Pheromones are cell type-specific signals used for communication between individuals of the same species. When faced with overcrowding or starvation, Caenorhabditis elegans secrete the pheromone daumone, which facilitates communication between individuals for adaptation to adverse environmental stimuli. Daumone signals C. elegans to enter the dauer stage, an enduring and non-ageing stage of the nematode life cycle with distinctive adaptive features and extended life. Because daumone is a key regulator of chemosensory processes in development and ageing, the chemical identification of daumone is important for elucidating features of the daumone-mediated signalling pathway. Here we report the isolation of natural daumone from C. elegans by large-scale purification, as well as the total chemical synthesis of daumone. We present the stereospecific chemical structure of purified daumone, a fatty acid derivative. We demonstrate that both natural and chemically synthesized daumones equally induce dauer larva formation in C. elegans (N2 strain) and certain dauer mutants, and also result in competition between food and daumone. These results should help to elucidate the daumone-mediated signalling pathway, which might in turn influence ageing and obesity research and the development of antinematodal drugs.
|Number of pages||5|
|Publication status||Published - 2005 Feb 3|
Bibliographical noteFunding Information:
Acknowledgements This study was supported by a grant to Y.K.P. from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea. We thank J.-M. Kim at KDR Biotech Co. for his support on this project, D.J. Chitwood at the USDA-ARS Nematology Lab for his critical reading and suggestions, R. Moyer at King College (USA) for editorial assistance, J. Lee at Seoul National University for discussions and the Caenorhabditis Genetics Center for kind provision of the C. elegans strains used in this study. Technical support from the LG Chem Research Center (Taejon, Korea) was appreciated.
Acknowledgements We thank H. Huber and K. O. Stetter for advice and spirited discussions, M. Thomm for the use of laboratory facilities, and J. Yuan and J. Sabina for critically reading the manuscript. This work was supported by grants from the National Institute of General Medical Sciences and the Department of Energy (to D.S.) and by the German Federal Ministry of Education and Research (BMBF) for the Bioinformatics Competence Center ‘Intergenomics’ (to D.J.).
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