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General Information
Symbol
Dmel\pucE69
Species
D. melanogaster
Name
FlyBase ID
FBal0032524
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
puc-lacZ, pucE69-lacZ, puc-lacZE69, puckered-lacZ, Puc:LacZ, pucLacZ
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{A92} insertion in the second intron.

Insertion components
P{A92}pucE69
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

pucE69 heterozygotes do not show obvious thorax defects.

The size of regenerated adult wings in pucE69 heterozygous mutants that were subjected to ablation of imaginal wing disc tissue during the larval stage, is not reduced compared to similarly treated controls.

Heterozygous pucE69 mutants display no perturbation to neuromuscular junction size.

pucE69/+ flies are more resistant to oxidative stress (paraquat), have extended lifespans, and have significantly better climbing ability (at 40 days old, but not younger) than wild type.

pucE69 heterozygotes exhibit a 25% frequency of ensheathment defects compared with only 11% in controls. pucE69 homozygotes exhibit a 50% frequency of ensheathment defects.

Wings of heterozygous pucE69 flies appear normal.

pucE69/+ flies are more resistant against paraquat toxicity than controls.

40% of stage 17 homozygous embryos show inversion of the normal left-right asymmetry of the anterior midgut and 5% do not show any left-right asymmetry.

Homozygotes have a larval cuticle with a puckered dorsal midline.

pucE69 heterozygous adults have signifcantly longer average and maximum life spans than wild-type.

In contrast to wild-type flies, pucE69/+ flies do not die in response to being fed with paraquat. However, the sensitivity of these flies to G148 is similar to wild-type flies. pucE69/+ males show significant extension of mean and maximal lifespan when compared to wild-type flies. Females show qualitatively similar lifespan data, although the extension of lifespan is less pronounced than in males. pucE69/+ flies and wild-type controls exhibit roughly equivalent sizes, reproductive activities and developmental timing. However, these mutants show a much stronger resistance to starvation than wild-type flies, and also contain significantly decreased levels of oxidized proteins.

Heterozygous embryos do not show cuticle defects.

Dorsal closure takes place in homozygous embryos but the leading edge cells do not differentiate properly. The dorsal ectoderm closes properly, but the two rows of cardioblasts do not migrate and join to form the heart tube at the dorsal midline, instead remaining separate.

Homozygous pucE69 cells do not survive in the eye disc.

Heterozygotes have wild-type wings. The number of dying cells in the late third larval instar wing disc is not increased compared to wild type.

Mutant embryos show a severe crinkling of the dorsal epidermis and a small, posterior, dorsal hole. The fine dorsal hairs are disrupted.

Homozygous embryos lack dorsal hairs along the dorsal midline, leaving a strip of naked cuticle along most of the midline. These embryos show puckering of the epidermis.

Dorsal closure proceeds normally in pucE69 cno3 double heterozygotes.

Homozygous embryos produce a mutant cuticle phenotype in the dorsal epidermis. After germband shortening the cells are not restricted to a straight line at the edge of the epidermis, but are seen to extend several cell diameters away from the edge. As dorsal closure proceeds these cells become increasingly disorganised so that by completion of dorsal closure they are haphazardly arranged in clusters at the dorsal midline. The shape of the dorsal-most cells is also abnormal, the cells do not elongate and consequently they do not generate a straight edge to the moving front of the epidermis during dorsal closure. The pattern of the cuticle secreted by these cells is also abnormal. Despite the abnormalities of the dorsalmost epidermal cells, dorsal closure does occur to completion.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

Cskj1D8, pucE69/puc[+] has visible phenotype, enhanceable by ASPP[+]/ASPP8

NOT Enhanced by
Statement
Reference

pucE69 has chemical resistant | dominant phenotype, non-enhanceable by ry506/ry506

Suppressed by
Statement
Reference

gfr1, pucE69/puc[+] has lethal | dominant phenotype, suppressible by bru305871/l(3)05871[+]

gfr1, pucE69/puc[+] has lethal | dominant phenotype, suppressible by Df(3L)Exel6119/+

