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General Information
Symbol
Dmel\rprUAS.cZa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Zhou
FlyBase ID
FBal0060907
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-rpr, UAS-reaper, P[UAS-reaper]
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference
UASt regulatory sequences drive expression of a rpr cDNA.
Allele components
Product class / Tool use(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
Expression of rprScer\UAS.cZa under the control of Scer\GAL4Myo31DF-NP0001 (combined with tub-Gal80[ts] for added temporal control) induces apoptosis but also leads to increased number of proliferating (EdU+) cells in the posterior midgut epithelium.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4ptc-559.1 is lethal, but are viable when Scer\GAL80αTub84B.PL is expressed in early development. Robust cell death is seen in the wing disc 12 hours after Scer\GAL4 de-repression. When larvae expressing rprScer\UAS.cZa under the control of Scer\GAL4ptc-559.1 are irradiated, less cell death is seen in the wing disc in comparison with irradiated controls. The cells in the A compartment are the first to benefit, but the protective effect is able to reach the P compartment.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4GMR.PF results in almost complete loss of ommatidia in the eye at 29[o]C. Only 20% of flies are able to eclose. Less severe phenotypes are seen at 24[o]C, with 56% of flies able to eclose. At 18[o]C only 0.5% of flies eclose.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4Gp150-52A induces a low level of cell death in embryonic CNS midline cells.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4btl.PU causes frequent gaps in the dorsal trunk. No loss of the salivary ducts is seen.
Expression of rprScer\UAS.cZa in the developing eye under the control of Scer\GAL4GMR.PF induces a small eye phenotype. Down-regulation of endogenous th protein through ectopic expression of rprScer\UAS.cZa in all four cells of the adult sensory organ, under the control of Scer\GAL4sca-109-68 results in the loss of bristles on the adult notum, indicating a defect in only the shaft cell. In SOP lineages that express rprScer\UAS.cZa, the SOP divdes four times, as in wild-type, makes the same five cell types and shows the same developmental time-course, beginning 16 hours after puparium formation.
Ectopic expression of rprScer\UAS.cZa, under the control of Scer\GAL4ninaE.PT induces a progressive loss of outer photoreceptor cells that can be visualised in tangential plastic retina sections of 2-day old flies.
Expression of rprScer\UAS.cZa using Scer\GAL4Gr66a.PD abolishes the L-canavanine-induced proboscis retraction seen in wild type flies.
The eclosion of flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 under photoperiod conditions lacks the prominent lights-on response seen in wild-type flies. Unlike in controls, advancing the lights on signal by one or two hours does not swell the leading edge of the eclosion distribution.
Stage 16 embryos expressing rprScer\UAS.cZa under the control of Scer\GAL4gcm-rA87.C show a strong reduction in the number of glial cells. The brain neuropile is distorted and is not compartmentalised in the mutant embryos (in wild type the neuropile is subdivided by glial septa into distinct compartments). The glial sheath that is normally formed by surface glia around the brain is missing in the mutant embryos. Late stage embryos expressing rprScer\UAS.cZa under the control of Scer\GAL4gcm-rA87.C show abnormalities in movement; peristaltic waves are absent and the embryos show incessant movement which consists of uncoordinated contractions of individual segments. The amplitude of the contractions is reduced compared to controls. Animals expressing rprScer\UAS.cZa under the control of Scer\GAL4nrv2.PS and raised at 18[o]C mostly develop to late larval stages. In these larvae, most glial cells are still present in the first instar, but glial cell death occurs during the second instar. Late larvae show severe behavioural defects, which are characterised by strongly reduced peristaltic movement and feeding and a constant "tremor" of the pharyngeal and body wall musculature.
Males expressing rprScer\UAS.cZa under the control of Scer\GAL4IFa.PT show no difference in male-female courtship behaviour compared to control males when naive males are allowed to court virgin wild-type females. However, the mutant males show significant male-male courtship behaviour when naive males are allowed to court males.
