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Abstract
All metazoan guts are in constant contact with diverse food-borne microorganisms.
The signaling mechanisms by which the host regulates gut-microbe interactions, however,
are not yet clear. Here, we show that phospholipase C-beta (PLCbeta) signaling modulates
dual oxidase (DUOX) activity to produce microbicidal reactive oxygen species (ROS)
essential for normal host survival. Gut-microbe contact rapidly activates PLCbeta
through Galphaq, which in turn mobilizes intracellular Ca(2+) through inositol 1,4,5-trisphosphate
generation for DUOX-dependent ROS production. PLCbeta mutant flies had a short life
span due to the uncontrolled propagation of an essential nutritional microbe, Saccharomyces
cerevisiae, in the gut. Gut-specific reintroduction of the PLCbeta restored efficient
DUOX-dependent microbe-eliminating capacity and normal host survival. These results
demonstrate that the Galphaq-PLCbeta-Ca(2+)-DUOX-ROS signaling pathway acts as a bona
fide first line of defense that enables gut epithelia to dynamically control yeast
during the Drosophila life cycle.