The ATAC Acetyltransferase Complex Coordinates MAP Kinases to Regulate JNK Target Genes

In response to extracellular cues, signal transduction activates downstream transcription factors like c-Jun to induce expression of target genes. We demonstrate that the ATAC (Ada two A containing) histone acetyltransferase (HAT) complex serves as a transcriptional cofactor for c-Jun at the Jun N-terminal kinase (JNK) target genes Jra and chickadee. ATAC subunits are required for c-Jun occupancy of these genes and for H4K16 acetylation at the Jra enhancer, promoter, and transcribed sequences. Under conditions of osmotic stress, ATAC colocalizes with c-Jun, recruits the upstream kinases Misshapen, MKK4, and JNK, and suppresses further activation of JNK. Relocalization of these MAPKs and suppression of JNK activation by ATAC are dependent on the CG10238 subunit of ATAC. Thus, ATAC governs the transcriptional response to MAP kinase signaling by serving as both a coactivator of transcription and as a suppressor of upstream signaling. [Display omitted] ► The ATAC acetyltransferase complex is a cofactor for c-jun-dependent transcription ► ATAC and MAP kinases localize to c-jun binding sites upon induction by osmotic stress ► ATAC is required for the localization of Jun and MAP kinases on JNK target genes ► ATAC suppresses the levels of JNK activation under osmotic stress