Journal
DEVELOPMENTAL CELL
Volume 16, Issue 3, Pages 386-397Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2008.12.015
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Funding
- Korea Ministry of Education, Science and Technology [R31-2008-000-10010-0]
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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 (PLC beta) signaling modulates dual oxidase (DUOX) activity to produce microbicidal reactive oxygen species (ROS) essential for normal host survival. Gut-microbe contact rapidly activates PLC beta through G alpha q, which in turn mobilizes intracellular Ca2+ through inositol 1,4,5-trisphosphate generation for DUOX-dependent ROS production. PLC beta 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 PLC beta restored efficient DUOX-dependent microbe-eliminating capacity and normal host survival. These results demonstrate that the G alpha q-PLC beta-Ca2+_ 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.
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