Allele Dmel\rpr^Scer\UAS.cZa

General Information
Symbol	Dmel\rpr^Scer\UAS.cZa	Species	D. melanogaster
Name	Saccharomyces cerevisiae UAS construct a of Zhou	FlyBase ID	FBal0060907
Feature type	allele	Associated gene	Dmel\rpr

Allele class
Mutagen	in vitro construct - regulatory fusion
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	in vitro construct - regulatory fusion (Zhou et al., 1997, McNabb et al., 1997, Chen et al., 1998)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Construct: A 0.9kb EcoRI fragment containing rpr cDNA is expressed under the control of Scer\UAS regulatory sequences. (McNabb et al., 1997) rpr cDNA cloned into pUAST. (Zhou et al., 1997)
Carried in construct	P{UAS-rpr.Z} (Clark et al., 2004, Keller et al., 2002, Rodriguez Moncalvo and Campos, 2005, Renn et al., 1999, Park et al., 2003, Robertson et al., 2003, Malpel et al., 2002, Mendes et al., 2009, Geisbrecht and Montell, 2004, Dewey et al., 2004, Wing et al., 2002, Lee and Park, 2004, Ryoo et al., 2002, Mergliano and Minden, 2003, Tanoue et al., 2004, Myat and Andrew, 2000, Baker et al., 1999, Wing et al., 1998, McNabb et al., 1997, Wing et al., 2001, Chen et al., 1998, Zhou et al., 1997, Kim et al., 2006, Wells et al., 2006, Lee et al., 2006, Ryoo et al., 2004, Perez-Garijo et al., 2005, Brun et al., 2006, Pereanu et al., 2007, Kanuka et al., 2005, Palgi et al., 2009, Picot et al., 2009, Mitri et al., 2009, Kuraishi et al., 2009, Morris et al., 2006, Koto et al., 2009, Hassan et al., 2005, Choi et al., 2008, Yoshii et al., 2005, Pereanu et al., 2007, Terhzaz et al., 2007, Schroeder et al., 2003, Fishilevich et al., 2010, Blanco et al., 2010, Wang et al., 2008, Fox and Spradling, 2009, Sinenko et al., 2011, Bahn et al., 2009, Ben-Shahar et al., 2010, McNabb and Truman, 2008)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| embryonic stage, with Scer\GAL4^gcm-rA87.C (Pereanu et al., 2007) behavior defective \| larval stage, with Scer\GAL4^nrv2.PS (Pereanu et al., 2007) cell death defective, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997) courtship behavior defective \| male, with Scer\GAL4^IFa.PT (Terhzaz et al., 2007) courtship behavior defective \| male, with Scer\GAL4^npf.1 (Lee et al., 2006) eclosion rhythm defective, with Scer\GAL4^Ccap.PP (Park et al., 2003) eclosion rhythm defective, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997, McNabb and Truman, 2008) feeding behavior defective, with Scer\GAL4^Gr66a.PD (Mitri et al., 2009) fertile, with Scer\GAL4^Akh.PL (Lee and Park, 2004) increased cell death, with Scer\GAL4^Ccap.PP (Clark et al., 2004) increased cell death, with Scer\GAL4^Eh.2.4 (Clark et al., 2004) increased cell death, with Scer\GAL4^en-e16E (Ryoo et al., 2002) increased cell death, with Scer\GAL4^GMR.PF (Wing et al., 1998, Wing et al., 2001) increased cell death, with Scer\GAL4^ninaE.PT (Mendes et al., 2009) increased cell death, with Scer\GAL4^P2.4.Pdf (Rodriguez Moncalvo and Campos, 2005) increased cell death, with Scer\GAL4^P2.4.Pdf, Scer\GAL4^Rh5.PT (Rodriguez Moncalvo and Campos, 2005) increased cell death, with Scer\GAL4^salm.PU (Blanco et al., 2010) increased cell death, with Scer\GAL4^slbo.2.6 (Geisbrecht and Montell, 2004) lethal (Morris et al., 2006) lethal, with Scer\GAL4^30A (Morris et al., 2006) lethal, with Scer\GAL4³¹ (Morris et al., 2006) lethal, with Scer\GAL4^32B (Morris et al., 2006) lethal, with Scer\GAL4^34B (Morris et al., 2006) lethal, with Scer\GAL4^71B (Morris et al., 2006) lethal, with Scer\GAL4^179Y (Morris et al., 2006) lethal, with Scer\GAL4³⁷³⁵ (Morris et al., 2006) lethal, with Scer\GAL4⁴⁹³⁵ (Morris et al., 2006) lethal, with Scer\GAL4^Act5C.PI (Morris et al., 2006) lethal, with Scer\GAL4^ap-md544 (Morris et al., 2006) lethal, with Scer\GAL4^arm.PS (Morris