Mutations in the Van Gogh gene result in the altered polarity of adult
Drosophila cuticular structures. On the wing, Van Gogh mutations caus
e an altered polarity pattern that is typical of mutations that inacti
vate the frizzled signaling/signal transduction pathway. The phenotype
however, differs from those seen previously, as the number of wing ce
lls forming more than one hair is intermediate between that seen previ
ously for typical frizzled-like or inturned-like mutations. Consistent
with Van Gogh being involved in the function of the frizzled signalin
g/signal transduction pathway, Van Gogh mutations show strong interact
ions with mutations in frizzled and prickle. Mitotic clones of Van Gog
h display domineering cell nonautonomy. In contrast to frizzled clones
, Van Gogh clones alter the polarity of cells proximal (and in part an
terior and posterior) but not distal to the clone. In further contrast
to frizzled clones, Van Gogh clones cause neighboring wild-type hairs
to point away from rather than toward the clone. This anti-frizzled t
ype of domineering nonautonomy and the strong genetic interactions see
n between frizzled and Van Gogh suggested the possibility that Van Gog
h was required for the noncell autonomous function of frizzled. As a t
est of this possibility we induced frizzled clones in a Van Gogh mutan
t background and Van Gogh clones in a frizzled mutant background. In b
oth cases the domineering nonautonomy was suppressed consistent with V
an Gogh being essential for frizzled signaling.