Generated through imprecise excision of P{EP}GLazEP2383. The deletion starts 12bp from the P{EP}GLazEP2383 start site and removes 2794bp, eliminating the transcription initiation site, the first coding exon, and part of the first intron of GLaz.
In the GLazΔ2/+ larval brain, LNv neurons show decreased dendritic volume.
GLazΔ2 mutants are more sensitive to oxidative and starvation stress. These effects are observed in both males and females.
GLazΔ2/Df(2R)Exel8057 flies exhibit sensitivity to oxidative stress to the same levels as GLazΔ2 homozygotes.
Homozygous GLazΔ2 flies exhibit a median survival time that is reduced by 19.3% and a maximum survival time reduced by 10.9%, compared to wild-type.
GLazΔ2/+ heterozygotes exhibit a median survival time that is reduced by 18.1% and a maximum survival time reduced by 12.7%, compared to wild-type.
Young GLazΔ2 homozygotes (<21 days) exhibit no differences in running, climbing, or flying ability compared to control flies. However, 21-day old flies, where the mortality risk has increased only slightly for the mutant males, have a significantly reduced climbing ability. These flies do not exhibit a difference in phototaxis or geotropism compared to controls.
After 24 hours of exposure to paraquat, four-day old GLazΔ2 mutant flies of both sexes perform significantly worse than controls in locomotor tests, such as phototaxis, geotropism and flight ability.
A significant increase in apoptotic cell death is observed in the aged GLazΔ2 brain (approximately 25 -/+6 TUNEL positive cells/section compared to 8 -/+ 4 cells/section in wild-type). Apoptosis in neural cells also increases when young GLazΔ2 flies are exposed to paraquat (95 -/+35 TUNEL-positive cells/section), while levels in a wild-type nervous system remain low (33 -/+ 6 TUNEL-positive cells/section).
Old GLazΔ2 flies exhibit an increase in apoptotic cells in the pericerebral fat body compared to controls. Upon paraquat feeding, apoptotic nuclei are observed in the abdominal and pericerebral fat body to a greater extent than in wild-type cells.
Both sexes of GLazΔ2 flies exhibit significantly lower wet and dry body weights compared to wild-type. Protein content does not differ between GLazΔ2 flies and controls, implying that the difference in weight can be attributed to a marked reduction in relative fat content of GLazΔ2 flies. The relative content of triglycerides in both young and old adults is significantly decreased in GLazΔ2 mutants. Both the pericerebral and the abdominal fat bodies are markedly reduced in size in GLazΔ2 mutants. Young adult GLazΔ2 flies of both sexes exhibit fewer and smaller lipid bodies, and aging worsens this effect with a reduction in the fat body mass. The limited lipid bodies present in old GLazΔ2 flies are accompanied by increased eosinophilia due to protein aggregates.
The concentration of free malondialdehyde (MDA), the main product derived from unstable lipid peroxides, is more than two times higher in GLazΔ2 flies than in control flies.
GLazΔ2/Df(2R)Exel8057 flies exhibit a survival curve upon paraquat or H2O2 exposure that is similar to GLazΔ2 homozygous flies.
GLazΔ2 has abnormal stress response phenotype, non-enhanceable by Spt-ISH1626
Spt-ISH1626/GLazΔ2 transheterozygotes exhibit survival curves similar to the control GLazΔ2/+ or wild-type flies upon exposure to paraquat or H2O2.
Transheterozygous flies GLazΔ2/Spt-ISH1626 flies are as resistant to paraquat or H2O2 as the controls heterozygous for either gene.
GLazΔ2 is rescued by GLaz4.2kb.GFP
When GLaz4.2kb.T:Avic\GFP is placed in a GLazΔ2 background, the survival upon paraquat treatment returns to control levels. Starvation sensitivity is also recovered, with a 66.2% increase in median survival time when comparing GLaz4.2kb.T:Avic\GFP GLazΔ2 to GLazΔ2 flies. The size and morphology of the fat body is also restored.