Regulation of sugar transporter activity for antibacterial defense in Arabidopsis
Dueling for sugars Bacteria thrive on sugar. So do plant cells. Yamada et al. now show how the fight for sugar plays out in the extracellular spaces around plant cells when pathogenic bacteria are invading the plant (see the Perspective by Dodds and Lagudah) In the model plant Arabidopsis, part of the defense response incited by the presence of pathogenic bacteria includes transcriptional and posttranscriptional regulation of sugar transporters. The resulting uptake of monosaccharides from the extracellular space makes life a little bit more difficult for the invading bacteria. Science, this issue p. 1427; see also p. 1377 Bacterial pathogens try to suck the sugar out of their target host plants, which respond by enhancing their own sugar transporter activity. Microbial pathogens strategically acquire metabolites from their hosts during infection. Here we show that the host can intervene to prevent such metabolite loss to pathogens. Phosphorylation dependent regulation of sugar transport protein 13 (STP13) is required for antibacterial defense in the plant Arabidopsis thaliana. STP13 physically associates with the flagellin receptor flagellin sensitive 2 (FLS2) and its co receptor BRASSINOSTEROID INSENSITIVE 1 associated receptor kinase 1 (BAK1) BAK1 phosphorylates STP13 at threonine 485, which enhances its monosaccharide uptake activity to compete with bacteria for extracellular sugars. Limiting the availability of extracellular sugar deprives bacteria of an energy source and restricts virulence factor delivery. Our results reveal that control of sugar uptake, managed by regulation of a host sugar transporter, is a defense strategy deployed against microbial infection. Competition for sugar thus shapes host pathogen interactions.
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