Flies that express rprScer\UAS.cZa under the control of Scer\GAL4Fmrf.PS show ablation of Tv neurons. These flies complete pupal ecdysis but show weaker pre-ecdysis contractions than controls. Flies that express rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 show ablation of VM neurons. These flies complete pupal ecdysis without severe defects or lethality but ecdysis is delayed by around 4 minutes, resulting in a longer period of pre-ecdysis. Expression of rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP results in ablation of the 27/704 neurons. These flies fail to initiate ecdysis contractions and cannot complete head eversion. Instead, they show prolonged pre-ecdysis contractions for about 25 minutes, followed by weak random contractions of the abdomen for the next 50 minutes.
Males in which most npf-expressing cells have been ablated (by expression of rprScer\UAS.cZa under the control of Scer\GAL4nf.1) display subnormal courtship activity toward virgin females, partly because of prolonged courtship initiation latency before commencement of active courtship. Males in which most npf-expressing cells have been ablated (by expression of rprScer\UAS.cZa under the control of Scer\GAL4nf.1) show subtle but consistently subnormal 'evening anticipation' (ie, the gradual increase in locomotor activity before the light-to-dark transition): after the quiescent midday period, activity levels are elevated slightly earlier compared to controls.
Expression of rprScer\UAS.cZa in pacemaker neurons under the control of Scer\GAL4P2.4.Pdf results in varying degrees of ablation of the normal compliment of eight PDF neurons per larval brain. However, this does not affect the larval response to light. Ablation of PDF neurons through expression of rprScer\UAS.cZa under the control of Scer\GAL4tim.Scer\UAS does not affect the larval response to light.
Severe lethality is seen when rprScer\UAS.cZa is expressed using Scer\GAL4GMR.PU, presumably due to leaky Scer\GAL4 expression. Animals also show a small-eye phenotype. Expression of rprScer\UAS.cZa using Scer\GAL4Rh3.PP does not cause any lethality. However, R7 photoreceptor neurons are absent in some ommatidia, and this phenotype worsens significantly with age.
Expression of rprScer\UAS.cZa, under the control of Scer\GAL4P2.4.Pdf, causes ablation of the LNv. This has no apparent effect on 5-HT arborization. Further, ablation of the LNv and Rh5 photoreceptors, by expression of rprScer\UAS.cZa driven by both Scer\GAL4P2.4.Pdf and Scer\GAL4Rh5.PT, does not affect 5-HT arborization.
Larvae that express rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 show ablation of the EH neurons. Only 31% of these larvae survive from first to third larval instar. The majority of dead larvae have fluid-filled trachea. Most Scer\GAL4Eh.2.4>rprScer\UAS.cZa larvae show similar ecdysis timings to wild-type larvae. However, Scer\GAL4Eh.2.4>rprScer\UAS.cZa larvae can occasionally show unusually light mouthpart pigmentation and differences in the amount of pigmentation between the two sides of the mouth plates. Larvae that express rprScer\UAS.cZa under the control of both Scer\GAL4Eh.2.4 and Scer\GAL4Ccap.PP show ablation of both the EH and CCAP neurons. These larvae also show a "buttoned-up" phenotype in which the mouthparts of the second instar are not shed and are present anterior to those of the third instar. The onset of pre-ecdysis is significantly delayed in these larvae compared to controls.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4slbo.2.6 results in apoptotic cells in stage 10 egg chambers, in contrast to wild-type egg chambers; TUNEL labeling is seen in the border cells, centripetal cells and posterior follicle cells.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL does not produce any noticeable defects in growth, metamorphosis, eclosion or longevity. Adults show normal reproductive capabilities and courtship behaviour. Hemolymph trehalose levels are reduced to 7-26% of normal levels in larvae expressing rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL, while glucose levels are unaffected. The triglyceride content of the fat body is normal. Flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL show resistance to starvation-induced death. Flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL show similar locomotor activity rhythms to wild-type flies when fed on 4% sucrose-agar medium. Under starvation conditions, most flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL do not show pronounced starvation-induced hyperactivity (which is seen in wild-type flies).
