Maintenance of histone crotonylation by YEATS2 and GCDH drives EMT in head and neck cancer [ChIP-seq]
Regulation of gene expression is an integral cellular process, fine-tuned by epigenetic marks like histone modifications. Perturbations in the activity or abundance of epigenetic factors can lead, or contribute to tumorigenesis in healthy cells. Remarkably, the addition of epigenetic marks is dependent on the metabolites produced during several essential cellular pathways. Here, we have explored the interplay between a highly expressed epigenetic factor YEATS2, and a metabolic enzyme GCDH in regulating epithelial to mesenchymal transition in head and neck cancer. We report the results of RNA-seq in YEATS2-silenced BICR10 cells to investigate the effect of YEATS2 in influencing gene expression globally. We have also performed ChIP-seq using YEATS2 antibody in BICR10 cells to obtain the globally occupied sites of YEATS2. Lastly, we report the changes in crotonylation at histone 3 lysine 27 (H3K27Cr) upon YEATS2 downregulation in BICR10 by performing ChIP-seq in shControl vs. shYEATS2 cells. Overall design: ChIP-seq for YEATS2 performed in BICR10 cells. ChIP-seq for H3K27Cr was performed in shControl vs shYEATS2 BICR10 cells.