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MEF2 is an in vivo immune-metabolic switch

Clark, R.I.; Tan, S.W.; Pean, C.B.; Roostalu, U.; Vivancos, V.; Bronda, K.; Pilatova, M.; Fu, J.; Walker, D.W.; Berdeaux, R.; Geissmann, F.; Dionne, M.S.

MEF2 is an in vivo immune-metabolic switch Thumbnail


Authors

S.W. Tan

C.B. Pean

U. Roostalu

V. Vivancos

K. Bronda

M. Pilatova

J. Fu

D.W. Walker

R. Berdeaux

F. Geissmann

M.S. Dionne



Abstract

Infections disturb metabolic homeostasis in many contexts, but the underlying connections are not completely understood. To address this, we use paired genetic and computational screens in Drosophila to identify transcriptional regulators of immunity and pathology and their associated target genes and physiologies. We show that Mef2 is required in the fat body for anabolic function and the immune response. Using genetic and biochemical approaches, we find that MEF2 is phosphorylated at a conserved site in healthy flies and promotes expression of lipogenic and glycogenic enzymes. Upon infection, this phosphorylation is lost, and the activity of MEF2 changes—MEF2 now associates with the TATA binding protein to bind a distinct TATA box sequence and promote antimicrobial peptide expression. The loss of phosphorylated MEF2 contributes to loss of anabolic enzyme expression in Gram-negative bacterial infection. MEF2 is thus a critical transcriptional switch in the adult fat body between metabolism and immunity.

Citation

Clark, R., Tan, S., Pean, C., Roostalu, U., Vivancos, V., Bronda, K., …Dionne, M. (2013). MEF2 is an in vivo immune-metabolic switch. Cell, 155(2), 435-447. https://doi.org/10.1016/j.cell.2013.09.007

Journal Article Type Article
Acceptance Date Sep 5, 2013
Online Publication Date Sep 26, 2013
Publication Date Oct 10, 2013
Deposit Date Aug 13, 2015
Publicly Available Date Jun 15, 2018
Journal Cell
Print ISSN 0092-8674
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 155
Issue 2
Pages 435-447
DOI https://doi.org/10.1016/j.cell.2013.09.007

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Publisher Licence URL
http://creativecommons.org/licenses/by/4.0/

Copyright Statement
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




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