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Acute carbon dioxide avoidance in Caenorhabditis elegans

Hallem, Elissa A. and Sternberg, Paul W. (2008) Acute carbon dioxide avoidance in Caenorhabditis elegans. Proceedings of the National Academy of Sciences of the United States of America, 105 (23). pp. 8038-8043. ISSN 0027-8424. PMCID PMC2430355.

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Carbon dioxide is produced as a by-product of cellular respiration by all aerobic organisms and thus serves for many animals as an important indicator of food, mates, and predators. However, whether free-living terrestrial nematodes such as Caenorhabditis elegans respond to CO2 was unclear. We have demonstrated that adult C. elegans display an acute avoidance response upon exposure to CO2 that is characterized by the cessation of forward movement and the rapid initiation of backward movement. This response is mediated by a cGMP signaling pathway that includes the cGMP-gated heteromeric channel TAX-2/TAX-4. CO2 avoidance is modulated by multiple signaling molecules, including the neuropeptide Y receptor NPR-1 and the calcineurin subunits TAX-6 and CNB-1. Nutritional status also modulates CO2 responsiveness via the insulin and TGFβ signaling pathways. CO2 response is mediated by a neural circuit that includes the BAG neurons, a pair of sensory neurons of previously unknown function. TAX-2/TAX-4 function in the BAG neurons to mediate acute CO2 avoidance. Our results demonstrate that C. elegans senses and responds to CO2 using multiple signaling pathways and a neural network that includes the BAG neurons and that this response is modulated by the physiological state of the worm.

Item Type:Article
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URLURL TypeDescription CentralArticle Information
Sternberg, Paul W.0000-0002-7699-0173
Additional Information:© 2008 by The National Academy of Sciences of the USA. Freely available online through the PNAS open access option. Edited by Martin Chalfie, Columbia University, New York, NY, and approved February 20, 2008 (received for review August 8, 2007). This article is a PNAS Direct Submission. We thank M. de Bono (MRC Laboratory of Molecular Biology, Cambridge, U.K.), C. Bargmann (HHMI and The Rockefeller University, New York, NY), J. Thomas (University of Washington, Seattle, WA), and the Caenorhabditis Genetics Center (University of Minnesota, Minneapolis, MN) for strains; D. Anderson (California Institute of Technology, Pasadena, CA) and members of our laboratory for insightful discussions; and J. Srinivasan (California Institute of Technology, Pasadena, CA) for discussion of other species. This work was supported by the Howard Hughes Medical Institute, of which P.W.S. is an investigator, and a Helen Hay Whitney postdoctoral fellowship (to E.A.H.). Author contributions: E.A.H. and P.W.S. designed research; E.A.H. performed research; E.A.H. analyzed data; and E.A.H. and P.W.S. wrote the paper. The authors declare no conflict of interest. This article contains supporting information online at
Funding AgencyGrant Number
Howard Hughes Medical Institute (HHMI)UNSPECIFIED
Helen Hay Whitney FoundationUNSPECIFIED
Subject Keywords:behavioral genetics; cGMP signaling; chemosensation
Issue or Number:23
PubMed Central ID:PMC2430355
Record Number:CaltechAUTHORS:HALpnas08
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:11012
Deposited By: Archive Administrator
Deposited On:23 Jun 2008
Last Modified:03 Oct 2019 00:15

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