Summary: p38 MAPK Regulates Expression of Immune
Response Genes and Contributes to Longevity
in C. elegans
Emily R. Troemel1,2
, Stephanie W. Chu3
, Valerie Reinke4
, Siu Sylvia Lee5[
, Frederick M. Ausubel1,2[
, Dennis H. Kim3[*
1 Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America, 2 Department of Molecular Biology, Massachusetts General Hospital,
Boston, Massachusetts, United States of America, 3 Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America,
4 Department of Genetics, Yale University School of Medicine, New Haven, Connecticut, United States of America, 5 Department of Molecular Biology and Genetics,
Cornell University, Ithaca, New York, United States of America
The PMK-1 p38 mitogen-activated protein kinase pathway and the DAF-2­DAF-16 insulin signaling pathway control
Caenorhabditis elegans intestinal innate immunity. pmk-1 loss-of-function mutants have enhanced sensitivity to
pathogens, while daf-2 loss-of-function mutants have enhanced resistance to pathogens that requires upregulation of
the DAF-16 transcription factor. We used genetic analysis to show that the pathogen resistance of daf-2 mutants also
requires PMK-1. However, genome-wide microarray analysis indicated that there was essentially no overlap between
genes positively regulated by PMK-1 and DAF-16, suggesting that they form parallel pathways to promote immunity.
We found that PMK-1 controls expression of candidate secreted antimicrobials, including C-type lectins, ShK toxins,

Source: Ausubel, Frederick M. - Department of Genetics, Harvard University

Collections: Biology and Medicine