7ubu: Difference between revisions
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== Function == | == Function == | ||
[https://www.uniprot.org/uniprot/CMT1_MAIZE CMT1_MAIZE] | [https://www.uniprot.org/uniprot/CMT1_MAIZE CMT1_MAIZE] | ||
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== Publication Abstract from PubMed == | |||
DNA methylation is an evolutionarily conserved epigenetic mechanism essential for transposon silencing and heterochromatin assembly. In plants, DNA methylation widely occurs in the CG, CHG, and CHH (H = A, C, or T) contexts, with the maintenance of CHG methylation mediated by CMT3 chromomethylase. However, how CMT3 interacts with the chromatin environment for faithful maintenance of CHG methylation is unclear. Here we report structure-function characterization of the H3K9me2-directed maintenance of CHG methylation by CMT3 and its Zea mays ortholog ZMET2. Base-specific interactions and DNA deformation coordinately underpin the substrate specificity of CMT3 and ZMET2, while a bivalent readout of H3K9me2 and H3K18 allosterically stimulates substrate binding. Disruption of the interaction with DNA or H3K9me2/H3K18 led to loss of CMT3/ZMET2 activity in vitro and impairment of genome-wide CHG methylation in vivo. Together, our study uncovers how the intricate interplay of CMT3, repressive histone marks, and DNA sequence mediates heterochromatic CHG methylation. | |||
Mechanistic basis for maintenance of CHG DNA methylation in plants.,Fang J, Jiang J, Leichter SM, Liu J, Biswal M, Khudaverdyan N, Zhong X, Song J Nat Commun. 2022 Jul 5;13(1):3877. doi: 10.1038/s41467-022-31627-3. PMID:35790763<ref>PMID:35790763</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
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== References == | |||
<references/> | |||
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</StructureSection> | </StructureSection> | ||
