H4K16 acylations fine-tune transcriptional response to short-chain acyl-CoA dehydrogenase deficiency (RNA-seq)
We investigated the combined effects of H4K16 acylations in vivo using a mouse model of short-chain acyl-CoA dehydrogenase deficiency (SCADD), 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: RNA-seq on WT and SCADD male mouse livers in 3 biological replicates.