et al., 2006) lethal, with Scer\GAL4^c323a (Morris et al., 2006) lethal, with Scer\GAL4^Cy6 (Morris et al., 2006) lethal, with Scer\GAL4^da.G32 (Morris et al., 2006) lethal, with Scer\GAL4^Dll-md23 (Morris et al., 2006) lethal, with Scer\GAL4^dpp.blk1 (Morris et al., 2006) lethal, with Scer\GAL4^en-e16E (Morris et al., 2006) lethal, with Scer\GAL4^ey.PH (Morris et al., 2006) lethal, with Scer\GAL4^GMR.PF (Wing et al., 1998, Wing et al., 2001, Morris et al., 2006) lethal, with Scer\GAL4^h-H10 (Morris et al., 2006) lethal, with Scer\GAL4^how-24B (Morris et al., 2006) lethal, with Scer\GAL4^hs.PB (Morris et al., 2006) lethal, with Scer\GAL4^nrv2.PS (Pereanu et al., 2007) lethal, with Scer\GAL4^ple.PF (Schroeder et al., 2003) lethal, with Scer\GAL4^prd.RG1 (Morris et al., 2006) lethal, with Scer\GAL4^sca-T3 (Morris et al., 2006) lethal, with Scer\GAL4^sev.EP (Morris et al., 2006) lethal, with Scer\GAL4^T80 (Morris et al., 2006) lethal, with Scer\GAL4^tsh-md621 (Morris et al., 2006) lethal, with Scer\GAL4^twi.2PE (Morris et al., 2006) lethal, with Scer\GAL4^twi.PG (Morris et al., 2006) lethal, with Scer\GAL4^wg.PM (Morris et al., 2006) lethal, with Scer\GAL4^αTub84B.PL (Morris et al., 2006) lethal \| embryonic stage, with Scer\GAL4^en-e16E (Ryoo et al., 2002) lethal \| pupal stage, with Scer\GAL4^Ccap.PP (Park et al., 2003) lethal \| pupal stage, with Scer\GAL4^GMR.PF (Keller et al., 2002) locomotor rhythm defective, with Scer\GAL4^P2.4.Pdf (Renn et al., 1999) locomotor rhythm defective \| male, with Scer\GAL4^npf.1 (Lee et al., 2006) neuroanatomy defective \| late embryonic stage, with Scer\GAL4^gcm-rA87.C (Pereanu et al., 2007) partially lethal - majority die, with Scer\GAL4^elav-C155 (Morris et al., 2006) partially lethal - majority die, with Scer\GAL4^GMR.PU (Kanuka et al., 2005) partially lethal - majority die \| larval stage, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997) viable, with Scer\GAL4^Akh.PL (Lee and Park, 2004) viable, with Scer\GAL4^rdgC.PK (Keller et al., 2002) viable, with Scer\GAL4^Rh3.PP (Kanuka et al., 2005) visible, with Scer\GAL4^Act88F.PD (Morris et al., 2006) visible, with Scer\GAL4^GMR.PF (Wing et al., 2001) visible, with Scer\GAL4^nos.PG (Morris et al., 2006)
Phenotype Manifest In
	abdominal dorsal/lateral multidendritic neuron, with Scer\GAL4^Ccap.PP (Kim et al., 2006) adult cuticle, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997) adult head, with Scer\GAL4^Ccap.PP (Park et al., 2003) border follicle cell, with Scer\GAL4^slbo.2.6 (Geisbrecht and Montell, 2004) centripetally migrating follicle cell, with Scer\GAL4^slbo.2.6 (Geisbrecht and Montell, 2004) EH neurosecretory neuron, with Scer\GAL4^Eh.2.4 (Kim et al., 2006, Clark et al., 2004) embryonic/larval brain \| late embryonic stage, with Scer\GAL4^gcm-rA87.C (Pereanu et al., 2007) embryonic/larval mouth, with Scer\GAL4^Ccap.PP, Scer\GAL4^Eh.2.4 (Clark et al., 2004) embryonic/larval mouth, with Scer\GAL4^Eh.2.4 (Clark et al., 2004) embryonic/larval trachea \| dorsal, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997) eye, with Scer\GAL4^GMR.PF (Wing et al., 2001, Koto et al., 2009) eye, with Scer\GAL4^GMR.PU (Kanuka et al., 2005) follicle cell, with Scer\GAL4^slbo.2.6 (Geisbrecht and Montell, 2004) glial cell \| larval stage, with Scer\GAL4^nrv2.PS (Pereanu et al., 2007) leg, with Scer\GAL4^Ccap.PP (Park et al., 2003) LNv neuron, with Scer\GAL4^P2.4.Pdf (Rodriguez Moncalvo and Campos, 2005) macrochaeta, with Scer\GAL4^nos.PG (Morris et al., 2006) macrochaeta, with Scer\GAL4^sca-109-68 (Koto et al., 2009) midline glial cell, with Scer\GAL4^Gp150-52A (Wing et al., 1998) neuron \| larval stage, with Scer\GAL4^Ccap.PP (Park et al., 2003, Clark et al., 2004) neuron \| larval stage, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997) neuropil