the RNAi recognizes it via artificial small RNAs, the repeated gene starts producing cognate small RNAs to autonomously maintain heterochromatin. This depends on the number of repeats and an anti-silencing factor Epe1, which removes H3K9me and derepresses transcription of genes underlying heterochromatin. Our results suggest that an anti-silencing factor generates sufficient transcripts for the activation of RNAi when repetitive DNA underlies silent heterochromatin.Competing Interest StatementThe authors have declared no competing interest.