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Autocatalytic differentiation of epigenetic modifications within the Arabidopsis genome
Author(s) -
Inagaki Soichi,
MiuraKamio Asuka,
Nakamura Yasukazu,
Lu Falong,
Cui Xia,
Cao Xiaofeng,
Kimura Hiroshi,
Saze Hidetoshi,
Kakutani Tetsuji
Publication year - 2010
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2010.227
Subject(s) - biology , epigenetics , genetics , demethylase , dna methylation , histone methylation , methylation , histone , histone methyltransferase , epigenetics of physical exercise , gene , gene expression
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.