R-loop resolution promotes co-transcriptional chromatin silencing

Congyao Xu, Zhe Wu, Hong-Chao Duan, Xiaofeng Fang, Guifang Jia () and Caroline Dean ()
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Congyao Xu: Cell and Developmental Biology, John Innes Centre
Zhe Wu: Cell and Developmental Biology, John Innes Centre
Hong-Chao Duan: Peking University
Xiaofeng Fang: Cell and Developmental Biology, John Innes Centre
Guifang Jia: Peking University
Caroline Dean: Cell and Developmental Biology, John Innes Centre

Nature Communications, 2021, vol. 12, issue 1, 1-9

Abstract: Abstract RNA-mediated chromatin silencing is central to genome regulation in many organisms. However, how nascent non-coding transcripts regulate chromatin is poorly understood. Here, through analysis of Arabidopsis FLC, we show that resolution of a nascent-transcript-induced R-loop promotes chromatin silencing. Stabilization of an antisense-induced R-loop at the 3′ end of FLC enables an RNA binding protein FCA, with its direct partner FY/WDR33 and other 3′-end processing factors, to polyadenylate the nascent antisense transcript. This clears the R-loop and recruits the chromatin modifiers demethylating H3K4me1. FCA immunoprecipitates with components of the m6A writer complex, and m6A modification affects dynamics of FCA nuclear condensates, and promotes FLC chromatin silencing. This mechanism also targets other loci in the Arabidopsis genome, and consistent with this fca and fy are hypersensitive to a DNA damage-inducing drug. These results show how modulation of R-loop stability by co-transcriptional RNA processing can trigger chromatin silencing.

Date: 2021
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DOI: 10.1038/s41467-021-22083-6

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