MoedsRNA.327-775.UAS, Scer\GAL4dpp.blk1, pucE69/puc[+] has visible phenotype, suppressible by Rho172R/Rho1[+]

pucE69 has long lived | dominant phenotype, suppressible by foxo25/foxo[+]

pucE69 has long lived | dominant phenotype, suppressible by foxo21/foxo[+]

pucE69 has long lived | dominant phenotype, suppressible by hep1

pucE69 has chemical resistant | dominant phenotype, suppressible by hep1

pucE69 has chemical resistant | dominant phenotype, suppressible by bsk2/bsk[+]

pucE69 has lethal | recessive phenotype, suppressible | partially by hep1

pucE69 has lethal | recessive phenotype, suppressible by hep1/hep1

NOT suppressed by
Statement
Reference

gfrx, pucE69/puc[+] has lethal | dominant phenotype, non-suppressible by Df(3L)H99/+

Enhancer of
Statement
Reference

pucE69/puc[+] is an enhancer of tumorigenic phenotype of Sox21a6

pucE69/puc[+] is an enhancer of visible phenotype of Rala35d

pucE69/puc[+] is an enhancer of visible | dominant phenotype of sdSG29.1

pucE69/puc[+] is an enhancer of visible phenotype of Scer\GAL4pnr-MD237, slprUASp.cPa

pucE69/puc[+] is an enhancer of visible phenotype of Rac1GMR.PN

pucE69/puc[+] is an enhancer of visible phenotype of dpphr56/dppd8

pucE69/puc[+] is an enhancer of visible | recessive phenotype of biomb-1

pucE69 is an enhancer of visible phenotype of tkv7/tkv427

Suppressor of
Statement
Reference

pucE69/puc[+] is a suppressor of visible | adult stage phenotype of Scer\GAL4pnr.PU, licGD7546

pucE69/puc[+] is a suppressor of visible | adult stage phenotype of mole02670

pucE69/puc[+] is a suppressor of stress response defective | adult stage phenotype of mole02670

pucE69/puc[+] is a suppressor of short lived phenotype of Mrp4M2/Mrp4M1

pucE69/puc[+] is a suppressor of short lived | conditional phenotype of Hayan1

pucE69/puc[+] is a suppressor of partially lethal - majority die | larval stage | conditional phenotype of Hayan1

pucE69/puc[+] is a suppressor of lethal phenotype of slprBS06

pucE69/puc[+] is a suppressor of visible | male phenotype of PSRUAS.cKa, Scer\GAL4Act5C.PU

pucE69/puc[+] is a suppressor of visible phenotype of Scer\GAL4pnr-MD237, slprD314Y.UASp

pucE69/puc[+] is a suppressor of chemical sensitive phenotype of hep1

pucE69/puc[+] is a suppressor of chemical sensitive | dominant phenotype of bsk2

pucE69 is a suppressor | partially of lethal phenotype of kay1/kay2

pucE69/puc[+] is a suppressor of lethal | recessive phenotype of Src42AJp45

pucE69 is a suppressor of visible phenotype of hepr39/hep1

pucE69 is a suppressor of visible phenotype of hepr75/hep1

pucE69/puc[+] is a suppressor of lethal phenotype of kay1/kay2

NOT Suppressor of
Statement
Reference
Other
Statement
Reference

bru305871/l(3)05871[+], gfr1, pucE69/puc[+] has viable phenotype

bru305871/l(3)05871[+], pucE69 has viable phenotype

ASPP[+]/ASPP8, Cskj1D8, pucE69/puc[+] has visible phenotype

chm14, pucE69/puc[+] has viable phenotype

chm14/chm[+], pucE69 has viable phenotype

Phenotype Manifest In
Enhanced by
Statement
Reference

Cskj1D8, pucE69/puc[+] has wing phenotype, enhanceable by ASPP[+]/ASPP8

Suppressed by
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

pucE69/puc[+] is an enhancer of adult anterior midgut epithelium phenotype of Sox21a6

pucE69/puc[+] is an enhancer of wing disc phenotype of Scer\GAL4ptc-559.1, Sin3AKK100700

pucE69/puc[+] is an enhancer of eye phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev

pucE69/puc[+] is an enhancer of eye | somatic clone phenotype of ebik16213

pucE69/puc[+] is an enhancer of adult thorax phenotype of Scer\GAL4pnr-MD237, slprUASp.cPa

