Imprecise excision of P{lacW}Dcp-1k05606 has left 40bp of P-element sequence at the insertion site leading to a frameshift in Dcp-1 and an in-frame stop codon within the 40-bp insertion.
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.
The arista of Dcp-1Prev1 flies appears wild type.
Dcp-1Prev1 pupal eyes appear wild type.
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.
Dcp-1Prev1 has abnormal cell death phenotype, enhanceable by DroncI29
Dcp-1Prev1 has decreased cell death phenotype, non-suppressible by DriceΔ1
Dcp-1Prev1 is an enhancer of abnormal cell death phenotype of DroncI29
Dcp-1[+]/Dcp-1Prev1 is an enhancer of lethal | pupal stage phenotype of DriceΔ1
Dcp-1Prev1 is an enhancer of abnormal developmental rate | pupal stage phenotype of DriceΔ1
Dcp-1Prev1 is an enhancer of decreased cell death | embryonic stage phenotype of Drice17
Dcp-1Prev1/Dcp-1Prev1 is a suppressor of increased cell death | oogenesis phenotype of DyroΔ6
DriceΔ1, Dcp-1[+], Dcp-1Prev1 is a suppressor of increased cell death phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev
Dcp-1Prev1 is a suppressor of abnormal neuroanatomy phenotype of Ank2f02001
Dcp-1[+]/Dcp-1Prev1 is a suppressor | partially of abnormal neuroanatomy phenotype of Ank2f02001
Dcp-1Prev1 is a non-suppressor of decreased cell death phenotype of DriceΔ1
Dcp-1Prev1 is a non-suppressor of partially lethal - majority die | larval stage phenotype of DriceΔ1
Dcp-1Prev1/Dcp-1Prev1 is a non-suppressor of visible phenotype of hidGMR.PG
Dcp-1Prev1, DriceΔ1 has increased cell death | recessive | P-stage phenotype
Dcp-1Prev1, Drice17 has abnormal cell death | P-stage phenotype
Dcp-1Prev1, DriceΔ1 has lethal | pharate adult stage phenotype
Dcp-1Prev1, DriceΔ1 has abnormal developmental rate | pupal stage phenotype
Dcp-1Prev1, Drice17 has abnormal cell death | germline clone phenotype
Dcp-1Prev1 has neuron phenotype, enhanceable by DroncI29
Dcp-1Prev1 has egg chamber | nutrition conditional phenotype, suppressible by sesBorg
Dcp-1Prev1 is an enhancer of neuron phenotype of DroncI29
Dcp-1[+]/Dcp-1Prev1 is an enhancer of arista phenotype of DriceΔ1
Dcp-1[+]/Dcp-1Prev1 is an enhancer of male genitalia phenotype of DriceΔ1
Dcp-1Prev1/Dcp-1Prev1 is a suppressor | partially of ovary phenotype of DyroΔ6
Dcp-1Prev1/Dcp-1Prev1 is a suppressor | partially of egg chamber | absent phenotype of DyroΔ6
DriceΔ1, Dcp-1[+], Dcp-1Prev1 is a suppressor of eye phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev
Dcp-1[+]/Dcp-1Prev1 is a suppressor | partially of embryonic/larval neuromuscular junction phenotype of Ank2f02001
Dcp-1Prev1 is a suppressor of embryonic/larval neuromuscular junction phenotype of Ank2f02001
Dcp-1Prev1/Dcp-1Prev1 is a non-suppressor of egg | absent phenotype of DyroΔ6
Dcp-1Prev1 is a non-suppressor of wing disc phenotype of DriceΔ1
Dcp-1Prev1/Dcp-1Prev1 is a non-suppressor of eye phenotype of hidGMR.PG
Dcp-1Prev1, DriceΔ1 has adult optic lobe | P-stage phenotype
Dcp-1Prev1, Drice17 has adult optic lobe | P-stage phenotype
Dcp-1Prev1, sesBorg has nurse cell phenotype
Dcp-1Prev1, DriceΔ1 has neuron phenotype
Dcp-1Prev1, Drice17 has egg chamber | germline clone phenotype
In DriceΔ1 and Dcp-1Prev1 double mutants, the number of apoptotic cells throughout the optic lobe is greatly reduced, though a few apoptotic cells are detectable in the some regions at 48h, when in wild type there are no apoptotic cells in these regions.