Expression of rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP results in the ablation of Ccap-expressing neurons in the larval central nervous system. Expression of rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP is not lethal during the larval stages. These animals are able to shed their old cuticle at the end of the moult to the 3rd instar. The initiation of ecdysis behaviour from the 2nd to 2rd larval instar occurs and the larvae use this behaviour to free themselves from the 2nd instar cuticle. The duration of events up to the onset of pre-ecdysis is normal, but there is a modest but significant lengthening of pre-ecdysis behaviour (although the pre-ecdysis behaviour itself is normal). The biting period, which occurs between the end of pre-ecdysis and ecdysis onset, and the duration of ecdysis itself, are significantly extended compared to wild type. The larvae show anterior to posterior peristaltic waves interspersed with the typically occurring posterior to anterior waves, which is never seen in wild-type animals. The waves moving in the anterior to posterior direction do not aid in breaking the old cuticle, so the time to successful shedding of the old cuticle is lengthened. Most animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP die during the pupal stage. Early pupal stage animals show defects such as incomplete head eversion, retracted posterior cuticle due to failure to transition from pre-ecdysis to ecdysis and incomplete shedding of tracheal lining. Pharate adults have defects in adult head formation and in leg and wing extension. Animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP initiate normal pre-ecdysis behaviour before pupal ecdysis, however, this behaviour lasts significantly longer than in controls and is not followed by head eversion. Instead, abdominal pre-ecdysis movements eventually cease and are followed by a period that resembles the postecdysis period seen in controls. About 10% of animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP form relatively normal heads at the end of metamorphosis, and these animals are usually able to exit from the pupal case. The developmental and behavioural events that normally occur at eclosion do occur in these animals, although there are differences in the duration or number of events compared to wild type. For example, tracheal filling takes longer than normal, while the ptilinum is deployed normally. The bouts of rapid anteriorly directed peristalses of ecdysis proper occur in these animals, but they are relatively ineffective at propelling the animal forward, because the abdomen is not distended by this time. Although most of these animals eventually succeed in eclosing, it takes much longer than normal. The eclosion profile of animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP is different from that of control animals; the temporal gate of eclosion is lengthened, with significant emergence occurring in the late night/predawn period. There is also a significant diminution in the amplitude of the eclosion burst that occurs immediately following lights-on. There is no consistent difference in the peak time of eclosion between animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Ccap.PP and control animals in light-dark or constant darkness conditions.
Most flies expressing rprScer\UAS.cZa under the control of Scer\GAL4GMR.PF die shortly after pupariation. Flies expressing rprScer\UAS.cZa under the control of Scer\GAL4rdgC.PK survive well to adulthood and show no defects in walking behaviour.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4Gp150-52A in embryos in the central nervous system midline does not induce ectopic cell death.
Flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 show a similar rise in heart rate during the last 10 hours of adult development (before eclosion) as seen in wild-type flies, differing significantly only during the smooth/grainy stage and grainy stage. Flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 fail to fill their tracheoles completely with air at any stage during the last 2.9 hours of development before eclosion, in contrast to wild type which have air filled tracheoles by 0.9 hours before eclosion. In contrast to wild-type flies, injection of M.sexta ecdysis-triggering hormone (ETH) is ineffective in inducing premature tracheal filling around the ventral CNS or in the tracheal sacs overlying the brain in flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4. Injection of M.sexta ETH into these flies at the grainy stage also has no effect on the heart rate, in contrast to wild-type flies. Very few flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 attempt to ecdyse after neck ligation and there is no stage dependent pattern to these ecdyses (this response differs from wild-type flies).
The locomotor activity of flies expressing rprScer\UAS.cZa under the control of Scer\GAL4P2.4.Pdf is not entirely normal. The flies are entrained during 12 hour light:12 hour dark (LD) cycles, but the evening locomotor phase is advanced by at least 0.5 hours compared to wild-type flies. 63% of flies are rhythmic for the entire duration of a 9 day period under constant darkness. The proportion of rhythmic individuals decreases over time under constant darkness. Flies that are persistently rhythmic tend to have short periods.