pucE69/puc[+] is an enhancer of microchaeta phenotype of Rala35d

pucE69/puc[+] is an enhancer of macrochaeta phenotype of Rala35d

pucE69/puc[+] is an enhancer of zonula adherens & disc epithelium proper phenotype of CskdsRNA.UAS, Scer\GAL4ptc-559.1

pucE69/puc[+] is an enhancer of wing phenotype of Scer\GAL4C-765, egrUAS.cMa

pucE69/puc[+] is an enhancer of eye phenotype of Rac1GMR.PN

pucE69/puc[+] is an enhancer of ommatidium phenotype of Rac1GMR.PN

pucE69/puc[+] is an enhancer of wing phenotype of dpphr56/dppd8

pucE69 is an enhancer of wing phenotype of tkv7/tkv427

pucE69 is an enhancer of wing disc phenotype of tkv7/tkv427

pucE69/puc[+] is an enhancer of wing phenotype of biomb-1

NOT Enhancer of
Statement
Reference

pucE69 is a non-enhancer of phenotype of Rho1rev220

Suppressor of
Statement
Reference

pucE69/puc[+] is a suppressor of tergum phenotype of Scer\GAL4pnr.PU, licGD7546

pucE69/puc[+] is a suppressor of wing phenotype of mole02670

pucE69/puc[+] is a suppressor of male genitalia phenotype of PSRUAS.cKa, Scer\GAL4Act5C.PU

pucE69/puc[+] is a suppressor | partially of adult thorax | pharate adult stage phenotype of chm14

pucE69 is a suppressor | partially of mesothoracic cleft phenotype of kay1/kay2

pucE69/puc[+] is a suppressor of phenotype of slpr3P5

pucE69/puc[+] is a suppressor of embryo | dorsal closure stage phenotype of slpr921

pucE69/puc[+] is a suppressor of adult thorax | dorsal phenotype of Src42AJp45

pucE69 is a suppressor of wing phenotype of hep1

pucE69 is a suppressor of leg phenotype of hep1

pucE69 is a suppressor of eye phenotype of hep1

pucE69 is a suppressor of wing disc phenotype of hep1

pucE69 is a suppressor of adult thorax phenotype of hepr39/hep1

pucE69 is a suppressor of chaeta phenotype of hepr39/hep1

pucE69 is a suppressor of imaginal disc phenotype of hepr39

pucE69 is a suppressor of wing disc phenotype of hepr39

pucE69 is a suppressor of adult thorax phenotype of hepr75/hep1

pucE69 is a suppressor of chaeta phenotype of hepr75/hep1

pucE69 is a suppressor of imaginal disc phenotype of hepr75

pucE69 is a suppressor of wing disc phenotype of hepr75

pucE69 is a suppressor of adult thorax | dorsal phenotype of kay2

NOT Suppressor of
Statement
Reference

pucE69 is a non-suppressor of bouton phenotype of Scer\GAL4elav-C155, kayFbz.UAS

pucE69/puc[+] is a non-suppressor of denticle belt phenotype of arm3

pucE69/puc[+] is a non-suppressor of embryonic epidermis | dorsal phenotype of arm3

pucE69/puc[+] is a non-suppressor of embryonic epidermis | ventral phenotype of arm3

pucE69 is a non-suppressor of phenotype of Rho1rev220

Other
Additional Comments
Genetic Interactions
Statement
Reference

The reduced size of regenerated adult wings characteristic for mole02670 heterozygous mutants that were subjected to ablation of the imaginal wing disc tissue during the larval stage can be rescued by combination with a single copy of pucE69.

Heterozygous combinations of pucE69 and Rab81 results in an increase in synaptic bouton number compared with wild-type.

One copy of pucE69 increases tumor formation in the anterior midgut of Sox21a6 mutant flies.

Reduced resistance to oxidative stress (paraquat) in Mrp4M2/Mrp4M2 flies is increased to significantly more than wild type levels with a single copy of pucE69. Reduced lifespan in Mrp4M1/Mrp4M2 flies is increased to significantly more than wild type levels with a single copy of pucE69. Reduced climbing ability in Mrp4M1/Mrp4M2 flies is rescued to wild type levels (at 10 and 30 days old) and increased beyond wild type levels (at 40 days old) by a single copy of pucE69.

