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Fig. 2. Reduction of Kul levels leads to loss of wing veins. (A) Wild-type wing.
(B) Expression of ds-kul in the central part of the wing by
sal-GAL4 led to loss of veins (arrow). This phenotype suggests that
Kul may normally be required for proper signaling by the Notch pathway. (C)
Overexpression of Kul by sal-GAL4 led to an expansion of veins
(arrow). (D) kul RNA is broadly distributed in the wing imaginal
disc. (E) Expression of ds-kul at the anterior-posterior boundary of
the wing disc by ptc-GAL4 led to elimination of endogenous
kul RNA within this domain (arrowhead). (F) Expression of
kul by the ptc-GAL4 driver exhibited a marked elevation in
kul RNA. (G) Overexpression of Kuz by sd-GAL4 led to an
expansion of veins (arrow), similar to Kul. (H) Expression of dskuz
by MS1096-GAL4 led to thickening of the veins, similar to a
kuz loss-of function phenotype. (I) The specificity of
ds-kul was monitored in S2 cells. HA-tagged Kul (Kul-HA) is detected
as a high molecular precursor, and as a mature protein lacking the pro-domain.
Co-expression of ds-kul eliminated expression of the protein. By
contrast, ds-kuz had no effect on the expression of Kul-HA. However,
ds-kul had no effect on the expression of Kuz-HA, while
ds-kuz eliminated the expression of the Kuz-HA protein. We conclude
that ds-kul is specific. Expression of UAS-GFP was used to
demonstrate similar transfection levels.
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