The acetyltransferase HAT1 moderates the NF-κB response by regulating the transcription factor PLZF

Anthony J. Sadler (), Bandar A. Suliman, Liang Yu, Xiangliang Yuan, Die Wang, Aaron T. Irving, Soroush T. Sarvestani, Ashish Banerjee, Ashley S. Mansell, Jun-Ping Liu, Steve Gerondakis, Bryan R. G. Williams and Dakang Xu ()
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Anthony J. Sadler: Hudson Institute of Medical Research
Bandar A. Suliman: Hudson Institute of Medical Research
Liang Yu: Hudson Institute of Medical Research
Xiangliang Yuan: Xin Hua Hospital, Shanghai Jiaotong University School of Medicine
Die Wang: Hudson Institute of Medical Research
Aaron T. Irving: Hudson Institute of Medical Research
Soroush T. Sarvestani: Hudson Institute of Medical Research
Ashish Banerjee: Hudson Institute of Medical Research
Ashley S. Mansell: Hudson Institute of Medical Research
Jun-Ping Liu: Institute of Ageing Research, Hangzhou Normal University School of Medicine
Steve Gerondakis: School of Biomedical Sciences, Monash University Clayton Campus
Bryan R. G. Williams: Hudson Institute of Medical Research
Dakang Xu: Hudson Institute of Medical Research

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract To date, the activities of protein kinases have formed the core of our understanding of cell signal transduction. Comprehension of the extent of protein acetylation has raised expectations that this alternate post-transcriptional modification will be shown to rival phosphorylation in its importance in mediating cellular responses. However, limited instances have been identified. Here we show that signalling from Toll-like or TNF-α receptors triggers the calcium/calmodulin-dependent protein kinase (CaMK2) to activate histone acetyltransferase-1 (HAT1), which then acetylates the transcriptional regulator PLZF. Acetylation of PLZF promotes the assembly of a repressor complex incorporating HDAC3 and the NF-κB p50 subunit that limits the NF-κB response. Accordingly, diminishing the activity of CaMK2, the expression levels of PLZF or HAT1, or mutating key residues that are covalently modified in PLZF and HAT1, curtails control of the production of inflammatory cytokines. These results identify a central role for acetylation in controlling the inflammatory NF-κB transcriptional programme.

Date: 2015
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DOI: 10.1038/ncomms7795

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