Histone H3.1 is a chromatin embedded redox sensor triggered by tumor cells developing adaptive phenotypic plasticity and multi-drug resistance [ChIP-Seq]
Chromatin structure is regulated through histone post-translational modifications as well as histone variants. Although highly homologous, histone variants display unique amino acid sequences associated with specialized functions in gene transcription regulation. Abnormal incorporation of histone variants into chromatin contributes to cancer initiation, progression, metastasis, as well as, therapy resistance. The current study reports a novel epigenetic function of histone H3.1 as a redox sensor embedded in heterochromatin. We found that this new function depends on oxidation by nuclear ROS and lead to changes in the transcriptional profile of MCF10A cells. Overall design: ChIP-seq for H3.1/H3.2 and H3.3 histone variants 4h or 24h after treatment with D-Alanine (ROS generated in the nucleus)