glial sheath \| late embryonic stage, with Scer\GAL4^gcm-rA87.C (Pereanu et al., 2007) outer photoreceptor cell, with Scer\GAL4^ninaE.PT (Mendes et al., 2009) Pdf neuron, with Scer\GAL4^P2.4.Pdf (Hassan et al., 2005) Pdf neuron, with Scer\GAL4^tim.Scer\UAS (Hassan et al., 2005) photoreceptor cell R5, with Scer\GAL4^Rh5.PT (Rodriguez Moncalvo and Campos, 2005) rhabdomere R7, with Scer\GAL4^Rh3.PP (Kanuka et al., 2005) Tv neuron, with Scer\GAL4^Fmrf.PS (Kim et al., 2006) wing, with Scer\GAL4^Ccap.PP (Park et al., 2003) wing, with Scer\GAL4^Eh.2.4 (McNabb et al., 1997) wing disc, with Scer\GAL4^salm.PU (Blanco et al., 2010) wing vein, with Scer\GAL4^Act88F.PD (Morris et al., 2006)
Detailed Description
	Statement Reference Expression of rpr[Scer\UAS.cZa] in the developing eye under the control of Scer\GAL4[GMR.PF] induces a small eye phenotype. Down-regulation of endogenous th protein through ectopic expression of rpr[Scer\UAS.cZa] in all four cells of the adult sensory organ, under the control of Scer\GAL4[sca-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 rpr[Scer\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. (Koto et al., 2009) Ectopic expression of rpr[Scer\UAS.cZa], under the control of Scer\GAL4[ninaE.PT] induces a progressive loss of outer photoreceptor cells that can be visualised in tangential plastic retina sections of 2-day old flies. (Mendes et al., 2009) Expression of rpr[Scer\UAS.cZa] using Scer\GAL4[Gr66a.PD] abolishes the L-canavanine-induced proboscis retraction seen in wild type flies. (Mitri et al., 2009) The eclosion of flies expressing rpr[Scer\UAS.cZa] under the control of Scer\GAL4[Eh.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. (McNabb and Truman, 2008) Stage 16 embryos expressing rpr[Scer\UAS.cZa] under the control of Scer\GAL4[gcm-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 rpr[Scer\UAS.cZa] under the control of Scer\GAL4[gcm-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 rpr[Scer\UAS.cZa] under the control of Scer\GAL4[nrv2.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. (Pereanu et al., 2007) Males expressing rpr[Scer\UAS.cZa] under the control of Scer\GAL4[IFa.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. (Terhzaz et al., 2007) Flies that express rpr^Scer\UAS.cZa under the control of Scer\GAL4^Fmrf.PS show ablation of Tv neurons. These flies complete pupal ecdysis but show weaker pre-ecdysis contractions than controls. Flies that express rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.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. (Kim et al., 2006) Males in which most npf-expressing cells have been ablated (by expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^nf.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^nf.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. (Lee et al., 2006) Expression of rpr[Scer\UAS.cZa] in pacemaker neurons under the control of Scer\GAL4[P2.4.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 rpr[Scer\UAS.cZa] under the control of Scer\GAL4[tim.Scer\UAS] does not affect the larval response to light. (Hassan et al., 2005) Severe lethality is seen when rpr[Scer\UAS.cZa] is expressed using Scer\GAL4[GMR.PU], presumably due to leaky Scer\GAL4 expression. Animals also show a small-eye phenotype. Expression of rpr[Scer\UAS.cZa] using Scer\GAL4[Rh3.PP] does not cause any lethality. However, R7 photoreceptor neurons are absent in some ommatidia, and this phenotype worsens significantly with age. (Kanuka et al., 2005) Expression of rpr^Scer\UAS.cZa, under the control of Scer\GAL4^P2.4.