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) sog^YL26/sog^P129D results in detached PCV. (D,D') In the stronger allelic combination sog^P1/sog^P129D, 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.