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Fig. 7. Reduction of Sog levels perturbs the PCV formation. (A) Overexpression of
UAS-tld(16) with da>Gal4 driver causes expanded pMad in
the PCV region and expanded PCV material and detachment of PCV from L5. (B)
Overexpression of UAS-tld(16) with en>Gal4 in a wild-type
background causes widening or absence of PCV. (C)
sogYL26/sogP129D results in detached PCV.
(D,D') In the stronger allelic combination
sogP1/sogP129D, partial to more complete loss
of PCV structures is observed in a larger percentage of animals (see text for
numbers). (E) Overexpression of two copies of UAS-tlr (X) with
A9>Gal4 does not affect PCV formation. (F) Overexpression of one
copy of UAS-tld(16) with A9>Gal4 driver produces detached
PCV in 16% of the animals (n=102). (G) Overexpression of
UAS-tld(16) and UAS-tlr(X) with A9>Gal4 driver
produces a range of crossvein defects, from detached PCV shown to almost
complete loss of PCV structures in 82% (n=192) of the adults.
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