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.
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.Attached Files
Published - Reddy2011p15523P_Natl_Acad_Sci_Usa.pdf
Supplemental Material - pnas.201108265SI.pdf
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Additional details
- PMCID
- PMC3150904
- Eprint ID
- 24969
- Resolver ID
- CaltechAUTHORS:20110822-094630738
- NIH
- GM084477
- Jane Coffin Childs Cancer Research Foundation
- Charles A. King Trust Foundation
- Canadian Cystic Fibrosis Foundation
- NSF
- Massachusetts Institute of Technology Swanson Career Development Award
- Created
-
2011-08-23Created from EPrint's datestamp field
- Updated
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2021-11-09Created from EPrint's last_modified field
- Caltech groups
- Division of Geological and Planetary Sciences