Leaky expression of GluRIICUAS.cMa (without a GAL4 driver) under the control of Scer\GAL4G14 in a GluRIIC2/Df(2L)ast1 mutant background results in a significant reduction in bouton number at muscles 6/7 and 4 NMJs compared to controls.
The ionophoretic response to glutamate at the neuromuscular junction is approximately 13-fold less than that of wild-type larvae in GluRIIC2/Df(2L)ast1 larvae carrying GluRIICScer\UAS.cMa in the absence of an Scer\GAL4 driver. In addition, these mutant animals show a 2.5-fold reduction in mean miniature excitatory junctional potential (mEJP) amplitude and a 14.4-fold reduction in mEJP frequency compared to wild type. At low calcium levels (0.47mM), there is no difference between the excitatory junctional current (EJC) amplitude of the mutant synapse and of the wild-type synapse. However, at high external calcium levels (1.5mM), the mutant synapses generate an EJC only 1/5 the size of the wild-type EJC.
Miniature excitatory junctional potentials (mEJPs) are virtually undetectable in third larval instar muscles of "weakly" rescued GluRIIC1/Df(2L)ast1 animals carrying GluRIICScer\UAS.cMa in the absence of an Scer\GAL4 driver; only rare and small events are seen.
Leaky expression of GluRIICScer\UAS.cMa in the absence of an Scer\GAL4 driver rescues the embryonic lethality of GluRIIC1/Df(2L)ast1 animals. These "weakly" rescued animals eclose as adults and have not obvious abnormalities with locomotion, flight or fertility.