The ATAC acetyltransferase complex coordinates MAP kinases to regulate JNK target genes.

Abstract:

: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.

journal_name

Cell

journal_title

Cell

authors

Suganuma T,Mushegian A,Swanson SK,Abmayr SM,Florens L,Washburn MP,Workman JL

doi

10.1016/j.cell.2010.07.045

subject

Has Abstract

pub_date

2010-09-03 00:00:00

pages

726-36

issue

5

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(10)00893-7

journal_volume

142

pub_type

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