Table 1.

Penetrance of vein pattern phenotypes upon manipulation of Abl and other Notch endosomal trafficking regulators

Genetic perturbationGain/loss of veins?Penetrance (% of wings)Regions affected
WT - 0% (N = 50) - 
AbldeGradFP (knockdown) Loss 29% (N = 70) PCV 
Notch54l9/+ Gain 94% (N = 54) L3, L4, L5 
Notch54l9/+; abl2/+ Gain 80% (N = 76) L3, L4, L5 
Su(dx) Gain 62% (N = 40) PCV, occasionally ACV, L4, L5, and interveins. 
Su(dx) + abl2/+ Gain 43% (N = 63) PCV 
Dx Loss 60% (N = 80) L4, occasionally L5, PCV 
Dx + abl2/+ Loss 71% (N = 44) L4, occasionally L5, and PCV 
Abl Gain 52% (N = 65) PCV 
AblK417N (kinase dead) Gain 4% (N = 48) PCV 
Abl + Su(dx) Gain 85% (N = 83) PCV, ACV, L4, L5, and interveins 
Su(dx)RNAi - 0% (N = 30) - 
Abl + Su(dx)RNAi Gain 18% (N = 60) PCV 
Nedd4RNAi - 0% (N = 40) - 
Abl + Nedd4RNAi Gain 24% (N = 54) PCV 
Nedd4S Gain 9% (N = 34) PCV 
Nedd4Lo Gain 90% (N = 42) L4, L5, ACV, and PCV 

All genetic perturbations, except the Notch54l9/+; abl2/+ interaction, used engrailed-Gal4 to drive expression of UAS transgenes in the posterior compartment of developing pupal wings (see Materials and methods). Abl knockdown (AbldeGradFP) was performed in an ablGFP/abl2 background. ACV/PCV, anterior/posterior cross vein.

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