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Vol. 16, No. 3, pp. 377-387, February 1, 2002
Department of Genetics, Howard Hughes Medical Institute, Harvard
Medical School, Boston, Massachusetts 02115, USA
The Jun kinase (JNK) pathway has been characterized for its role in
stimulating AP-1 activity and for modulating the balance between cell
growth and death during development, inflammation, and cancer. Six
families of mammalian kinases acting at the level of JNKKK have emerged
as upstream regulators of JNK activity (MLK, LZK, TAK, ASK, MEKK, and
TPL); however, the specificity underlying which kinase is utilized for
transducing a distinct signal is poorly understood. In
Drosophila, JNK signaling plays a central role in dorsal
closure, controlling cell fate and cell sheet morphogenesis during
embryogenesis. Notably, in the fly genome, there are single homologs of
each of the mammalian JNKKK families. Here, we identify mutations in
one of those, a mixed lineage kinase, named slipper (slpr), and show that it is required for JNK activation during dorsal closure. Furthermore, our results show that other putative JNKKKs cannot compensate for the loss of slpr function and,
thus, may regulate other JNK or MAPK-dependent processes.
[Key Words: JNK; morphogenesis; dorsal closure; kinase]
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