G9a-mediated methylation of ERα links the PHF20/MOF histone acetyltransferase complex to hormonal gene expression

Xi Zhang, Danni Peng, Yuanxin Xi, Chao Yuan, Cari A. Sagum, Brianna J. Klein, Kaori Tanaka, Hong Wen, Tatiana G. Kutateladze, Wei Li, Mark T. Bedford and Xiaobing Shi ()
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Xi Zhang: The University of Texas MD Anderson Cancer Center
Danni Peng: The University of Texas MD Anderson Cancer Center
Yuanxin Xi: Dan L. Duncan Cancer Center, Baylor College of Medicine
Chao Yuan: The University of Texas MD Anderson Cancer Center
Cari A. Sagum: The University of Texas MD Anderson Cancer Center
Brianna J. Klein: University of Colorado School of Medicine
Kaori Tanaka: The University of Texas MD Anderson Cancer Center
Hong Wen: The University of Texas MD Anderson Cancer Center
Tatiana G. Kutateladze: University of Colorado School of Medicine
Wei Li: Dan L. Duncan Cancer Center, Baylor College of Medicine
Mark T. Bedford: The University of Texas MD Anderson Cancer Center
Xiaobing Shi: The University of Texas MD Anderson Cancer Center

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract The euchromatin histone methyltransferase 2 (also known as G9a) methylates histone H3K9 to repress gene expression, but it also acts as a coactivator for some nuclear receptors. The molecular mechanisms underlying this activation remain elusive. Here we show that G9a functions as a coactivator of the endogenous oestrogen receptor α (ERα) in breast cancer cells in a histone methylation-independent manner. G9a dimethylates ERα at K235 both in vitro and in cells. Dimethylation of ERαK235 is recognized by the Tudor domain of PHF20, which recruits the MOF histone acetyltransferase (HAT) complex to ERα target gene promoters to deposit histone H4K16 acetylation promoting active transcription. Together, our data suggest the molecular mechanism by which G9a functions as an ERα coactivator. Along with the PHF20/MOF complex, G9a links the crosstalk between ERα methylation and histone acetylation that governs the epigenetic regulation of hormonal gene expression.

Date: 2016
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DOI: 10.1038/ncomms10810

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