NnaDPL90 mutants hatch from their eggs in normal numbers with no defects in cuticle patterning. However, NnaDPL90 third instar larvae are much thinner than their control siblings. NnaDPL90 males die between the late second instar larval stage and early pupal stage. NnaDPL90 mutants that survive to produce pupal cases initiate morphogenesis but die before head eversion. Almost all NnaDPL90 male flies that survive past head eversion do complete morphogenesis, and then eclose as "escaper" males. The frequency of escaper NnaDPL90 males is approximately 40% of expected Mendelian ratios. The cuticles of NnaDPL90 escaper males are normal, but the wings are smaller than those of controls and always appear droopy and opaque.
Charting of NnaDPL90 escaper male lifespan reveals continuous, relatively uniform, and decreased survival, suggesting that there isn't a particular crisis stage or time-dependent nature to their demise.
18-day old NnaDPL90 male fly heads do not display evidence of vacuolization or gross neurodegeneration in the brain parenchyma. However, areas of thinning, cell loss, and vacuole formation in retinal photoreceptor neurons are found. Two-day old NnaDPL90 mutant heads exhibit less severe photoreceptor degeneration. The ommatidial array is severely disrupted in 5-day old NnaDPL90 escaper males retina.
Four-day old NnaDPL90 escaper males score extremely poorly on the Benzer countercurrent assay for phototaxis, indicating a severe loss of eyesight.
Seven-day old NnaDPL90 escaper males exhibit a number of electron-dense degenerating retina cells, typical of apoptosis. Endoplasmic reticulum, highly studded with ribosomes in neurons at moderate to advanced stages of degeneration are also found. Unlike mitochondria with well-defined cristae and lumens of normal size, NnaDPL90 mitochondria exhibit decreased numbers of cristae, and the lumens of the cristae are swollen and irregular. Many NnaDPL90 mitochondria have vacuoles, a feature never seen in wild-type.
Mitochondrial complex I, II and V exhibit marked reductions in activity in NnaDPL90 larval samples. NnaDPL90 flies exhibit significantly decreased survival when exposed to 2,4-dinitrophenol at either a high or a low concentration. NnaDPL90 escaper males are exquisitely susceptible to oligomycin at high concentrations, but, at low concentrations, both NnaDPL90 and control flies are resistant, suggesting a distinct threshold for toxicity.
Nna1PL90 has abnormal visual behavior phenotype, suppressible by BacA\p35UAS.cHa/Scer\GAL4ey.PU
Nna1PL90 has abnormal visual behavior phenotype, non-suppressible by Avic\GFPUAS.cUa/Scer\GAL4ey.PU
Nna1PL90 has eye phenotype, suppressible by BacA\p35UAS.cHa/Scer\GAL4ey.PU
Nna1PL90 has ommatidium phenotype, suppressible by BacA\p35UAS.cHa/Scer\GAL4ey.PU
Nna1PL90 has eye phenotype, non-suppressible by Avic\GFPUAS.cUa/Scer\GAL4ey.PU
Nna1PL90 has ommatidium phenotype, non-suppressible by Avic\GFPUAS.cUa/Scer\GAL4ey.PU
Expression of Avic\GFPScer\UAS.cUa in the developing retina under the control of Scer\GAL4ey.PU fails to suppress the retinal degeneration phenotype (and associated loss of eyesight) found in NnaDPL90 mutants.
Expression of BacA\p35Scer\UAS.cHa in the developing retina under the control of Scer\GAL4ey.PU suppresses the retinal degeneration phenotype (and associated loss of eyesight) found in NnaDPL90 mutants, indicating that altered apoptotic pathway activity is contributing to the NnaDPL90 escaper male phenotype.
Nna1PL90 is rescued by Scer\GAL4Nna1.1.3/Nna1RB.UAS
Nna1PL90 is rescued by Nna1RB.UAS/Scer\GAL4ey.PU
Nna1PL90 is not rescued by Scer\GAL4Nna1.1.3/Nna1RA.UAS
Expression of NnaDRB.Scer\UAS under the control of Scer\GAL4NnaD.1.3 rescues the larval lethality seen in NnaDPL90 mutants.
Expression of NnaDRA.Scer\UAS under the control of Scer\GAL4NnaD.1.3 does not rescue the larval lethality seen in NnaDPL90 mutants.
Expression of NnaDRB.Scer\UAS in the developing retina under the control of Scer\GAL4ey.PU full rescues the retinal degeneration phenotype (and associated loss of eyesight) found in NnaDPL90 mutants.