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J Biol Chem, Vol. 274, Issue 42, 29599-29602, October 15, 1999
From the Laboratory of Biological Chemistry, NIA, National
Institutes of Health, Baltimore, Maryland 21224
Cells respond to environmental stress with
activation of c-Jun N-terminal kinase (JNK) and p38. Recent studies
have implicated Gadd45 and two related proteins, MyD118/Gadd45
and
CR6/Gadd45
, as initiators of JNK/p38 signaling via their interaction
with an upstream kinase MTK1. It was proposed that stress-induced
expression of the Gadd45-related proteins leads to MTK1 activation and
subsequent JNK/p38 activation. Using embryo fibroblasts from
gadd45-null mice, we have addressed the requirement for
Gadd45 in mediating JNK/p38 activation during acute stress. Comparison
of JNK/p38 activities in response to methyl methanesulfonate, hydrogen
peroxide, UVC irradiation, sorbitol, and anisomycin treatment of
gadd45+/+ and
gadd45
/ fibroblasts revealed no deficiency
in JNK/p38 activation in gadd45/
fibroblasts. In addition, in wild type cells, JNK and p38 activation significantly preceded gadd45 induction with all stresses.
Examination of myd118/gadd45 and
cr6/gadd45 expression in
gadd45+/+ and
gadd45/ fibroblasts revealed similar
induction patterns in the two cell types, which, like
gadd45 expression, was delayed relative to JNK/p38 activation. We conclude that gadd45 expression is
not required for activation of JNK/p38 by environmental stresses, nor
are stress-induced increases in myd118/gadd45 and
cr6/gadd45 expression necessary for kinase
activation in response to such insults.
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