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General Information
Symbol
Dmel\pucUAS.cMa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Martin-Blanco
FlyBase ID
FBal0086366
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-puc, UAS-puc2A, UAS-puckered, UAS-puc2A, UASpuc
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
A puc cDNA is expressed under the control of UASt regulatory sequences.
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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 1 )
 
Expression of pucScer\UAS.cMa ameliorates tumor-like growth and invasion when Ras85DV12.Scer\UAS is expressed in l(2)gl4 mutant cells.
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
dorsal mesothoracic disc & peripodial epithelium & prepupa, with Scer\GAL4Act5C.PI
dorsal mesothoracic disc & peripodial epithelium & prepupa, with Scer\GAL4Act5C.PI, pucE69
dorsal mesothoracic disc & peripodial stalk & prepupa, with Scer\GAL4Act5C.PI
dorsal mesothoracic disc & peripodial stalk & prepupa, with Scer\GAL4Act5C.PI, pucE69
Detailed Description
Statement
Reference
Expression of pucScer\UAS.cMa under the control of Scer\GAL4GMR.PF has no effect on eye size.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4twi.PG has no effect on ventral furrow formation.
Embryos expressing pucScer\UAS.cMa under the control of Scer\GAL4ptc-559.1 completely lack cell intercalation and mixer cell shifting at the segment boundary during dorsal closure (in the abdominal segments of wild-type embryos at the end of dorsal closure, a mixer cell moves across the segment boundary from the anterior compartment to the posterior compartment and two cells from the ventral ectoderm intercalate into the leading edge, posterior to the mixer cell).
Overexpression of pucScer\UAS.cMa driven by Scer\GAL4Abd-B-LDN induces abnormal male terminalia rotation without genital arch defects. Overexpression of pucScer\UAS.cMa driven by Scer\GAL4en-e16E and Scer\GAL4ptc-559.1 induces abnormal male terminalia rotation and genital arch defects.
Wing imaginal discs expressing pucScer\UAS.cMa under the control of Scer\GAL4Bx-MS1096-KE are reduced in size compared to controls.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4hs.PU using heat shock during 10.5 to 11.5 AEL results in left-right asymmetry defects in the anterior midgut, with a number of embryos showing inversion of the normal asymmetry. Overexpression using heat shock during 4.5 to 5.5 AEL has does not induce defects in anterior midgut left-right asymmetry.
Expression of pucScer\UAS.cMa in the developing retina under the control of Scer\GAL4GMR.PF results in a few mild R axon misrouting defects.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4ey.PH does not affect eye size.
Expression of pucScer\UAS.cMa in the posterior compartment of the wing disc, driven by Scer\GAL4en-e16E, prevents normal wound healing in the posterior part of the disc in around 60% of cases. Wound healing in the anterior part of the disc, where pucScer\UAS.cMa is not expressed, is unaffected.
Overexpression of pucScer\UAS.cMa in the notum of wing imaginal discs under the regulation of Scer\GAL4ap-md544 induces a marked cleft in the thorax.
When pucScer\UAS.cMa is driven by Scer\GAL4e22c or Scer\GAL469B a strong dorsal closure defect is observed.
Expression of puc driven by Scer\GAL4dpp.blk1 and Scer\GAL4en-e16E causes rotation of the male terminalia and dorsal split. Spermiduct and sperm pump are misrotated.
Shortly after pupariation begins in wild-type flies, the wing discs move so that their peripodial side is in apposition with the larval epidermis. This fails completely in pucScer\UAS.cMa; Scer\GAL4Act5C.PI flies. (Scer\GAL4Act5C.PI induced from Scer\GAL4Scer\FRT.Act5C at 48-60 hours before puparium formation). Less severe phenotypes are seen in animals which also heterozygous for pucE69. In many cases disc eversion and spreading fails. In the least sever cases, eversion and spreading occurs normally but fusion to adjacent discs fails.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4hs.2sev does not affect eye development. Expression of pucScer\UAS.cMa under the control of Scer\GAL4en-GAL4-54 does not affect wing development. Expression of pucScer\UAS.cMa under the control of Scer\GAL469B causes a dorsal closure defect in embryos.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4elav-C155 results in a 25-30% decrease in EJC amplitude (synaptic strength) and bouton number at the larval neuromuscular junction.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4hs.PB using heat shock results in variably short eggs with dorsal appendage defects within 24 hours of expression. Expression of pucScer\UAS.cMa in large clones in the follicle cells under the control of Scer\GAL4Act5C.PP results in defective egg chambers composed of a significant mass of nurse cell material connected to a small chorion encased egg.
Expression of pucScer\UAS.cMa, when driven by Scer\GAL4pnr-MD237 leads to a mild thorax closure defect in adult flies.
