GluRIIASP16/GluRIIASP16 Cskc04256/Cskc04256 Src42Ak10108/+ third instar larvae show significant decreases in mEPSP (decreased quantal size) but do not show significant compensatory homeostatic increases in quantal content (similar to GluRIIASP16/GluRIIASP16 Cskc04256/Cskc04256 double mutants) at the NMJ. GluRIIASP16/GluRIIASP16 Src42Ak10108/+ third instar larvae look similar to GluRIIASP16/GluRIIASP16 larvae (significant decreases in mEPSP and compensatory homeostatic increases in quantal content) at the NMJ.
A Src42Ak10108/+ ; Src64Bko/+ trans-heterozygous background partially suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.
Src42AE1/Src42Ak10108 ; Src64Bko/Src64Bko double mutants exhibit severe defects in Fas2-positive axons, with Fas2-positive ipsilateral axons often crossing the midline inappropriately. eg-positive commissural neurons do not exhibit defects in these mutants.
Synthetic lethality is found in p130CAS1 homozygotes with a Src42Ak10108 heterozygous or homozygous background, with fewer than 46% of the double mutant embryos hatch. 90% of the cuticles of the double mutants have holes in or absence of the head cuticle and 10% of the double mutants exhibit additional germ band retraction defects.
Fails to complement three (unnamed) alleles of the SK2-4 complementation group.