Fig. 4. Expression of wild-type CG8667 restores neuropeptide levels in dimm mutants (left) and increases normal neuropeptide levels in wild-type animals (right). (A) LK immunostaining of the A1-A7 neurons in the ventral nerve cord in animals heterozygous for the Rev8 or Rev4 deficiencies. The P{UAS-dimm::Myc} transgene, which contains the entire predicted CG8667 ORF, was present on the Rev8 chromosome. (B) Markedly reduced LK immunostaining in dimm^-/- (Rev8/Rev4) animals. (C) Staining levels in A1-A7 were restored to normal in Rev8/Rev4 animals by inclusion of the c127-Gal4 element. The A1-7 LK-positive neurons were all GFP positive at this stage (C'). (D) Mean pixel intensity (intensity index) for four pairs of LK-positive neurons in the three genotypes (NS, heterozygous versus rescue; P<0.01, homozygous versus rescue). (E) LK immunostaining of the Br1 neuron in the lateral brain of an animal wild type for dimm and containing one copy of the UAS-dimm::myc transgene. (F) LK-immunostaining in Br1 (soma and arbor) is markedly increased, and a neighboring neuron Br2 becomes LK positive, when UAS-dimm-Myc is driven by ap-GAL4. Br1 was identified based on the retained shape of its axonal arbor. (F') Anti-Myc immunostaining of the specimen in F reveals that Br1 and Br2 neuron are both ap-GAL4 positive. Scale bar, 50 µm in C; 20 µm in F. (G) Mean pixel intensity (intensity index) for the Br1 LK-positive neuron in the two genotypes (P<0.001).

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