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Vol. 15, No. 6, pp. 658-671, March 15, 2001
Departments of 1 Developmental Biology,
2 Genetics, and 3 Pathology, Howard Hughes Medical
Institute, Beckman Center B300, Stanford University School of
Medicine, Stanford, California 94305, USA; 4 Department of
Biology, Kraus Natural Science Building, University of Michigan, Ann
Arbor, Michigan 48109, USA
In Drosophila embryos the protein Naked cuticle (Nkd) limits
the effects of the Wnt signal Wingless (Wg) during early segmentation. nkd loss of function results in segment polarity defects and
embryonic death, but how nkd affects Wnt signaling is unknown.
Using ectopic expression, we find that Nkd affects, in a
cell-autonomous manner, a transduction step between the Wnt signaling
components Dishevelled (Dsh) and Zeste-white 3 kinase (Zw3). Zw3 is
essential for repressing Wg target-gene transcription in the absence of
a Wg signal, and the role of Wg is to relieve this inhibition. Our
double-mutant analysis shows that, in contrast to Zw3, Nkd acts when
the Wg pathway is active to restrain signal transduction. Yeast two
hybrid and in vitro experiments indicate that Nkd directly binds to the basic-PDZ region of Dsh. Specially timed Nkd overexpression is capable
of abolishing Dsh function in a distinct signaling pathway that
controls planar-cell polarity. Our results suggest that Nkd acts
directly through Dsh to limit Wg activity and thus determines how
efficiently Wnt signals stabilize Armadillo (Arm)/
-catenin and
activate downstream genes.
[Key Words: Wnt/wingless; naked cuticle; dishevelled; zeste-white 3; segmentation; Drosophila]
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