The cell invasion phenotype seen when Sin3AKK100700 is expressed under the control of Scer\GAL4ptc-559.1 is enhanced in a pucE69/+ background.

pucE69/+ enhances the mild rough eye phenotype seen in eyes containing large ebik16213 clones.

A pucE69/+ mutant background suppresses the mortality induced when homozygous Hayan1 mutants are wounded at either the larval or adult stages.

pucE69 dominantly suppresses the wing notching phenotype seen in Df(1)N-54l9 heterozygotes (the penetrance of the phenotype is significantly decreased in the double heterozygotes).

Heterozygous pucE69 mutant flies expressing MoedsRNA.327-775.Scer\UAS under the control of Scer\GAL4dpp.blk1 exhibit a severely reduced or rudimentary wing phenotype.

Rho172R/+ strongly suppresses the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.

Co-expression of hepdsRNA.Scer\UAS suppresses the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.

Co-expression of slprdsRNA.Scer\UAS.NIG suppresses the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.

Co-expression of Tak1dsRNA.Scer\UAS suppresses the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.

Co-expression of Tak1K46R.M.Scer\UAS suppresses the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.

Co-expression of Pk92BK618M.Scer\UAS has no effect on the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.

Heterozygous pucE69 mutant flies expressing Rho1Scer\UAS.cMa under the control of Scer\GAL4dpp.blk1 exhibit a severely reduced or rudimentary wing phenotype.

pucE69 restores viability to slprBS06/Y males.

pucE69/+ strongly enhances the thorax closure defects of Scer\GAL4pnr-MD237 slprScer\UAS.P\T.cPa flies - the scutellum is smaller, and more bristles are lost.

Expression of Axud1Scer\UAS.cGa with Scer\GAL4salm-EPv in a heterozygous pucE69 background significantly enhances the reduction in wing size.

Introduction of a single copy of pucE69 into the Scer\GAL4GMR.PF, egrScer\UAS.cIa background dramatically enhances the reduced eye phenotype, with flies displaying a prominent black lesion in place of the eye.

The reduced eye phenotype caused by expression of Rab11N124I.Scer\UAS under the control of Scer\GAL4GMR.PF is enhanced if the flies also carry pucE69/+.

Heterozygosity for Atg1Δ3D, Atg1EY09216 or Atg600096 reverts the resistance to paraquat toxicity seen in pucE69/+ animals.

The genital rotation defect seen in males expressing PSRScer\UAS.cKa under the control of either Scer\GAL4Act5C is suppressed by pucE69/+.

pucE69/+ Cskj1D8/+ double heterozygotes have a notched wing phenotype, and third larval instar wing discs show ectopic apoptosis within the wing pouch.

The ectopic apoptosis seen in the wing discs of pucE69/+ Cskj1D8/+ double heterozygotes is enhanced if they are also heterozygous for ASPP8, resulting in adults with a severely reduced wing size. These adults also have leg deformities.

The wing discs of ASPP8/ASPP8 pucE69/+ third instar larvae show a moderate ectopic patch of apoptotic cells. Adults of this genotype do not show wing notching.

Only 20% of embryos derived from DokPG155 germ-line clones that are also heterozygous for pucE69 show a dorsal closure phenotype, compared to 48% of DokPG155 germ-line clones without a puc mutation. The rescued embryos have small holes in the cuticle.

A pucE69/+ background dramatically enhances the lkb1Scer\UAS.cLa-Scer\GAL4Bx-MS1096 small wing phenotype.

The severity of the thoracic cleft seen in chm14 pharate adults is suppressed by heterozygosity for pucE69.

The narrowed scutellum phenotype seen in flies expressing slprScer\UAS.P\T.cPa under the control of Scer\GAL4pnr-MD237 is enhanced by pucE69/+, such that the scutellum is essentially eliminated.

The cleft notum phenotype seen in flies expressing slprD314Y.Scer\UAS.P\T under the control of Scer\GAL4pnr-MD237 is suppressed almost to wild type by pucE69/+.

pucE69/+ strongly enhances the loss of apical profile, delamination and subsequent migration and cell death increase seen in cells at the posterior edge of theptc expression domain in CskIR.Scer\UAS Scer\GAL4ptc-559.1 third instar larvae.

