title: Caenorhabditis elegans NPR-1-mediated behaviors are suppressed in the presence of mucoid bacteria.
abstract: Caenorhabditis elegans exhibits a diverse range of behaviors in response to bacteria. The presence of bacterial food influences C. elegans aerotaxis, aggregation, locomotion, and pathogen avoidance behaviors through the activity of the NPR-1 neuropeptide receptor. Here, we show that mucoid strains of bacteria that produce an exopolysaccharide matrix do not induce NPR-1-dependent behaviors. In the presence of mucoid strains of bacteria, the C. elegans laboratory wild-type (WT) strain N2 exhibits behaviors characteristic of wild isolates and mutants with reduced NPR-1 activity. Specifically, N2 exhibits lawn bordering and roaming behavior on mucoid nonpathogenic bacteria and loss of pathogen avoidance on mucoid Pseudomonas aeruginosa. Alginate biosynthesis by laboratory and clinical isolates of mucoid P. aeruginosa is necessary and sufficient to attenuate NPR-1-mediated behavior and it suppresses C. elegans pathogen avoidance behavior. Our data suggest that the specific interaction with nonmucoid bacteria induces NPR-1-dependent behaviors of C. elegans. These observations provide an example of how exopolysaccharide matrix biosynthesis by a community of bacteria may inhibit specific host responses to microbes.
authors.affiliation: Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
authors.forename: Kirthi C
authors.initials: KC
authors.lastname: Reddy
authors.forename: Ryan C
authors.initials: RC
authors.lastname: Hunter
authors.forename: Nikhil
authors.initials: N
authors.lastname: Bhatla
authors.forename: Dianne K
authors.initials: DK
authors.lastname: Newman
authors.forename: Dennis H
authors.initials: DH
authors.lastname: Kim
mesh_terms: D000464:Alginates / Q000378:metabolism; D000818:Animals; D030801:Animals, Genetically Modified; D016956:Burkholderia cepacia / Q000378:metabolism / Q000502:physiology; D017173:Caenorhabditis elegans / Q000235:genetics / Q000382:microbiology / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism*; D004926:Escherichia coli / Q000378:metabolism / Q000502:physiology; D020723:Glucuronic Acid / Q000378:metabolism; D006162:Guanylate Cyclase / Q000235:genetics; D006603:Hexuronic Acids / Q000378:metabolism; D054884:Host-Pathogen Interactions; D006801:Humans; D008124:Locomotion / Q000235:genetics / Q000502:physiology; D008954:Models, Biological; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000235:genetics; D010100:Oxygen / Q000378:metabolism; D011135:Polysaccharides, Bacterial / Q000378:metabolism; D011552:Pseudomonas Infections / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000378:metabolism* / Q000502:physiology; D017476:Receptors, Neuropeptide Y / Q000235:genetics / Q000378:metabolism*; D013045:Species Specificity; D050916:TRPV Cation Channels; D050051:Transient Receptor Potential Channels / Q000235:genetics
chemical_list: D000464:Alginates; D029742:Caenorhabditis elegans Proteins; D006603:Hexuronic Acids; C468272:NPR-1 protein, C elegans; D009419:Nerve Tissue Proteins; C108820:OSM-9 protein, C elegans; D011135:Polysaccharides, Bacterial; D017476:Receptors, Neuropeptide Y; D050916:TRPV Cation Channels; D050051:Transient Receptor Potential Channels; C064841:exopolysaccharide, Pseudomonas; D020723:Glucuronic Acid; C488166:GCY-35 protein, C elegans; D006162:Guanylate Cyclase; D010100:Oxygen