A 4.3 kb deletion that removes the first 433 amino-terminal codons of the Gba1b gene and the carboxy-terminal 33 codons of the Gba1a gene, and completely removes the intervening gene, Qsox4. This deletion allele results in the production of a hybrid transcript fusing the amino terminal Gba1a coding sequence to the carboxy terminal Gba1b sequences, but does not create an in-frame fusion of the coding sequences, and therefore is not expected to yield a chimeric glucocerebrosidase protein. Given that this deletion eliminates the presumptive promoter and >3/4 of the amino terminal coding sequence of Gba1b, and results in ~75% reduced expression of a transcript lacking the final 33 codons of Gba1a, it is likely a null allele of Gba1b and a hypomorphic allele of Gba1a. The residual expression of the fusion transcript is nearly undetectable in heads from homozygotes.
Df(3R)GBA1ΔTT/Df(3R)GBA1ΔTT and Df(3R)GBA1ΔTT/+ mutants are viable, fertile and have no detectable morphological abnormalities. Df(3R)GBA1ΔTT/Df(3R)GBA1ΔTT (but not Df(3R)GBA1ΔTT/+) mutants are short lived, exhibit delayed recovery from heat-induced paralysis, display a progressive climbing defect. Df(3R)GBA1ΔTT/Df(3R)GBA1ΔTT mutants display increased vacuolization in the brain, but no significant loss of dopaminergic neurons, as compared to controls. Df(3R)GBA1ΔTT/Df(3R)GBA1ΔTT and Df(3R)GBA1ΔTT/+ mutants both exhibit bang sensitivity, and defective long term (but not short term) memory and latency to initiate courtship in a courtship assay.