ATAC-seq analysis of brain chromatin in Drosophila melanogaster chromodomain helicase DNA binding protein 1 (CHD1) deletion mutants

CHD1 is a conserved ATP-dependent chromatin remodeling factor with roles in transcriptional regulation and chromatin assembly. We show that deletion of Chd1 causes multiple behavioral and metabolic defects. In particular, it diminishes food-intake and results in shortened lifespan of mutant flies. These phenotypes are at least partially caused by widespread upregulation of transcription in the fly brain. Mass spec analysis showed significantly reduced amounts of chromatin-bound H3.3 in Chd1-mutant heads. ATAC-seq experiments of wildtype, Chd1-deletion and H3.3-deletion brains revealed substantial changes in chromatin accessibility in the absence of CHD1 that resemble the changes observed with H3.3-deletion mutants. The results suggest that CHD1 is required for H3.3 assembly in the brain thereby ensuring proper maintenance of chromatin structure and regulation of transcription.