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 rpr^Scer\UAS.cZa driven by both Scer\GAL4^P2.4.Pdf and Scer\GAL4^Rh5.PT, does not affect 5-HT arborization. (Rodriguez Moncalvo and Campos, 2005) Larvae that express rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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\GAL4^Eh.2.4>rpr^Scer\UAS.cZa larvae show similar ecdysis timings to wild-type larvae. However, Scer\GAL4^Eh.2.4>rpr^Scer\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 rpr^Scer\UAS.cZa under the control of both Scer\GAL4^Eh.2.4 and Scer\GAL4^Ccap.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. (Clark et al., 2004) Expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^slbo.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. (Geisbrecht and Montell, 2004) Expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.PL, while glucose levels are unaffected. The triglyceride content of the fat body is normal. Flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.PL show resistance to starvation-induced death. Flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.PL show similar locomotor activity rhythms to wild-type flies when fed on 4% sucrose-agar medium. Under starvation conditions, most flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.PL do not show pronounced starvation-induced hyperactivity (which is seen in wild-type flies). (Lee and Park, 2004) Expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.PP results in the ablation of Ccap-expressing neurons in the larval central nervous system. Expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Ccap.PP and control animals in light-dark or constant darkness conditions. (Park et al., 2003) Most flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^GMR.PF die shortly after pupariation. Flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^rdgC.PK survive well to adulthood and show no defects in walking behaviour. (Keller et al., 2002) Expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^Gp150-52A in embryos in the central nervous system midline does not induce ectopic cell death. (Wing et al., 2002) Flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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). (Baker et al., 1999) The locomotor activity of flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^P2.4.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. (Renn et al., 1999) Expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.2.4. The neurons appear to disintegrate progressively. 30%-34% of animals expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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 rpr^Scer\UAS.cZa under the control of Scer\GAL4^Eh.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. (McNabb et al., 1997) Scer\GAL4^Gp150-52A-mediated expression of rpr^Scer\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). (Zhou et al., 1997)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference BacA\p35^Scer\UAS.cHa, Scer\GAL4^αTub84B.PZ, rpr^Scer\UAS.cZa has hyperplasia \| somatic clone phenotype, suppressible by puc^Scer\UAS.cMa (Ryoo et al., 2004) rpr^Scer\UAS.cZa has increased cell death phenotype, suppressible by ninaA[+]/ninaA^E110V/Scer\GAL4^ninaE.PT (Mendes et al., 2009) Scer\GAL4^en-e16E, rpr^Scer\UAS.cZa has increased cell death phenotype, suppressible by BacA\p35^Scer\UAS.cHa, Scer\GAL4^en-e16E (Ryoo et al., 2002) Scer\GAL4^en-e16E, rpr^Scer\UAS.cZa has lethal \| embryonic stage phenotype, suppressible by BacA\p35^Scer\UAS.cHa, Scer\GAL4^en-e16E (Ryoo et al., 2002) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has increased cell death phenotype, suppressible \| partially by th^SL (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has increased cell death phenotype, suppressible by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has lethal phenotype, suppressible by