Genomics

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Targeted H3R26 deimination specifically facilitates ER binding by modifying nucleosome structure


ABSTRACT: The precise mechanisms by which hormone receptors bind to DNA in the context of chromatin remain unclear. Here we report that the genomic distributions of estrogen receptor (ER) and H3R26 deimination (H3R26Cit) in breast cancer cells are strikingly coincident, linearly correlated, and observed as early as 2 minutes following estradiol treatment. Paired-end MNase ChIP-seq indicates that the charge-neutral H3R26Cit modification facilitates ER binding to DNA by altering the fine structure of the nucleosome. Clinically, we find that PAD2 and H3R26Cit levels correlate with ER expression in breast tumors and that high PAD2 expression is associated with increased survival in ER+ breast cancer patients. Our study suggests that PAD2-mediated histone deimination is fundamental to ER signaling in breast cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58177 | GEO | 2014/08/04

SECONDARY ACCESSION(S): PRJNA251512

REPOSITORIES: GEO

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