H4K16 acylations fine-tune transcriptional response during metabolic perturbations (ChIP-seq)
We studied the combined effects of the H4K16 acylations in vivo using a mouse model of the metabolic disorder propionic acidemia (PA), which causes metabolic challenges and systemic shifts in acyl-CoA ratios. Our findings indicate that H4K16 acylations modulate transcriptional responses in a concerted manner, providing insights into an adaptive chromatin regulation in response to metabolic stress. Overall design: H4K16ac, H4K16pr, H4K16bu, H4K5ac, H4K5pr, H4K12ac, H4K12pr, H3K27ac, H3K9ac ChIP-seq on WT and PA female mouse livers in 2 biological replicates.