Iap2^Scer\UAS.cWa, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Wing et al., 1998) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has lethal phenotype, suppressible by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has lethal phenotype, suppressible by th^SL (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has visible phenotype, suppressible \| partially by th^SL (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has visible phenotype, suppressible by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^IFa.PT, rpr^Scer\UAS.cZa has courtship behavior defective \| male phenotype, suppressible by BacA\p35^Scer\UAS.cHa, Scer\GAL4^IFa.PT (Terhzaz et al., 2007) Scer\GAL4^P2.4.Pdf, rpr^Scer\UAS.cZa has locomotor rhythm defective phenotype, suppressible \| partially by BacA\p35^Scer\UAS.cHa, Scer\GAL4^P2.4.Pdf (Renn et al., 1999)
Suppressor of
Statement Reference Scer\GAL4^vg.PM/rpr^Scer\UAS.cZa is a suppressor \| partially of lethal \| pupal stage phenotype of Scer\GAL4^vg.PM, stwl^UY823 (Brun et al., 2006)
Other
Statement Reference BacA\p35^Scer\UAS.cHa, Scer\GAL4^en-e16E, rpr^Scer\UAS.cZa has viable phenotype (Ryoo et al., 2002, Ryoo et al., 2002) BacA\p35^Scer\UAS.cHa, Scer\GAL4^tub.PU, rpr^Scer\UAS.cZa, wg^l-17 has tumorigenic \| somatic clone phenotype (Perez-Garijo et al., 2005) BacA\p35^Scer\UAS.cHa, Scer\GAL4^αTub84B.PZ, rpr^Scer\UAS.cZa has hyperplasia \| somatic clone phenotype (Ryoo et al., 2004) Scer\GAL4¹¹¹⁸, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has neuroanatomy defective phenotype (Malpel et al., 2002, Malpel et al., 2002) Scer\GAL4^Gp150-52A, morgue^EP2367, rpr^Scer\UAS.cZa has increased cell death phenotype (Wing et al., 2002, Wing et al., 2002) Scer\GAL4^nrv2.PS, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has increased cell death \| temperature conditional phenotype (Pereanu et al., 2007, Pereanu et al., 2007) Scer\GAL4^nrv2.PS, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has lethal \| temperature conditional phenotype (Pereanu et al., 2007, Pereanu et al., 2007) Scer\GAL4^nrv2.PS, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has neuroanatomy defective \| temperature conditional phenotype (Pereanu et al., 2007, Pereanu et al., 2007) Scer\GAL4^P2.4.Pdf, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has behavior defective phenotype (Yoshii et al., 2005) Scer\GAL4^tub.PU, rpr^Scer\UAS.cZa, wg^l-17 has tumorigenic \| somatic clone phenotype (Perez-Garijo et al., 2005, Perez-Garijo et al., 2005, Perez-Garijo et al., 2005)
Phenotype Manifest In
Enhanced by
Statement Reference Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has midline glial cell phenotype, enhanceable by grim^Scer\UAS.cNa/Scer\GAL4^Gp150-52A (Wing et al., 1998)
Suppressed by
Statement Reference BacA\p35^Scer\UAS.cHa, Scer\GAL4^αTub84B.PZ, rpr^Scer\UAS.cZa has wing disc \| somatic clone phenotype, suppressible by puc^Scer\UAS.cMa (Ryoo et al., 2004) rpr^Scer\UAS.cZa has outer photoreceptor cell phenotype, suppressible by ninaA[+]/ninaA^E110V/Scer\GAL4^ninaE.PT (Mendes et al., 2009) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has eye phenotype, suppressible \| partially by th^SL (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has eye phenotype, suppressible by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has eye phenotype, suppressible by th^{Scer\UAS.T:Avic\GFP-YFP.Venus}/Scer\GAL4^GMR.PF (Koto et al., 2009) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has eye phenotype, suppressible by th^{Scer\UAS.T:Zzzz\FLAG}/Scer\GAL4^GMR.PF (Koto et al., 2009) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has midline glial cell phenotype, suppressible by Scer\GAL4^Gp150-52A/Iap2^Scer\UAS.cWa (Wing et al., 1998) Scer\GAL4^Gp150-52A, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has ventral midline phenotype, suppressible \| partially by Scer\GAL4^Gp150-52A/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^Gp150-52A, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has ventral midline phenotype, suppressible \| partially by th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^Rh3.PP, rpr^Scer\UAS.cZa has rhabdomere R7 phenotype, suppressible by BacA\p35^Scer\UAS.cHa, Scer\GAL4^Rh3.PP (Kanuka et al., 2005)
