The wings of ArkCD4 flies that survive to adulthood gradually melanize within 5 days after eclosion. Necrotic cells are also observed in the wings of 5-day-old flies.
ArkCD4 flies are hypersusceptible to starvation stress compared to wild type.
2.1 +/- 1.1 surviving EW3-sib cells are seen in homozygous larvae (these cells die during embryogenesis in wild type).
Surviving EW3-sib cells are seen in ArkCD4/Ark82 larvae (these cells die during embryogenesis in wild type) and the average number of surviving cells is increased if the female parent is homozygous for ArkCD4.
The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed in ArkCD4 mutant homozygotes. Between 0 and two bursCCAP neurons are seen at 3-5 days.
The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed in ArkCD4/Ark82 mutants. On average 3.9 bursCCAP neurons are seen at 3-5 days.
Homozygous debclE26 mutant larvae do not display any NMJ degeneration or changes in NMJ morphology.
Flies develop melanized blemishes in the wing in a progressive manner - wings are normal at eclosion, but blemishes are evident by day 14.
Homozygous adult ArkCD4 mutants exhibit wing blemishes.
On the first day of eclosion, the dorsal and ventral wing cuticles of wild-type animals become tightly merged, with no intervening tissue evident between the dorsal and ventral cuticles. However, even 14 days after eclosion, cells and cell remnants remain situated between the dorsal and ventral cuticles in ArkCD4 mutants. There is evidence of intact cells soon after eclosion and ectopic cellular material 24 hours after eclosion.
The apoptotic response to irradiation is significantly decreased in mutant embryos compared to wild type.
ArkCD4 mutants exhibit a delay in programmed cell death in Crz-expressing neurons in the ventral nerve cord during pupation.
Flies homozygous for ArkCD4 exhibit suppression of dendritic branch removal.
Adults homozygous for ArkCD4 develop melanized spots on their wings as they age.
Homozygous mutants have normal aristae.
A few neuroblasts ectopically survive in the abdominal neuromeres of homozygous larvae, in contrast to wild type where most of these neuroblasts undergo apoptosis by the end of embryogenesis.
There is a significant increase in the number of midline glia (~8 cells/segment) in mutants. On exposure to ionising radiation, mutant stage 9 embryos show very few sparsely distributed apoptotic cells, compared to wild-type embryos at the same stage where widespread cell death. No evidence is seen for extra photoreceptor cells in mutant pupal eyes.
Most homozygotes survive to adulthood, although at a lower frequency than heterozygous siblings. Many homozygotes derived from heterozygous parents have melanotic tumours and abnormalities affecting the wings and/or bristles. Most affected flies have severe wing defects similar to a 'gnarled' or 'wrinkled' phenotype, while others have wing blisters or burnt 'notched' wings. 3% of flies have melanotic tumours inside the body, while in 7% of flies, melanotic tumours are seen protruding from the body next to the haltere. Among flies with extra bristles, most have one extra anterior scutellar bristle, while a few have two extra anterior scutellar bristles and/or an extra posterior scutellar bristle. Homozygotes derived from homozygous parents have impaired viability and fecundity and have an increased penetrance and expression of similar defects to those seen in homozygotes derived from heterozygous parents. Most homozygous larvae have a significantly overgrown central nervous system (CNS) compared to wild type. Occasionally, hyperplasia of the CNS is seen in the brain lobes only, while in other cases the ventral nerve cord is abnormally extended. Homozygous embryos show markedly reduced levels of apoptosis compared to wild type. The reduction in number of apoptotic cells is most noticeable in the CNS and epidermis.