2002 East Coast Worm Meeting abstract 6
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
| 1 | Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA |
| 2 | Department of Molecular Biology, Graduate School of Science, Nagoya University and CREST, Japan Science and Technology Corporation, Chikusa-ku, Nagoya 464-8602, Japan |
| 3 | Department of Genetics, Stanford University School of Medicine, 300 Pasteur Drive, Room M337, Stanford, CA 94305-5120 |
We used a Caenorhabditis elegans-Pseudomonas aeruginosa pathogenesis system to perform a genetic screen for C. elegans mutants with enhanced susceptibility to pathogens (esp). The screen identified two genes required for host defense: esp-2, encoding SEK-1, a C. elegans MAP kinase kinase homologous to the mammalian MKK3/6 and MKK4 classes of MAP kinase kinases, and esp-8, encoding NSY-1, an ortholog of the mammalian MAP kinase kinase kinase, ASK-1. esp-2/sek-1 and esp-8/nsy-1 mutants showed diminished levels of p38 MAP kinase activation, and RNAi of a C. elegans p38 MAP kinase ortholog, pmk-1, gave an Esp phenotype. These findings provide direct genetic evidence for the involvement of the evolutionarily conserved p38 MAP kinase pathway in C. elegans immunity. Combined with data from other organisms, our results suggest that a stress-activated MAP kinase signaling cassette is an ancient feature of innate immune responses in diverse species.