NOT suppressed by
Statement Reference Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa has eye phenotype, non-suppressible by th^{N117K.H283Y.Scer\UAS.T:Avic\GFP-YFP.Venus}/Scer\GAL4^GMR.PF (Koto et al., 2009)
Enhancer of
Statement Reference Scer\GAL4^Gp150-52A/rpr^Scer\UAS.cZa is an enhancer of midline glial cell phenotype of Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa (Wing et al., 1998)
Other
Statement Reference BacA\p35^Scer\UAS.cHa, Scer\GAL4^αTub84B.PZ, rpr^Scer\UAS.cZa has wing disc \| somatic clone phenotype (Ryoo et al., 2004) Scer\GAL4¹¹¹⁸, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has larval LN period neuron phenotype (Malpel et al., 2002, Malpel et al., 2002) Scer\GAL4^Gp150-52A, grim::rpr^rg.Scer\UAS, rpr^Scer\UAS.cZa has ventral midline phenotype (Wing et al., 2001, Wing et al., 2001) Scer\GAL4^Gp150-52A, morgue^EP2367, rpr^Scer\UAS.cZa has midline glial cell phenotype (Wing et al., 2002, Wing et al., 2002) Scer\GAL4^Gp150-52A, morgue^EP2367, rpr^Scer\UAS.cZa has presumptive embryonic/larval central nervous system phenotype (Wing et al., 2002, Wing et al., 2002) Scer\GAL4^nrv2.PS, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has embryonic/larval ganglionic branch \| temperature conditional phenotype (Pereanu et al., 2007, Pereanu et al., 2007) Scer\GAL4^nrv2.PS, W^Scer\UAS.cZa, rpr^Scer\UAS.cZa has glial cell \| temperature conditional phenotype (Pereanu et al., 2007, Pereanu et al., 2007) Scer\GAL4^ple.PF, W^Scer\UAS.cZa, grim^{Scer\UAS.cOCa}, rpr^Scer\UAS.cZa has neurite & dopaminergic neuron phenotype (Palgi et al., 2009)
Additional Comments
Genetic Interactions
Statement Reference Co-expression of W[Scer\UAS.cZa] and rpr[Scer\UAS.cZa] in the posterior signalling center under the control of Scer\GAL4[Antp-10] has no effect on lamellocyte differentiation. (Sinenko et al., 2011) Expression of th[Scer\UAS.T:Zzzz\FLAG] or th[Scer\UAS.T:Avic\GFP-YFP.Venus] in the developing eye under the control of Scer\GAL4[GMR.PF] suppresses the rpr[Scer\UAS.cZa]-induced 'small-eye' phenotype. Expression of th[N117K.H283Y.Scer\UAS.T:Avic\GFP-YFP.Venus] in the developing eye under the control of Scer\GAL4[GMR.PF] fails to suppress the 'small-eye' phenotype found in rpr[Scer\UAS.cZa]; Scer\GAL4[GMR.PF] flies. (Koto et al., 2009) Loss of one genomic copy of ninaA, using the amorphic allele ninaA[E110V], protects the outer photoreceptor cells from rpr[Scer\UAS.cZa]-induced apoptosis. This anti-apoptotic effect is dose-dependent, as complete loss of ninaA leads to further protection. (Mendes et al., 2009) Co-expression of W[Scer\UAS.cZa], grim[Scer\UAS.cOCa] and rpr[Scer\UAS.cZa] under the control of Scer\GAL4[ple.PF] results in the volume of DA neurites being significantly diminished compared to controls. (Palgi et al., 2009) Expression of both rpr[Scer\UAS.cZa] and W[Scer\UAS.cZa] in the cortex and neuropile glia from late embryonic stage onwards, under the control of Scer\GAL4[nrv2.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. (Pereanu et al., 2007) Males co-expressing rpr[Scer\UAS.cZa] and W[Scer\UAS.cZa] under the control of Scer\GAL4[IFa.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 rpr[Scer\UAS.cZa] and W[Scer\UAS.cZa] under the control of Scer\GAL4[IFa.PT] copulate more rapidly with male flies than control females. (Terhzaz et al., 2007) Animals co-expressing rpr[Scer\UAS.cZa] and W[Scer\UAS.cZa] under the control of Scer\GAL4[P2.4.