Expression of rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 results in semilethality, with most animals dying during the larval period, crawling out of the food before dying. Most of the larvae have tracheal abnormalities; 80% have dorsal tracheae filled with fluid. Old tracheae are seen inside new ones. Eh expressing neurons die during the first or second larval stages in animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4. The neurons appear to disintegrate progressively. 30%-34% of animals expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4 eclose as fertile, viable adults. Defects are seen during pre-eclosion, when the timing of inflation of the trachea relative to ptilinum extension is altered compared to wild-type (tracheal inflation is delayed in approximately a third of cases). There is also a dramatic increase in the latency from ptilinum extension to adult emergence. The organisation of eclosion behaviour into bouts that is seen in wild-type flies is absent in flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Eh.2.4. These flies display the four characteristic eclosion behaviours (head expansion, head thrusts, thoracic contractions and abdominal contractions), but once these behaviours begin they are performed almost continuously without periods of quiescence. The behaviours also seem weaker than in wild-type flies. The flies fail to undergo normal postemergence expansion and hardening of the adult cuticle after they have eclosed, and more than two-thirds of flies fail to undergo wing expansion. The eclosion of the flies under photoperiod conditions lacks the prominent lights-on response seen in wild-type flies, although the flies show a robust free-running eclosion rhythm under constant darkness.
Scer\GAL4Gp150-52A-mediated expression of rprScer\UAS.cZa alone is not sufficient to induce substantial apoptosis in the embryonic CNS midline cells. The midline cells survive and are capable of carrying out normal axon guidance functions (axon scaffold organisation is normal).
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Statement
Reference
Suppressor of
Other
Statement
Reference
Scer\GAL4nrv2.PS, hidUAS.cZa, rprUAS.cZa has lethal | temperature conditional phenotype
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Suppressor of
Other
Statement
Reference
Scer\GAL4nrv2.PS, hidUAS.cZa, rprUAS.cZa has glial cell | temperature conditional phenotype
Additional Comments
Genetic Interactions
Statement
Reference
Co-expression of WScer\UAS.cZa and rprScer\UAS.cZa under the control of Scer\GAL4ptc-559.1 is lethal, but is viable when Scer\GAL80αTub84B.PL is expressed until the third instar larval stage. Robust cell death is seen in the wing disc 12 hours after Scer\GAL4 de-repression. When larvae expressing WScer\UAS.cZa and rprScer\UAS.cZa under the control of Scer\GAL4ptc-559.1 are irradiated (and expression is repressed until 12 hours prior to irradiation using Scer\GAL80αTub84B.PL), less cell death is seen in the wing disc in comparison with irradiated controls. A heterozygous Df(3L)banΔ1 background has no effect on the amount of cell death, but when de-repression occurs 6 hours prior to irradiation (which results in a less dramatic reduction in cell death compared to 12 hours), heterozygous Df(3L)banΔ1 partially suppresses the level of protection seen when WScer\UAS.cZa and rprScer\UAS.cZa are expressed alone. When wing discs containing WScer\UAS.cZa and rprScer\UAS.cZa expressing clones (repressed during early development using Scer\GAL80αTub84B.PL)) are irradiated, less cell death is seen outside of the clones in comparison with irradiated controls.
Expression of thScer\UAS.T:Hsap\MYC.cBa almost completely restores the eye phenotypes seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4GMR.PF at 29[o]C. Eye size is 98% of control and no roughness or other morphological abnormalities are observed. The loss of viability seen in flies expressing rprScer\UAS.cZa is rescued upon co-expression of thScer\UAS.T:Hsap\MYC.cBa.
Expression of morgueScer\UAS.cZa enhances the embryonic CNS midline cell death phenotype seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4Gp150-52A. Expression of morgueG421A.Scer\UAS enhances the embryonic CNS midline cell death phenotype seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4Gp150-52A. Expression of morgueG421C.Scer\UAS enhances the embryonic CNS midline cell death phenotype seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4Gp150-52A. Expression of morgueG421S.Scer\UAS enhances the embryonic CNS midline cell death phenotype seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4Gp150-52A.