In Drice17 and Dcp-1Prev1 double mutants, the number of apoptotic cells is reduced compared to wild type between 0-24h APF, and is slightly increased between 48-72h APF.
Degenerating midstage egg chambers from nutrient-deprived sesBorg/+; Dcp-1Prev1/Dcp-1Prev1 flies contain persisting nurse cell nuclei and an accumulation of ref(2)P protein.
Ovarioles from fed sesBorg/sesBorg; Dcp-1Prev1/Dcp-1Prev1 flies arrested during mid-oogenesis, and these midstage egg chambers contain condensed and fragmented nurse cell nuclei and reduced ref(2)P levels.
Dcp-1Prev1; IceΔ1 double mutants exhibit a block on cell death after irradiation.
A Dcp-1Prev1; IceΔ1 double mutant background fails to abolish the ability of Icefl.5'3'UTR mutants to induce cell death, although induction is at a reduced rate compared to in a IceΔ1 single mutant background.
Homozygous Dcp-1Prev1 suppresses the NMJ degeneration seen in Ank2f02001 mutants. One copy of Dcp-1Prev1 is also able to partially suppress the phenotype.
Dcp-1Prev1; NcI29 double mutants exhibit an arrest of vCrz programmed cell death with all 16 vCrz neurons retained at 7 and 16 hours after puparium formation, compared to apoptosis of these neurons in wild-type controls.
Dcp-1Prev1 ; NcI24/NcI29 IceΔ1 triple mutant larvae undergo cell death with morphology similar to the midgut of wild-type animals when analysed from -4 to -1 hours relative to puparium formation.
Females containing Dcp-1Prev1 Ice17 double mutant germline clones have persisting nurse cell nuclei in 21% of stage 14 egg chambers.
Developmental apoptosis in the eye disc is completely absent in Dcp-1Prev1 ; IceΔ2C8 double homozygous third instar larvae.
The reduction in adult eye size caused by expression of WGMR.PG is not suppressed if the eye is made homozygous for Dcp-1Prev1 (using the eyFLP method).
The lethality of IceΔ1 is enhanced by Dcp-1Prev1 : less than 1% of Dcp-1Prev1/+, IceΔ1/IceΔ1 animals eclose and Dcp-1Prev1/Dcp-1Prev1; IceΔ1/IceΔ1 animals die prior to, or during, early pupal stages. Almost all Dcp-1Prev1/Dcp-1Prev1; IceΔ1/IceΔ1 pupae arrest development prior to head inversion.
Dcp-1Prev1/+, IceΔ1 flies show an increased number of lateral branches on the arista compared to IceΔ1 single mutant flies. Additionally, the genitalia misrotation phenotype of IceΔ1 flies is increased to full penetrance in Dcp-1Prev1/+, IceΔ1 flies.
Ice17 Dcp-1Prev1 double mutant embryos derived from mutant female germline clones (so lacking maternal and zygotic function of Ice and Dcp-1 show significantly reduced levels of apoptosis compared to Ice17 single maternal and zygotic mutant embryos, containing only a few dying cells.
A Dcp-1Prev1/+; IceΔ1/IceΔ1 background strongly suppresses the adult eye size defect found upon expression of Mmus\Gria1Lc.Scer\UAS under the control of Scer\GAL4hs.2sev.
Dcp-1Prev1 is rescued by Scer\GAL4VP16.nanos.UTR/Dcp-1ΔN.UASp
Dcp-1Prev1 is rescued by Dcp-1t4.4
A Dcp-1Prev1 heterozygous or homozygous background abolishes the ability of Dcp-1Ice.5'3'UTR mutants to induce cell death.
The presence of egg chambers lacking follicle cells in nutrient deprived Dcp-1Prev1 homozygotes is prevented by Dcp-1t4.4.
rawdcp-1 has been identified as a second-site mutation on the Dcp-1Prev1 chromosome.