期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 117, 期 26, 页码 15316-15321出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2007268117
关键词
non-coding RNA; chromatin; polycomb; FLC; Arabidopsis
资金
- Biotechnology and Biological Sciences Research Council Institute Strategic Programme Genes in the Environment [BB/P013511/1]
- European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie Grant [800318]
- ERC Advanced Grant [EPISWITCH-833254]
- Wellcome Trust [203149]
- European Research Council (ERC) under the European Union [639253]
- Wellcome Senior Investigator grant [210654/Z/18/Z]
- European Research Council (ERC) [639253] Funding Source: European Research Council (ERC)
- Marie Curie Actions (MSCA) [800318] Funding Source: Marie Curie Actions (MSCA)
- BBSRC [BB/L009714/1, BBS/E/J/000PR9773] Funding Source: UKRI
- Wellcome Trust [210654/Z/18/Z] Funding Source: Wellcome Trust
Noncoding RNA plays essential roles in transcriptional control and chromatin silencing. At Arabidopsis thaliana FLC, antisense transcription quantitatively influences transcriptional output, but the mechanism by which this occurs is still unclear. Proximal polyadenylation of the antisense transcripts by FCA, an RNA-binding protein that physically interacts with RNA 3' processing factors, reduces FLC transcription. This process genetically requires FLD, a homolog of the H3K4 demethylase LSD1. However, the mechanism linking RNA processing to FLD function had not been established. Here, we show that FLD tightly associates with LUMINIDEPENDENS (LD) and SET DOMAIN GROUP 26 (SDG26) in vivo, and, together, they prevent accumulation of monomethylated H3K4 (H3K4me1) over the FLC gene body. SDG26 interacts with the RNA 3' processing factor FY (WDR33), thus linking activities for proximal polyadenylation of the antisense transcripts to FLD/LD/SDG26-associated H3K4 demethylation. We propose this demethylation antagonizes an active transcription module, thus reducing H3K36me3 accumulation and increasing H3K27me3. Consistent with this view, we show that Polycomb Repressive Complex 2 (PRC2) silencing is genetically required by FCA to repress FLC. Overall, our work provides insights into RNA-mediated chromatin silencing.
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