Co-expression of WScer\UAS.cZa and rprScer\UAS.cZa in the posterior signalling center under the control of Scer\GAL4Antp-10 has no effect on lamellocyte differentiation.
Expression of thScer\UAS.T:Zzzz\FLAG or thScer\UAS.T:Avic\GFP-YFP.Venus in the developing eye under the control of Scer\GAL4GMR.PF suppresses the rprScer\UAS.cZa-induced 'small-eye' phenotype. Expression of thN117K.H283Y.Scer\UAS.T:Avic\GFP-YFP.Venus in the developing eye under the control of Scer\GAL4GMR.PF fails to suppress the 'small-eye' phenotype found in rprScer\UAS.cZa; Scer\GAL4GMR.PF flies.
Loss of one genomic copy of ninaA, using the amorphic allele ninaAE110V, protects the outer photoreceptor cells from rprScer\UAS.cZa-induced apoptosis. This anti-apoptotic effect is dose-dependent, as complete loss of ninaA leads to further protection.
Co-expression of WScer\UAS.cZa, grimScer\UAS.cOCa and rprScer\UAS.cZa under the control of Scer\GAL4ple.PF results in the volume of DA neurites being significantly diminished compared to controls.
Scer\GAL4Hml.PG-, Scer\GAL4Pxn.PS- or Scer\GAL4srp.D.cCa-mediated expression of rprScer\UAS.cZa and WScer\UAS.cZa ablates larval hemocytes. Scer\GAL4srp.D.cCa-mediated expression of rprScer\UAS.cZa and WScer\UAS.cZa leads to a high lethality rate during early larval development - these larvae are devoid of hemocytes and rarely reach the third instar larval stage.
Expression of both rprScer\UAS.cZa and WScer\UAS.cZa in the cortex and neuropile glia from late embryonic stage onwards, under the control of Scer\GAL4nrv2.PS at 18[o]C and switching to a high temperature (25[o]C) shortly after hatching allows most animals to develop to late larval stages. In these larvae, glial cell death sets in around hatching and is more or less complete by the early 2nd instar. These larval brains exhibit a greatly increased number of intra-neuropilar tracheal branches. Six or more secondary branches split off the perineuropilar plexus at variable positions and penetrate the neuropile. Larvae lacking cortex and neuropile glia (but retaining surface glia) show severe behavioural deficits, characterised by reduced peristaltic movement and feeding, and a constant 'tremor' of the pharyngeal and body wall musculature.
Males co-expressing rprScer\UAS.cZa and WScer\UAS.cZa under the control of Scer\GAL4IFa.PT show no difference in male-female courtship behaviour compared to control males when naive males are allowed to court virgin wild-type females. However, the mutant males show significant male-male courtship behaviour when naive males are allowed to court males. Females co-expressing rprScer\UAS.cZa and WScer\UAS.cZa under the control of Scer\GAL4IFa.PT copulate more rapidly with male flies than control females.
Animals co-expressing rprScer\UAS.cZa and WScer\UAS.cZa under the control of Scer\GAL4P2.4.Pdf are arrhythmic for locomotor activity under constant light conditions at a constant temperature of 25[o]C, but become rhythmic almost immediately after being exposed to a temperature cycle of 12 hours at 25[o]C and 12 hours at 30[o]C. There is a peak at the beginning of the cryophase and a smaller peak at the early thermophase. The flies show a dispersed anticipatory activity starting around the middle of the thermophase, although transient cycles are not clear.
Co-expression of BacA\p35Scer\UAS.cHa partially restores hemolymph trehalose levels in larvae expressing rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL. Co-expression of BacA\p35Scer\UAS.cHa partially reduces the resistance to starvation-induced death seen in flies expressing rprScer\UAS.cZa under the control of Scer\GAL4Akh.PL.
The electroantennogram (EAG) rhythm in response to ethyl acetate (measured on the second day of constant darkness conditions) in flies co-expressing rprScer\UAS.cZa and WScer\UAS.cZa under the control of Scer\GAL4P2.4.Pdf is similar to that of wild-type flies.
