Journal
EMBO JOURNAL
Volume 29, Issue 20, Pages 3496-3506Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/emboj.2010.227
Keywords
chromatin; DNA methylation; histone demethylase; IBM1; transposon
Categories
Funding
- Mitsubishi Foundation
- Takeda Science Foundation
- Japanese Ministry of Education, Culture, Sports, Science and Technology [19207002, 19060014]
- National Basic Research Program of China [200903941500, 2005CB522400]
- National Natural Science Foundation of China [30930048]
- Grants-in-Aid for Scientific Research [19060014, 21570196, 19207002] Funding Source: KAKEN
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In diverse eukaryotes, constitutively silent sequences, such as transposons and repeats, are marked by methylation at histone H3 lysine 9 (H3K9me). Although selective H3K9me is critical for maintaining genome integrity, mechanisms to exclude H3K9me from active genes remain largely unexplored. Here, we show in Arabidopsis that the exclusion depends on a histone demethylase gene, IBM1 (increase in BONSAI methylation). Loss-of-function ibm1 mutation results in ectopic H3K9me and non-CG methylation in thousands of genes. The ibm1-induced genic H3K9me depends on both histone methylase KYP/SUVH4 and DNA methylase CMT3, suggesting interdependence of two epigenetic marks H3K9me and non-CG methylation. Notably, IBM1 enhances loss of H3K9me in transcriptionally de-repressed sequences. Furthermore, disruption of transcription in genes induces ectopic non-CG methylation, which mimics the loss of IBM1 function. We propose that active chromatin is stabilized by an autocatalytic loop of transcription and H3K9 demethylation. This process counteracts a similarly autocatalytic accumulation of silent epigenetic marks, H3K9me and non-CG methylation. The EMBO Journal (2010) 29, 3496-3506. doi:10.1038/emboj.2010.227; Published online 10 September 2010 Subject Categories: chromatin & transcription; plant biology
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