Toll-like Receptor Signaling Promotes Development and Function of Sensory Neurons Required for a C. elegans Pathogen-Avoidance Behavior

被引:89
作者
Brandt, Julia P. [1 ,2 ]
Ringstad, Niels [1 ,2 ]
机构
[1] NYU, Mol Neurobiol Program, Skirball Inst Biomol Med, Langone Med Ctr,Helen L & Martin S Kimmel Ctr Bio, New York, NY 10016 USA
[2] NYU, Langone Med Ctr, Dept Cell Biol, New York, NY 10016 USA
关键词
CARBON-DIOXIDE AVOIDANCE; MAP KINASE PATHWAY; CAENORHABDITIS-ELEGANS; KAPPA-B; SENSING NEURONS; RECOGNITION RECEPTORS; SERRATIA-MARCESCENS; INNATE IMMUNITY; ACTIVATION; OXYGEN;
D O I
10.1016/j.cub.2015.07.037
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Toll-like receptors (TLRs) play critical roles in innate immunity in many animal species. The sole TLR of C. elegans-TOL-1-is required for a pathogen-avoidance behavior, yet how it promotes this behavior is unknown. We show that for pathogen avoidance TOL-1 signaling is required in the chemosensory BAG neurons, where it regulates gene expression and is necessary for their chemosensory function. Genetic studies revealed that TOL-1 acts together with many conserved components of TLR signaling. BAG neurons are activated by carbon dioxide (CO2), and we found that this modality is required for pathogen avoidance. TLR signaling can therefore mediate host responses to microbes through an unexpected mechanism: by promoting the development and function of chemosensory neurons that surveil the metabolic activity of environmental microbes.
引用
收藏
页码:2228 / 2237
页数:10
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