Third instar larvae co-expressing both rprScer\UAS.cZa and WScer\UAS.cZa under the control of Scer\GAL41118 have no obvious defects in the Bolwig's nerve axonal projections although the lateral neurons are completely missing.
Co-expression of BacA\p35Scer\UAS.cHa completely blocks cell death caused by expression of rprScer\UAS.cZa under the control of Scer\GAL4en-e16E. Animals expressing both BacA\p35Scer\UAS.cHa and rprScer\UAS.cZa under the control of Scer\GAL4en-e16E survive to adulthood with largely normal wings.
Co-expression of rprScer\UAS.cZa and morgueEP2367 under the control of Scer\GAL4Gp150-52A in embryos in the central nervous system midline results in a dramatic loss of midline glia and neurons.
Co-expression of WScer\UAS.cZa and rprScer\UAS.cZa (when driven by Scer\GAL4Gp150-52A) results in ectopic midline cell death. The addition of thScer\UAS.T:Ivir\HA1 suppresses this phenotype, sometimes to wild-type.
The locomotor activity defects of flies expressing rprScer\UAS.cZa under the control of Scer\GAL4P2.4.Pdf are partially suppressed by coexpression of BacA\p35Scer\UAS.cHa.
When grimScer\UAS.cNa and rprScer\UAS.cZa are coexpressed, all the midline glia and some VUM neurons are eliminated. When grimScer\UAS.cNa and WScer\UAS.cZa are coexpressed, all the midline glia and VUM neurons are eliminated.
Mediated expression of both rprScer\UAS.cZa and WScer\UAS.cZa causes a striking loss of glial cells, significant defects in axon guidance scaffold are detected. VUM neurons exhibit greatly reduced sensitivity: cells are normal in position, number and morphology. Two copies of each construct completely eliminates all midline glia and dramatic loss of VUM neurons. Results indicate all midline glia are capable of undergoing cell death and suggests the midline neurons and glia may have different sensitivities to rpr and W expression. Simultaneous expression of BacA\p35Scer\UAS.cHa causes no ectopic cell death demonstrating that midline cell death induced by rpr and W require the functions or one or more caspases.
Xenogenetic Interactions
Statement
Reference
Expression of BacA\p35Scer\UAS.P\T.cBa rescues the eye phenotypes seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4GMR.PF at 24[o]C. In females, eye size is increased compared to wild type (but is still small compared to the expression of BacA\p35Scer\UAS.P\T.cBa alone), whereas in males the eye size seen is comparable to that seen in wild type. Expression of BacA\p35Scer\UAS.P\T.cBa eliminates eye roughness in both males and females. Expression of Zzzz\E4orf4Scer\UAS.cPa partially suppresses the semi-lethality seen when rprScer\UAS.cZa is expressed under the control of Scer\GAL4GMR.PF at 18[o]C. 27.4% of pupae eclose (compared to 0.5%). The reduction in eye size is also partially suppressed.
Co-expression of BacA\p35Scer\UAS.cHa suppresses the male-male courtship seen in males expressing rprScer\UAS.cZa under the control of Scer\GAL4IFa.PT.
Coexpression of BacA\p35Scer\UAS.cHa rescues the loss of R7 neurons caused by Scer\GAL4Rh3.PP-mediated expression of rprScer\UAS.cZa.
Co-expression of rprScer\UAS.cZa with BacA\p35Scer\UAS.cHa (both under the control of Scer\GAL4unspecified) in wgl-17 wing disc clones results in most or all of the cells in the clone being `undead'. None of these clones are associated with large, neoplastic outgrowths, and they grow slowly, forming abnormally small clones.
rprScer\UAS.cZa; BacA\p35Scer\UAS.cHa; Scer\GAL4αTub84B.PZ somatic clones in the wing disc cause significant overgrowth of this disc. This overgrowth in suppressed by pucScer\UAS.cMa.
Complementation and Rescue Data
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Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
rprScer\UAS.cZa
rprUAS.cMa
rprUAS.cZa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Zhou
Secondary FlyBase IDs
  • FBal0082291
References (68)