The dendritogenesis defects in the embryonic aCC motoneurons characteristic for embryos expressing either Dscam1HMS01859 or dockJF02810 RNAi under the control of Scer\GAL4eve.RN2 are partially suppressed by co-expression of PakScer\UAS.T:Myr-Src64B : the reduced dendritic number is fully restored but the region containing primary dendritic processes is expanded compared to controls. This rescue effect is however blocked in the presence of either Cdc426 or Cdc424 (in hemizygous state). No suppression of the loss of dendritic tips is observed upon co-expression with PakScer\UAS.T:Lhem\EosFP-m2.
The Cdc424/+ heterozygous mutation does not suppress or enhance the GluRIIASP16 NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc424/+ , GluRIIASP16 double mutants, compared to wild-type or GluRIIASP16 controls.
Cdc424/+ has very little effect on the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is 10% compared to 9% for control flies expressing LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E in an otherwise wild-type background). The frequency of the malformed leg phenotype seen in Sb63b/+ heterozygotes (8%) is not increased if the flies are also heterozygous for Cdc424/+ (6%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is not increased if the flies are also heterozygous for Cdc424/+ (8%).
Expression of Cdc42Scer\UAS.cLa under the control of Scer\GAL4elav.PLu rescues the dendritic caliber and branching pattern phenotype of Cdc424 mutants in VS1 neurons. However, this expression is unable to rescue many of the VS1 defects such as dendrites being significantly longer than in wild-type and reduction of well developed dendritic spines.