scb^Vol-3 embryos exhibit a gap between the dorsal epidermis and the peripheral amnioserosa, with the cells barely connected with filipodia. The border between the two epidermal cells appears unchanged. In contrast, the interface between dorsal epidermal cells remain tight.

scb^Vol-3 embryos exhibit a mild phenotype in the trachea, showing a stalled dorsal branch extension.

Time-lapse of scb^Vol-3 embryos indicates varying degrees of defects in dorsal closure, ranging from partial scarring in the dorsal epidermis to a complete dorsal open phenotype. Even when dorsal closure occurs, scb^Vol-3 embryos show slack dorsal epidermis leading edges, with discontinuous F-actin accumulation. Mutant embryos take twice as long to complete dorsal closure as controls. In more severe cases, the edges of the dorsal epidermis suddenly separate from the peripheral amnioserosa as they approach the dorsal midline and start to show abnormal F-actin accumulation.

Despite the separation of the dorsal epidermis and the peripheral amnioserosa in scb^Vol-3 embryos, the dorsal epidermis from the opposing sides continue to seal the gap, albeit at a delayed stage compared to controls. Following completion of dorsal closure, the peripheral amnioserosa remains associated with the dorsal epidermis, subsequently delaying entry into apoptosis.

The nuclei of peripheral amnioserosa and dorsal epidermal cells are occasionally separated at the start of dorsal closure, unlike in wild-type, where they overlap.

The scb^Vol-3 allele shows a partially dominant phenotype after single-trial short program training in an olfactory learning assay and a completely dominant phenotype after two-trial conditioning (massed or spaced).

Embryos hatch normally but show locomotor defects in the larval stages. Most die during the second or third instar, few pupate and non survive to adult stages. Nmjs show no obvious defects in neuronal pathfinding or synaptogenesis. At hatching CNS morphology, peripheral nerve branching, neuromuscular patterning and nmj distribution all appear normal. However, starting at mid-2nd instar, larvae begin to show nmj overgrowth: terminals are enlarged with 60-100% more synaptic terminal branches and 30-40% more synaptic boutons than controls. At physiological levels of external Ca²⁺ mutant nmjs show normal transmission. At reduced external Ca²⁺ levels EJC amplitudes are increased over those of controls (least pronounced for scb^Vol-2, but highly significant for scb^Vol-1, scb^Vol-3 and scb^Vol-4. scb^Vol-1, scb^Vol-3 and scb^Vol-4 show reduced slope of the logarithmic relationship between EJC amplitude and external Ca²⁺ concentration, indicating reduced Ca²⁺ dependence of transmission. mEJC variability, amplitude (indicative of postsynaptic glutamate receptor density) is indistinguishable from wild type. Mutants show significant defects in two forms of short-term facilitation, paired pulse and frequency dependent short term facilitation. Mutants show impaired augmentation of transmission amplitude upon prolonged stimulation at intermediate frequencies.