Both Dcp-1Prev1 homozygotes (in a cleaned-up background by recombination) and Dcp-1k05606/Dcp-1Prev1 transheterozygotes do not show protection against (injury-induced) Wallerian degeneration in third instar larval motoneurons.
Dcp-1Prev1 homozygotes do not exhibit a significant proportion of hyperplastic testes, as compared to controls.
In Dcp-1Prev1 mutant optic lobes, the peak number of apoptotic cells is unchanged as compared to wild-type, at 24h APF, but the decrease of number of apoptotic cells following the peak is slower. By 72h APF, however, the number of apoptotic cells is similar to wild-type. The spatial distribution of apoptotic cells is very similar to wild type between 0-36h APF, but there were apoptotic cells in some regions of the optic lobe at 48h that do not have apoptotic cells in wild type. Cell corpse clearance is normal between 0-24h APF and in late pupal stages, but is reduced throughout the optic lobe in areas of cell death at 36h APF.
After amino acid deprivation, degenerating midstage egg chambers from Dcp-1Prev1 flies contain a reduction in the percentage of autolysosomes compared with controls. Non-degenerating midstage egg chambers from starved Dcp-1Prev1 flies also display reduced autophagic flux.
Fed Dcp-1Prev1 flies expressing Avic\GFPE.Scer\UAS.P\T.T:Hsap\Mito-COX8A in the germline contain mitochondria with an altered morphology even in the absence of starvation. Approximately 54% of midstage egg chambers from Dcp-1Prev1 flies contain mitochondria that are elongated and overly connected, whereas only 39% of midstage egg chambers contain mitochondria that are healthy.
ATP levels are significantly increased in ovaries from Dcp-1Prev1 flies subjected to starvation conditions.
As in wild type, no bursCCAP neuron somata are seen in the ventral nerve cord of Dcp-1Prev1 mutant flies at 3-5 days post-eclosion. However the usual post-eclosion cell death is slightly delayed. Some neurites are still present at 3-5 days.
Dcp-1Prev1 mutant flies exhibit slightly increased levels of spermatogonial cyst death compared to controls.
Engulfment of nurse cells by follicle cells is largely inhibited in homozygous Dcp-1Prev1 mutant starvation-induced degenerating egg chambers. Most follicle cells fail to enlarge and display thinning out of the membranes.
Dcp-1Prev1 mutants display a significant delay of ~1hr in the rate of cell death, reaching the wild-type plateau level 4hrs after irradiation.
Dcp-1Prev1 mutants do not exhibit a difference in survival rate compared to wild-type controls.
Homozygous Dcp-1Prev1 mutants are viable and do not display any defects in NMJ integrity or growth.
Dcp-1Prev1 mutants exhibit an average of 9 vCrz somata at 7 hours after puparium formation, with no vCrz somata at 16 hours after puparium formation. The general morphology of vCrz neurons at 7 hours after puparium formation was comparable to those of wild-type at 4-5 hours after puparium formation, indicating that programmed cell death has been slowed down in the absence of Dcp-1 function.
Dcp-1Prev1 mutants exhibit a mild reduction in dendritic branch pruning at 18 hours after puparium formation.
Nutrient-deprived Dcp-1Prev1 mutant flies display reduced levels of autophagy (punctate Lysotracker staining) in region two of the germarium and in stage eight degenerating egg chambers compared to controls.
Fewer apoptotic (TUNEL positive) cells are seen in region two cysts in nutrient-deprived Dcp-1Prev1 mutant flies than are seen in wild type.
Developmental apoptosis is significantly reduced in homozygous third instar eye discs.
γ-ray induced apoptosis is not suppressed in homozygous third instar wing discs.
Dcp-1Prev1 homozygotes are viable and fertile. The ovaries of these flies are largely normal, but have occasional egg chambers lacking follicle cells. This phenotype is exacerbated by nutrient deprivation to a much greater degree than in wild-type. Degeneration of egg chambers correlates with ectopic expression of cell-death markers.