Ectopic expression of ringerScer\UAS.cMa under the control of Scer\GAL4eve.PU leads to defects in placement of embryonic eve-positive neurons (the phenotype is strongest in RP2 neurons) as well as disruption of axonal bundles. Expression under the Scer\GAL4Act5C.PU driver results in axonal stalling in embryos.
Cultured neurons (primary cultures from larval brains) expressing ringerScer\UAS.cMa under the control of Scer\GAL4elav-C155 show axonal extension defects and tend to have much shorter axons than control wild-type neurons.
Scer\GAL4elav-C155/ringerUAS.cMa partially rescues ringer915
Scer\GAL4eve.PU/ringerUAS.cMa partially rescues ringer915
The axonal targeting defects and eve-positive neurons placement errors characteristic for ringer915 homozygous mutant embryos are partially rescued by expression of ringerScer\UAS.cMa under the control of the Scer\GAL4elav-C155 or the Scer\GAL4eve.PU driver, respectively. However, the axonal extension defects observed in cultured ringer915 neurons (primary cultures from larval brains) is not significantly rescued by Scer\GAL4elav-C155-driven expression of ringerScer\UAS.cMa.