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Caenorhabditis elegans NPR-1–mediated behaviors are suppressed in the presence of mucoid bacteria

Reddy, Kirthi C. and Hunter, Ryan C. and Bhatla, Nikhil and Newman, Dianne K. and Kim, Dennis H. (2011) Caenorhabditis elegans NPR-1–mediated behaviors are suppressed in the presence of mucoid bacteria. Proceedings of the National Academy of Sciences of the United States of America, 108 (31). pp. 12887-12892. ISSN 0027-8424. PMCID PMC3150904.

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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.

Item Type:Article
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URLURL TypeDescription DOIArticle CentralArticle
Hunter, Ryan C.0000-0003-3841-1676
Newman, Dianne K.0000-0003-1647-1918
Additional Information:© 2011 National Academy of Sciences. Edited by Frederick M. Ausubel, Harvard Medical School and Massachusetts General Hospital, Boston, MA, and approved June 30, 2011 (received for review May 23, 2011). Published online before print July 18, 2011. We thank F. Ausubel and G. Walker for bacterial strains, and C. Bargmann for C. elegans strains. C. elegans strains were also provided by the Caenorhabditis Genetics Center, which is supported by the National Institutes of Health (NIH). K.C.R. was supported by Postdoctoral Fellowships from the Jane Coffin Childs Cancer Research Foundation and the Charles A. King Trust Foundation. R.C.H. was supported by a Canadian Cystic Fibrosis Foundation Postdoctoral Fellowship. N.B. was supported by a National Science Foundation Graduate Research Fellowship. D.K.N. is an Investigator of the Howard Hughes Medical Insitute. This work was supported by NIH GM084477, a Burroughs Wellcome Fund Career Award in the Biomedical Sciences, and a Swanson Career Development Award (Massachusetts Institute of Technology) (to D.H.K.). Author contributions: K.C.R. and D.H.K. designed research; K.C.R. and R.C.H. performed research; R.C.H., N.B., and D.K.N. contributed new reagents/analytic tools; K.C.R., R.C.H., N.B., D.K.N., and D.H.K. analyzed data; and K.C.R. and D.H.K. wrote the paper.
Funding AgencyGrant Number
Jane Coffin Childs Cancer Research FoundationUNSPECIFIED
Charles A. King Trust FoundationUNSPECIFIED
Canadian Cystic Fibrosis FoundationUNSPECIFIED
Massachusetts Institute of Technology Swanson Career Development AwardUNSPECIFIED
Issue or Number:31
PubMed Central ID:PMC3150904
Record Number:CaltechAUTHORS:20110822-094630738
Persistent URL:
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:24969
Deposited By: Tony Diaz
Deposited On:23 Aug 2011 16:07
Last Modified:09 Mar 2020 13:18

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