The c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protei
n kinase (MAPK) family, was shown to be involved in the response to various
stresses in cultured cells. However, there is little in vivo evidence indi
cating a role for a JNK pathway in the stress response of an organism. We i
dentified the Caenorhabditis elegans mek-1 gene, which encodes a 347 amino
acid protein highly homologous to mammalian MKK7, an activator of JNK, Mek-
1 reporter fusion proteins are expressed in pharyngeal muscle, uterus, a po
rtion of intestine, and neurons. A mek-1 deletion mutant is hypersensitive
to copper and cadmium ions and to starvation. A wild-type mek-1 transgene r
escued the hypersensitivity to the metal ions. Double mutants of mek-1 with
an eat-5, eat-II or eat-18 mutation, which are characterized by a limited
feeding defect, showed distinct growth defects under normal conditions. Exp
ression of an activated form of MEK-1 in the whole animal or specifically i
n the pharynx inhibited pharyngeal pumping. These results suggest a role fo
r mek-1 in stress responses, with a focus in the pharynx and/or intestine.