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Histone methylation and epigenetic gene regulation
Histone posttranslational modification plays crucial roles in epigenetic regulation of chromatin structure and function. Since first histone lysine methyltransferase has been discovered in 2000, roles of histone methylation and their mechanisms of action were extensively studied. Combination of different methylation levels (mono-, di- or tri-methylation) and target sites are translated into functionally distinct nuclear processes as “histone codes”. Initially, histone methylation was thought to be quite stable and an irreversible modification, but recent discovery of protein demethylases changed all that. We have studied two mammalian histone H3 lysine 9 (H3K9) methyltransferases, G9a and GLP, both of which are essential for mouse early embryogenesis and regulate H3K9 mono- and di-methylation mostly on euchromatin. In this presentation, I’d like to talk about another mammalian H3K9 methyltransferase, ESET/SETDB1. Since homozygous mutations of ESET result in early embryonic lethality (around a peri-implantation stage between 3.5 and 5.5 dpc) and no ESET-deficient ES cells are established, it is not shown that how ESET is crucial for H3K9 methylation in vivo. To further elucidate how ESET is important for H3K9 methylation in vivo, we established ESET conditional knockout mice and ES cells. We also performed ChIP-chip analysis of ESET to identify ESET target genes (genome loci). Based on those obtained data, I will discuss the molecular functions and biological roles of ESET.
Toshiyuki Matsui, Yoichi Shinkai
Institute for Virus Research and Grad. School of Biostudies, Kyoto University
国際シンポジウム「 DecodingEpigenetic Code」
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