Expression of pucScer\UAS.cMa in the posterior region of the follicular epithelium under the control of Scer\GAL4E4 has no effect on egg morphology or the embryo. Expression of pucScer\UAS.cMa in the anterior region of the main body follicle cells under the control of Scer\GAL455B results in a significant alteration in dorsal appendage shape and size. Micropyles are usually very reduced in size. Expression of pucScer\UAS.cMa in the follicle cells using either Scer\GAL4T155 or Scer\GAL4CY2 results in dorsal appendage and micropyle defects. Expression of pucScer\UAS.cMa in the anterior region of the main body follicle cells under the control of Scer\GAL455B results in a significant alteration in dorsal appendage shape and size. Micropyles are usually very reduced in size. Expression of pucScer\UAS.cMa using Scer\GAL4slbo.2.6 results in eggs with strongly shortened micropyles but normal dorsal appendages.
The expression of pucScer\UAS.cMa driven by Scer\GAL4LE results in adults with a mild thorax cleft phenotype.
When expression is driven by Scer\GAL4arm.T:Hsim\VP16 the dorsal surface of the embryos are completely open.
When expression is driven by Scer\GAL4hs.2sev the eyes of the flies can be mildly or occasionally very rough. Eyes show tissue polarity defects in tangential sections.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4pnr-MD237 or Scer\GAL4ap-md544 results in the appearance of a cleft in the thorax.
Embryos expressing pucScer\UAS.cMa under the control of Scer\GAL4hs.PB fail to achieve dorsal closure and have a large dorsal opening if they are heat shocked between 4 and 5 hours after egg laying (AEL). Most embryos heat shocked between 5 and 7 hours AEL have a dorsal hole or a phenotype similar to puc loss of function alleles. Embryos heat shocked after 7 hours AEL have a puc loss of function phenotype. Dorsal epidermal cells of embryos expressing pucScer\UAS.cMa under the control of Scer\GAL4arm.PS do not change their shape during the time of dorsal closure, in contrast to wild-type.
Flies expressing pucScer\UAS.cMa in the scutellum under the control of Scer\GAL4455.2 have ectopic macrochaetae in the scutellum. Wing vein pattern is normal in these flies. Flies expressing pucScer\UAS.cMa in the eye under the control of Scer\GAL4GMR.PF lack many accessory cells. Most ommatidia have the normal pattern of photoreceptors cells.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
Statement
Reference
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
Statement
Reference
Scer\GAL4Bx-MS1096-KE/pucUAS.cMa is a suppressor | partially of actin filament & dorsal mesothoracic disc phenotype of Scer\GAL4Bx-MS1096-KE, Vps4DN.UAS.Tag:HA
Scer\GAL4wex1.rev, Scer\GAL4wex1.for, pucUAS.cMa is a suppressor of embryonic leading edge cell & actomyosin phenotype of FERgof
Scer\GAL4wex1.rev, Scer\GAL4wex1.for, pucUAS.cMa is a suppressor of embryonic leading edge cell & filopodium phenotype of FERgof
pucUAS.cMa/Scer\GAL4ey.PH is a suppressor | partially of eye | ventral phenotype of L2
pucUAS.cMa is a suppressor of zonula adherens & disc epithelium proper phenotype of CskdsRNA.UAS, Scer\GAL4ptc-559.1
pucUAS.cMa is a suppressor of wing phenotype of Scer\GAL4C-765, egrUAS.cMa
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference
The extensive cell death in the pouch region of wing discs in third instar larvae as well as the small and deformed wings in adults expressing His1:CG31617NIG.31617R under the control of Scer\GAL4nub.PU are significantly suppressed by co-expression of pucScer\UAS.cMa.
The partial or complete loss of the wing anterior crossvein in flies expressing fmtGD6928 under the control of Scer\GAL4ptc.PU is suppressed by co-expression of pucScer\UAS.cMa.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4bun-GSG5961 and Scer\GAL4GSG5966 (along with RU486 to induce expression via the GeneSwitch system) in the gut fully restores growth of wild type clones in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones in the posterior midgut, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones. ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing pucScer\UAS.cMa under the control of Scer\GAL4tub.PU also show suppressed growth. Expression of pucScer\UAS.cMa in host tissue only, under the control of Scer\GAL4GSG2326, severely suppresses growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4tub.PU does not suppress the photoreceptor differentiation defects or increased cell death seen in Vps43B1 mutant eye disc clones.
Co-expression of pucScer\UAS.cMa results in suppression of the tumorigenesis observed in the mutant domain in flies expressing Rab5GD10492 under the control of Scer\GAL4salm.EPv (in combination with a Gal80[ts] transgene to restrict expression to the third instar larval stage) in the wing pouch.
Expression of Ras85DV12.Scer\UAS under the control of Scer\GAL4Scer\FRT.Act5C in l(2)gl4 mutant cells in eye-antennal discs using the ey-FLP/MARCM system results in tumor-like growth with invasive migration into the ventral nerve cord of the CNS. The growth and invasion of these tumors is dramatically suppressed upon co-expression of pucScer\UAS.cMa.
