The expression of Rac1DN.UAS.cUa under the control of Scer\GAL4da.G32 leads to severe cuticle defects in the embryo.
Flies with expression of Rac1DN.Scer\UAS.cUa driven by Scer\GAL4ics-G4 are more sensitive to ethanol-induced sedation than controls.
Expression of dominantly negative Rac1DN.Scer\UAS under the control of Scer\GAL4whir3 causes ethanol-sensitivity.
Rac1DN.UAS.cUa, Scer\GAL4ics-G4 has chemical sensitive | adult stage phenotype, non-suppressible by icsG4/icsG4
Rac1DN.UAS.cUa/Scer\GAL4ics-G4 is a suppressor of chemical resistant | adult stage phenotype of icsG4
Rac1DN.UAS.cUa/Scer\GAL4ppk.PU is a suppressor of increased cell growth rate | second instar larval stage | conditional phenotype of RtcaΔ
Rac1DN.UAS.cUa, Scer\GAL4da.G32 has embryonic/larval cuticle | maternal effect | embryonic stage phenotype, non-suppressible by cystUASp.R, Scer\GAL4da.G32
Rac1DN.UAS.cUa, Scer\GAL4da.G32 has embryonic/larval cuticle | maternal effect | embryonic stage phenotype, non-suppressible by cystN.UASp.R, Scer\GAL4da.G32
Scer\GAL4ics-G4>Rac1DN.Scer\UAS.cUa;icsG4/icsG4 flies have the same increased sensitivity to ethanol-induced sedation seen in Scer\GAL4ics-G4>Rac1DN.Scer\UAS.cUa flies, unlike ethanol-resistant icsG4/icsG4 flies.
Overexpression of Rac1DN.Scer\UAS.cUa driven by Scer\GAL4ppk.PU abolishes enhancement of CNS axon regeneration seen in RtcaΔ/RtcaΔ larvae.