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MEF2 is an in vivo immune-metabolic switch.

Clark, R.I. and Tan, S.W. and Pean, C.B. and Roostalu, U. and Vivancos, V. and Bronda, K. and Pilatova, M. and Fu, J. and Walker, D.W. and Berdeaux, R. and Geissmann, F. and Dionne, M.S. (2013) 'MEF2 is an in vivo immune-metabolic switch.', Cell., 155 (2). pp. 435-447.


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.

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Publisher 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.
Date accepted:05 September 2013
Date deposited:15 June 2018
Date of first online publication:26 September 2013
Date first made open access:No date available

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