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. (Yoshii et al., 2005) Co-expression of BacA\p35^Scer\UAS.cHa partially restores hemolymph trehalose levels in larvae expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.PL. Co-expression of BacA\p35^Scer\UAS.cHa partially reduces the resistance to starvation-induced death seen in flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^Akh.PL. (Lee and Park, 2004) The electroantennogram (EAG) rhythm in response to ethyl acetate (measured on the second day of constant darkness conditions) in flies co-expressing rpr^Scer\UAS.cZa and W^Scer\UAS.cZa under the control of Scer\GAL4^P2.4.Pdf is similar to that of wild-type flies. (Tanoue et al., 2004) Third instar larvae co-expressing both rpr^Scer\UAS.cZa and W^Scer\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. (Malpel et al., 2002) Co-expression of BacA\p35^Scer\UAS.cHa completely blocks cell death caused by expression of rpr^Scer\UAS.cZa under the control of Scer\GAL4^en-e16E. Animals expressing both BacA\p35^Scer\UAS.cHa and rpr^Scer\UAS.cZa under the control of Scer\GAL4^en-e16E survive to adulthood with largely normal wings. (Ryoo et al., 2002) Co-expression of rpr^Scer\UAS.cZa and morgue^EP2367 under the control of Scer\GAL4^Gp150-52A in embryos in the central nervous system midline results in a dramatic loss of midline glia and neurons. (Wing et al., 2002) Co-expression of W^Scer\UAS.cZa and rpr^Scer\UAS.cZa (when driven by Scer\GAL4^Gp150-52A) results in ectopic midline cell death. The addition of th^{Scer\UAS.T:Ivir\HA1} suppresses this phenotype, sometimes to wild-type. (Wing et al., 2001) The locomotor activity defects of flies expressing rpr^Scer\UAS.cZa under the control of Scer\GAL4^P2.4.Pdf are partially suppressed by coexpression of BacA\p35^Scer\UAS.cHa. (Renn et al., 1999) When grim^Scer\UAS.cNa and rpr^Scer\UAS.cZa are coexpressed, all the midline glia and some VUM neurons are eliminated. When grim^Scer\UAS.cNa and W^Scer\UAS.cZa are coexpressed, all the midline glia and VUM neurons are eliminated. (Wing et al., 1998) Mediated expression of both rpr^Scer\UAS.cZa and W^Scer\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\p35^Scer\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. (Zhou et al., 1997)
Xenogenetic Interactions
Statement Reference Co-expression of BacA\p35[Scer\UAS.cHa] suppresses the male-male courtship seen in males expressing rpr[Scer\UAS.cZa] under the control of Scer\GAL4[IFa.PT]. (Terhzaz et al., 2007) Coexpression of BacA\p35[Scer\UAS.cHa] rescues the loss of R7 neurons caused by Scer\GAL4[Rh3.PP]-mediated expression of rpr[Scer\UAS.cZa]. (Kanuka et al., 2005) Co-expression of rpr^Scer\UAS.cZa with BacA\p35^Scer\UAS.cHa (both under the control of Scer\GAL4^unspecified) in wg^l-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. (Perez-Garijo et al., 2005) rpr^Scer\UAS.cZa; BacA\p35^Scer\UAS.cHa; Scer\GAL4^αTub84B.PZ somatic clones in the wing disc cause significant overgrowth of this disc. This overgrowth in suppressed by puc^Scer\UAS.cMa. (Ryoo et al., 2004)
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
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Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	rpr^Scer\UAS.cZa rpr^UAS.cMa rpr^UAS.cZa
Name Synonym	Saccharomyces cerevisiae UAS construct a of Zhou (Zhou et al., 1997)
Secondary FlyBase IDs
	FBal0082291
References ( 50 )

Generate a list of	All references relating to this allele ( 50 )

List References by type	Research paper ( 49 ) Supplementary material ( 1 )
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Allele Dmel\rprScer\UAS.cZa

Allele Dmel\rpr^Scer\UAS.cZa