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Nucleic Acids Research Advance Access originally published online on April 30, 2009
Nucleic Acids Research 2009 37(12):3969-3980; doi:10.1093/nar/gkp270
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Nucleic Acids Research, 2009, Vol. 37, No. 12 3969-3980
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

A glycolytic burst drives glucose induction of global histone acetylation by picNuA4 and SAGA

R. Magnus N. Friis, Bob P. Wu, Stacey N. Reinke, Darren J. Hockman, Brian D. Sykes and Michael C. Schultz*

Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada T6G 2H7

*To whom correspondence should be addressed. Tel: +780 492 9144; Fax: +780 492 9556; Email: michael.schultz{at}ualberta.ca

Received February 4, 2009. Revised April 2, 2009. Accepted April 11, 2009.

Little is known about what enzyme complexes or mechanisms control global lysine acetylation in the amino-terminal tails of the histones. Here, we show that glucose induces overall acetylation of H3 K9, 18, 27 and H4 K5, 8, 12 in quiescent yeast cells mainly by stimulating two KATs, Gcn5 and Esa1. Genetic and pharmacological perturbation of carbon metabolism, combined with 1H-NMR metabolic profiling, revealed that glucose induction of KAT activity directly depends on increased glucose catabolism. Glucose-inducible Esa1 and Gcn5 activities predominantly reside in the picNuA4 and SAGA complexes, respectively, and act on chromatin by an untargeted mechanism. We conclude that direct metabolic regulation of globally acting KATs can be a potent driving force for reconfiguration of overall histone acetylation in response to a physiological cue.


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