mutant eye clones exhibit extra ommatidial pigment cells in the pupal retina.
transheterozygotes exhibit a delay in vCrz neuron apoptosis. At 7 hours after puparium formation 75% vCrz neurons are still present although these all die by 48 hours after puparium formation.
mosaic wings retain Disc\RFPhs.DsRedT4.T:nls5
-positive wing epithelial cells 4-11 days after eclosion, whereas control epithelial cells undergo apoptosis moments after eclosion.
Wing blemishes are not seen in Nc51
Programmed cell death inCrz
-expressing neurons in the ventral nerve cord is significantly delayed in Nc51
mutants. Approximately 12 neurons still survive at 7 hours after pupal formation, while the number is reduced to approximately 8 at 16 hours after pupal formation, and none at 48 hours after pupal formation.
mutants exhibit a delay in programmed cell death in Crz
-expressing neurons in the ventral nerve cord during pupation.
Dendrites of Nc51
mutant C4da neuron clones appear normal at larval stages. However, unlike wild-type, these neurons fail to properly prune their larval dendrites during metamorphosis and most display relatively intact primary and secondary larval dendritic arbors at 18 hours after puparium formation.
mutant third instar larvae have melanotic nodules found in the hemocoel or in association with He
-positive lymph glands. They also show gut melanisation not accompanied by tissue overgrowth or hemocyte encapsulation.
homozygous embryos hatch at the normal time, but the larvae develop more slowly than wild-type. These larvae fail to pupariate, but continue to grow for some time after controls pupariate. The resulting giant larvae die at 10-12 days after wild-type larvae pupariate. Unlike wild-type larvae, these larvae are not induced to pupariate early by feeding with ecdysone at the mid-third instar.
homozygous larvae fail to exhibit cell death in the larval midgut ,as wild-type larvae do, at end of the third larval instar (assayed by Tunel staining) or in response to feeding with ecdysone at mid-third instar (assayed by acridine orange staining).
homozygous embryos display head involution defects. Post-embryonic growth of these animals is slower than in wild-type and both larval moults and pupation are delayed. However, once they do reach the wandering late third instar larval stage, these larvae are generally bigger wild-type counterparts and have larger and sometimes deformed discs and brain. They also exhibit hyperplasia of the blood cells. These animals die during early pupal stages, sometimes with visible melanotic tumors.
homozygous embryos laid by NcKG02994
mothers do not hatch and have more severe head involution defects than Nc51
homozygotes laid by wild-type mothers. These have embryos decreased levels of cell death, as assayed by tunel staining, in the epidermis at stage 12 and the ventral nerve cord at stage 15/16. Consistent with a reduction in cell death, increases in cell number are see in multiple cases: Extra cells are associated with Bolwig's organ at stage 15 and extra cells are present in the ventral nerve cord at late embryonic stages
adults have a higher frequency of post-alar bristle duplication than NcKG02994
Adult eyes completely populated by Nc51
homozygous somatic clone cells are normal sized but rough. This is not due to supernumerary photoreceptor cells, however, ommatidial pre-clusters are irregularly spaced immediately posterior to the furrow in late third instar eye discs of this genotype.
No obvious defects are present in the wings of newly eclosed flies carrying Nc51
homozygous clones. But, the wings of these flies develop melanized blotches as they age.
Cultured hemocytes isolated from third instar Nc51
homozygous larvae are much less sensitive to induction of apoptosis by a variety of pro-apoptotic agents (cycloheximide, Actinomycin D, etoposide (Topoisomerase II inhibitor), ethanol, and smac mimetic) than wild-type controls. In addition, levels of constitutive apoptosis in these cells are significantly lower than controls.