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A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans

Molecular pathways involved in dauer formation, an alternate larval stage that allows Caenorhabditis elegans to survive adverse environmental conditions during development, also modulate longevity and metabolism. The decision to proceed with reproductive development or undergo diapause depends on fo...

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Autores principales: Khanna, Amit, Kumar, Jitendra, Vargas, Misha A., Barrett, LaKisha, Katewa, Subhash, Li, Patrick, McCloskey, Tom, Sharma, Amit, Naudé, Nicole, Nelson, Christopher, Brem, Rachel, Killilea, David W., Mooney, Sean D., Gill, Matthew, Kapahi, Pankaj
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5153853/
https://www.ncbi.nlm.nih.gov/pubmed/27958277
http://dx.doi.org/10.1038/srep38764
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author Khanna, Amit
Kumar, Jitendra
Vargas, Misha A.
Barrett, LaKisha
Katewa, Subhash
Li, Patrick
McCloskey, Tom
Sharma, Amit
Naudé, Nicole
Nelson, Christopher
Brem, Rachel
Killilea, David W.
Mooney, Sean D.
Gill, Matthew
Kapahi, Pankaj
author_facet Khanna, Amit
Kumar, Jitendra
Vargas, Misha A.
Barrett, LaKisha
Katewa, Subhash
Li, Patrick
McCloskey, Tom
Sharma, Amit
Naudé, Nicole
Nelson, Christopher
Brem, Rachel
Killilea, David W.
Mooney, Sean D.
Gill, Matthew
Kapahi, Pankaj
author_sort Khanna, Amit
collection PubMed
description Molecular pathways involved in dauer formation, an alternate larval stage that allows Caenorhabditis elegans to survive adverse environmental conditions during development, also modulate longevity and metabolism. The decision to proceed with reproductive development or undergo diapause depends on food abundance, population density, and temperature. In recent years, the chemical identities of pheromone signals that modulate dauer entry have been characterized. However, signals derived from bacteria, the major source of nutrients for C. elegans, remain poorly characterized. To systematically identify bacterial components that influence dauer formation and aging in C. elegans, we utilized the individual gene deletion mutants in E. coli (K12). We identified 56 diverse E. coli deletion mutants that enhance dauer formation in an insulin-like receptor mutant (daf-2) background. We describe the mechanism of action of a bacterial mutant cyaA, that is defective in the production of cyclic AMP, which extends lifespan and enhances dauer formation through the modulation of TGF-β (daf-7) signaling in C. elegans. Our results demonstrate the importance of bacterial components in influencing developmental decisions and lifespan in C. elegans. Furthermore, we demonstrate that C. elegans is a useful model to study bacterial-host interactions.
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spelling pubmed-51538532016-12-28 A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans Khanna, Amit Kumar, Jitendra Vargas, Misha A. Barrett, LaKisha Katewa, Subhash Li, Patrick McCloskey, Tom Sharma, Amit Naudé, Nicole Nelson, Christopher Brem, Rachel Killilea, David W. Mooney, Sean D. Gill, Matthew Kapahi, Pankaj Sci Rep Article Molecular pathways involved in dauer formation, an alternate larval stage that allows Caenorhabditis elegans to survive adverse environmental conditions during development, also modulate longevity and metabolism. The decision to proceed with reproductive development or undergo diapause depends on food abundance, population density, and temperature. In recent years, the chemical identities of pheromone signals that modulate dauer entry have been characterized. However, signals derived from bacteria, the major source of nutrients for C. elegans, remain poorly characterized. To systematically identify bacterial components that influence dauer formation and aging in C. elegans, we utilized the individual gene deletion mutants in E. coli (K12). We identified 56 diverse E. coli deletion mutants that enhance dauer formation in an insulin-like receptor mutant (daf-2) background. We describe the mechanism of action of a bacterial mutant cyaA, that is defective in the production of cyclic AMP, which extends lifespan and enhances dauer formation through the modulation of TGF-β (daf-7) signaling in C. elegans. Our results demonstrate the importance of bacterial components in influencing developmental decisions and lifespan in C. elegans. Furthermore, we demonstrate that C. elegans is a useful model to study bacterial-host interactions. Nature Publishing Group 2016-12-13 /pmc/articles/PMC5153853/ /pubmed/27958277 http://dx.doi.org/10.1038/srep38764 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Khanna, Amit
Kumar, Jitendra
Vargas, Misha A.
Barrett, LaKisha
Katewa, Subhash
Li, Patrick
McCloskey, Tom
Sharma, Amit
Naudé, Nicole
Nelson, Christopher
Brem, Rachel
Killilea, David W.
Mooney, Sean D.
Gill, Matthew
Kapahi, Pankaj
A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans
title A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans
title_full A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans
title_fullStr A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans
title_full_unstemmed A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans
title_short A genome-wide screen of bacterial mutants that enhance dauer formation in C. elegans
title_sort genome-wide screen of bacterial mutants that enhance dauer formation in c. elegans
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5153853/
https://www.ncbi.nlm.nih.gov/pubmed/27958277
http://dx.doi.org/10.1038/srep38764
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