Journal
EMBO JOURNAL
Volume 22, Issue 4, Pages 893-904Publisher
OXFORD UNIV PRESS
DOI: 10.1093/emboj/cdg094
Keywords
acetylation; cytokine; helix-loop-helix; STAT; transcription
Categories
Funding
- NCI NIH HHS [R01 CA077553, CA77553] Funding Source: Medline
- NIAID NIH HHS [R21 AI033597, R01 AI033597, AI33597] Funding Source: Medline
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Transcriptional activation is associated commonly with recruitment of histone acetylases, while repression involves histone deacetylases (HDACs). Here, we provide evidence to suggest that STAT5 activates gene expression by recruiting HDAC. The interleukin-3 (IL-3)-dependent expression of the Id-1 gene, encoding a helix-loop-helix (HLH) transcriptional inhibitor, is activated by both C/EBPbeta and STAT5 transcription factors bound to its pro-B-cell enhancer (PBE), but is inhibited by HDAC inhibitors in Ba/F3 cells. STAT5 interacts with HDAC1 in the PBE region, resulting in deacetylation of histones, as well as C/EBPbeta, whose acetylation diminishes its DNA-binding activity. Consistently, expression of an acetylation-resistant mutant of C/EBPbeta results in IL-3-independent expression of the Id-1 gene. Thus, we propose a novel mechanism by which STAT5 mediates the deacetylation of C/EBPbeta, allowing transcriptional activation.
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