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
Celljournal_title
Cellauthors
Suganuma T,Mushegian A,Swanson SK,Abmayr SM,Florens L,Washburn MP,Workman JLdoi
10.1016/j.cell.2010.07.045subject
Has Abstractpub_date
2010-09-03 00:00:00pages
726-36issue
5eissn
0092-8674issn
1097-4172pii
S0092-8674(10)00893-7journal_volume
142pub_type
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