Editors' ChoiceTranscription

Acetylation Flips the Transcription Switch

See allHide authors and affiliations

Science's STKE  14 Aug 2001:
Vol. 2001, Issue 95, pp. tw7
DOI: 10.1126/stke.2001.95.tw7

Cells respond to external challenges such as viral infection by adjusting gene expression. Viral infection activates the expression of interferon-β (INF-β) via a protein complex, termed the enhanceosome, that forms on the gene's promoter. The interferon enhanceosome recruits two acetyltransferases, PCAF and CBP, that not only acetylate the histone components of nucleosomes but also acetylate the enhanceosome itself. Munshi et al. (see the Perspective by Struhl) report that PCAF acetylation of the enhanceosome protein HMG-I at the Lys71 residue stabilizes the enhancesome and protects it from CBP acetylation. However, acetylation of HMG-I by CBP at Lys65 leads to the dissociation of the enhanceosome from the DNA molecule. Therefore, the enhanceosome is a dynamic complex that is acted upon by competing acetylations to create a switch that turns transcription on or off.

N. Munshi, T. Agalioti, S. Lomvardas, M. Merika, G. Chen, D. Thanos, Coordination of a transcriptional switch by HMGI(Y) acetylation. Science 293, 1133-1136 (2001). [Abstract] [Full Text]

K. Struhl, A paradigm for precision. Science 293, 1054-1055 (2001). [Full Text]

Stay Connected to Science Signaling