Open AccessG9a/GLP Complex Maintains Imprinted DNA Methylation in Embryonic Stem Cells
Author(s) -
Tuo Zhang,
Ausma Termanis,
Burak Özkan,
Xun X. Bao,
Jayne Culley,
Flávia de Lima Alves,
Juri Rappsilber,
Bernard Ramsahoye,
Irina Stancheva
Publication year - 2016
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2016.03.007
Subject(s) - genomic imprinting , dna methylation , biology , methyltransferase , imprinting (psychology) , epigenetics , histone methylation , methylation , histone , rna directed dna methylation , epigenomics , microbiology and biotechnology , histone methyltransferase , genetics , dna , gene , gene expression
DNA methylation at imprinting control regions (ICRs) is established in gametes in a sex-specific manner and has to be stably maintained during development and in somatic cells to ensure the correct monoallelic expression of imprinted genes. In addition to DNA methylation, the ICRs are marked by allele-specific histone modifications. Whether these marks are essential for maintenance of genomic imprinting is largely unclear. Here, we show that the histone H3 lysine 9 methylases G9a and GLP are required for stable maintenance of imprinted DNA methylation in embryonic stem cells; however, their catalytic activity and the G9a/GLP-dependent H3K9me2 mark are completely dispensable for imprinting maintenance despite the genome-wide loss of non-imprinted DNA methylation in H3K9me2-depleted cells. We provide additional evidence that the G9a/GLP complex protects imprinted DNA methylation by recruitment of de novo DNA methyltransferases, which antagonize TET dioxygenass-dependent erosion of DNA methylation at ICRs.
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