The reduced survival rate after natural infection with "Ecc-15" (P.carotovorum.carotovorum) that is seen in flies expressing IrcdsRNA.Scer\UAS under the control of Scer\GAL4da.G32 is partially rescued by pucE69/+.

The increase in average and maximum lifespan seen in pucE69/+ adults is dominantly suppressed by foxo21 or foxo25.

Recovery of arr2 homozygous somatic clones in third instar wing discs (induced at around 60 hours after egg laying) is reduced by the presence of pucE69/+ (10/25 twinspots vs 21/29 in a wild-type background).

pucE69/+; hep1/Y mutant flies have a decreased mortality rate in response to paraquat compared to hep1/Y single mutants, but an increased mortality rate compared to pucE69/+ single mutants. Likewise, pucE69/+; bsk2/+ have a decreased sensitivity to paraquat compared to bsk2/+ single mutants and an increased mortality rate compared to pucE69/+ single mutants. The response of pucE69/+ flies to paraquat is not affected when flies have a ry506 genetic background. pucE69/+ flies with a hep1/Y background have a less pronounced extension of lifespan than pucE69/+ single mutant flies.

pucE69 Sac1L2F double heterozygous embryos show defects in the dorsal cuticle (anterior head holes and/or puckering). pucE69 shows no genetic interactions with Sac12107 or Sac1BG02228. Sac1L16C interacts genetically with pucE69.

biomb-1, pucE69 double heterozygotes exhibit a strong wing notch and cell death increase phenotype. These phenotypes are suppressed by the addition of fu1.

The dorsal closure phenotype caused by expression of egScer\UAS.cDa under the control of Scer\GAL4pnr-MD237 is suppressed by pucE69. The dorsal closure phenotype caused by expression of knrlScer\UAS.cLa under the control of Scer\GAL4pnr-MD237 is suppressed by pucE69.

Heterozygosity for pucE69 enhances the wing phenotype due to P{UAS-eiger.M}weak with Scer\GAL4C-765. pucE69/+ enhances the eye ablation phentoype of egrScer\UAS.cMa; Scer\GAL4GMR.PF animals.

The severe dorsal open phenotype of slpr921/Y embryos is significantly rescued by pucE69/+. pucE69/+ rescues slpr3P5/Y animals to adulthood. The mutant male flies are weakly viable with no gross morphological defects.

Dominantly suppresses the lethality and cleft thorax phenotypes of Src42AJp45 homozygotes.

Homozygous escapers show mildly roughened eyes that display typical planar polarity defects.

Dominantly enhances the wing notching phenotype of dppd8/dpphr56, tkv7/tkv427 or biomb-1/Y flies. Dominantly enhances the appearance of an apoptotic cluster of cells in the primordial wing tip of the late third larval instar tkv7/tkv427 wing disc. The appearance of the cluster of apoptotic cells is suppressed in hepr75/Y ; tkv7/tkv427; pucE69/+ larvae.

The lethality of the kay1/kay2 combination is rescued by one copy of pucE69; the rescued flies have a thoracic cleft phenotype ranging from strong to very mild. Rescues the thoracic cleft phenotype of kay2 homozygotes. The lethality of embryos which are maternally and zygotically hep1 is rescued by one copy of pucE69. The lethality of pucE69 homozygotes is rescued if the flies are also homozygous or hemizygous for hep1. The rescued flies look remarkably normal, except some females have macrochaetae with a kink. Dominantly enhances the scutellar phenotype caused by hepScer\UAS.cBa expressed under the control of Scer\GAL4pnr-MD237.

Dominantly partially suppresses the dorsal open phenotype of hep1 hemizygous embryos.

Xenogenetic Interactions
Statement
Reference

A pucE69/+ background increases the severity the reduced adult eye size phenotype found in Scer\GAL4hs.2sev->Mmus\Gria1Lc.Scer\UAS flies.

A pucE69/+ background further enhances the rescue found in BacA\p35GMR.PH;Scer\GAL4hs.2sev->Mmus\Gria1Lc.Scer\UAS flies.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Reversion to wild-type is associated with loss of the P{A92} element. JNK activity is increased twofold compared to wild-type and ERK activity is similar to wild-type in extracts of homozygous embryos.

Loss of the P{A92} insertion results in reversion of the puc phenotype to wild type.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (77)