Imprecise excision causing a deletion of 816 nucleotides of genomic sequence that removes the first exon of scb short.
Mutant animals show reduced 1 hour memory and normal age-related memory impairment.
Single-trial short program training in an olfactory learning assay shows that scbVol-1 flies perform poorly immediately after conditioning. Single-trial training fails to induce any conditioning whatsoever. The scbVol-2 allele is partially dominant for performance after single-trial and two-trial massed conditioning. The scbVol-2 phenotype after two massed trials or two spaced trials is completely dominant.
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 scbVol-2, but highly significant for scbVol-1, scbVol-3 and scbVol-4. scbVol-2 shows normal dependence on external Ca2+. Mutants show normal augmentation of transmission amplitude upon prolonged stimulation at intermediate frequencies, but a dramatic decrease in transmission amplitude after tetanus, compared to wild type.
Mutations produce a memory deficit as shown in the odour avoidance test. Neither sensorimotor nor gross anatomical defects can account for the memory deficit. Conditional expression of scb short just before behavioural training is sufficient to fully rescue the memory deficit. Rescue is completely reversible.
Mutation disrupts the expression of scb short form.