Citation

BibTex format

@article{Grimes:2022:10.1101/2022.11.25.517956,
author = {Grimes, K and Beckwith, EJ and Pearson, WH and Jacobson, J and Chaudhari, S and Aughey, GN and Larrouy-Maumus, G and Southall, TD and Dionne, MS},
doi = {10.1101/2022.11.25.517956},
title = {A serine-folate metabolic unit controls resistance and tolerance of infection},
url = {http://dx.doi.org/10.1101/2022.11.25.517956},
year = {2022}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - <jats:title>Abstract</jats:title><jats:p>Immune activation drives metabolic change in most animals. Immune-induced metabolic change is most conspicuous as a driver of pathology in serious or prolonged infection, but it is normally expected to be important to support immune function and recovery. Many of the signalling mechanisms linking immune detection with metabolic regulation, and their specific consequences, are unknown. Here, we show that<jats:italic>Drosophila melanogaster</jats:italic>respond to many bacterial infections by altering expression of genes of the folate cycle and associated enzymes of amino acid metabolism. The net result of these changes is increased flow of carbon from glycolysis into serine and glycine synthesis and a shift of folate cycle activity from the cytosol into the mitochondrion. Immune-induced transcriptional induction of<jats:italic>astray</jats:italic>and<jats:italic>Nmdmc</jats:italic>, the two most-induced of these enzymes, depends on<jats:italic>Dif</jats:italic>and<jats:italic>foxo</jats:italic>. Loss of<jats:italic>astray</jats:italic>or<jats:italic>Nmdmc</jats:italic>results in infection-specific immune defects. Our work thus shows a key mechanism that connects immune-induced changes in metabolic signalling with the serine-folate metabolic unit to result in changed immune function.</jats:p>
AU - Grimes,K
AU - Beckwith,EJ
AU - Pearson,WH
AU - Jacobson,J
AU - Chaudhari,S
AU - Aughey,GN
AU - Larrouy-Maumus,G
AU - Southall,TD
AU - Dionne,MS
DO - 10.1101/2022.11.25.517956
PY - 2022///
TI - A serine-folate metabolic unit controls resistance and tolerance of infection
UR - http://dx.doi.org/10.1101/2022.11.25.517956
ER -

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