Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ATAC-Seq)

Mice harboring a liver-specific carnitine palmityltransferase 2 (Cpt2) knockout exhibit drastic lipid accumulation following a 24hr fast. Crossing Cpt2L-/- mice with Pparα-/- mice provides a model to drive ligand-activated Pparα signaling in liver. We use this to investigate unique patterns of Pparα target gene transcription and demonstrate the requirement for ligand-activated Pparα in maintaining transcriptionally permissive genomic architecture in liver, including regulation of promoters and enhancer elements during periods of nutrient deprivation. ATAC-seq on liver tissue from 9wk old male wild-type, Cpt2 liver knockout, Ppar⍺ knockout, and Cpt2 L-/- ;Ppar⍺ -/- double knockout mice fasted for 24 hours.