H4K16 acylations fine-tune transcriptional response during metabolic perturbations (ATAC-seq)
We studied the concerted 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 act in vivo in a coordinated manner, allowing fine-tuning of transcriptional responses to metabolic stresses. Our work provides insights into the adaptive mechanisms of chromatin regulation in response to metabolic challenges. Overall design: ATAC-seq on WT and PA female mouse livers in 2 biological replicates.