Mar 18, 2009

Regulation of DUOX by the Galphaq-phospholipase Cbeta-Ca2+ pathway in Drosophila gut immunity

Developmental Cell
Eun-Mi HaWon-Jae Lee

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.

Mentioned in this Paper

Microorganism
Metabolic Process, Cellular
YME1L1 gene
Biochemical Pathway
Immune System
Calcium [EPC]
SLC25A29 gene
Calcium
Saccharomyces cerevisiae allergenic extract
Agar

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