The reduced wing phenotype caused by expression of DLPEY09290 under the control of Scer\GAL4Bx-MS1096 is suppressed by co-expression of pucScer\UAS.cMa.
Blocking JNK signaling by expression of pucScer\UAS.cMa dramatically suppresses the growth and invasion behaviours of Ras85DV12.Scer\UAS/l(2)gl4 tumours.
Inactivation of JNK signaling, through the expression of pucScer\UAS.cMa, dramatically suppresses the Ras85DV12.Scer\UAS/l(2)gl4 mutant tumour growth and invasion, and rescues animals to pupal stage.
Co-expression of pucScer\UAS.cMa suppresses the cell invasion phenotype (migration into the posterior compartment) seen in anterior cells in the wing disc expressing Vha44Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ptc-559.1.
Coexpression of pucScer\UAS.cMa rescues the delay at pupariation of Scer\GAL4rn-GAL4-5, Syx7GD2767 animals. Coexpression of pucScer\UAS.cMa rescues the delay at pupariation of Scer\GAL4rn-GAL4-5, RpL7GD11462 animals.
Co-expression of pucScer\UAS.cMa does not suppress the small, rough eye phenotype found upon expression of nopoScer\UAS.cUa under the control of Scer\GAL4GMR.PF. egrScer\UAS.cIa-induced cell death is partially suppressed by co-expression of pucScer\UAS.cMa, under the control of Scer\GAL4GMR.PF.
The cell invasion phenotype seen in cells expressing sds22GD11788 under the control of Scer\GAL4ptc-559.1 along the anterior-posterior compartment boundary of the wing disc is suppressed if the cells are also co-expressing pucScer\UAS.cMa, but the abnormal apical folding phenotype is not suppressed.
Co-expression of pucScer\UAS.cMa suppresses the increased apoptosis and increased fraction of mitotic cells phenotypes seen in Scer\GAL4nub-AC-62, hppyScer\UAS.cMa discs.
Clones of cells co-expressing nabEP642 and pucScer\UAS.cMa in the wing imaginal disc (under the control of Scer\GAL4Scer\FRT.Rnor\CD2.Act5C) exhibit a block on overgrowth.
Co-expression of pucScer\UAS.cMa with scafScer\UAS.cRa driven by Scer\GAL4en-e16E enhances the male terminalia rotation phenotype observed when pucScer\UAS.cMa is expressed alone.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4tub.PU strongly suppresses the apoptosis that is seen in mahj1 or l(2)gl4 clones in the wing disc. Basal extrusion of mutant cells is not fully blocked in these discs.
Scer\GAL4GMR.PU-mediated co-expression of egrecto-60.Scer\UAS.T:Ivir\HA1,T:Zzzz\FLAG and pucScer\UAS.cMa results in a novel 'hanging-eye' phenotype. When co-expressed in wing disc clones, this combination induces apoptosis in neighbouring cells.
The disruption of the actin cytoskeleton that is seen in the wing imaginal discs of animals expressing Vps4DN.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Bx-MS1096-KE is partially suppressed by co-expression of pucScer\UAS.cMa. Wing imaginal discs co-expressing both pucScer\UAS.cMa and Vps4DN.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Bx-MS1096-KE are larger in size compared to controls.
The reduced eye size caused by expression of Rab11N124I.Scer\UAS under the control of Scer\GAL4GMR.PF is significantly suppressed by co-expression of pucScer\UAS.cMa.
Co-expression of pucScer\UAS.cMa ameliorates the eye defects caused by expression of Sir2Scer\UAS.cGa under the control of Scer\GAL4GMR.PU.
Expression of pucScer\UAS.cMa (which inhibits cell death) in vgnull clones results in clone survival in the prospective wing blade of the larval wing disc. Clone survival depends on the position along the proximal-distal axis of growth, clones being recovered at a higher frequency and larger size in the proximal territories of the vg expression domain. These clones tend to be extruded during larval stages and fail to appear in the adult wing.
Vps25N55 ArkH16/pucScer\UAS.cMa mosaic eye discs are severely overgrown.
The Fps85Dgof embryonic phenotype is rescued by expression of pucScer\UAS.cMa under the control of Scer\GAL4wex1.for and Scer\GAL4wex1.rev (the Scer\GAL4 alleles carried on the P{GawB-wex1}Fps85Dgof construct whose insertion causes the Fps85Dgof allele). pucScer\UAS.cMa, Fps85Dgof embryos complete dorsal closure at normal rates and show no axon misrouting at the ventral midline.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4ey.PH results in rescue of the ventral eye loss of L2/+ mutants in 36% of cases.
pucScer\UAS.cMa suppresses the loss of apical profile, delamination and subsequent migration and cell death increase seen in cells at the posterior edge of the ptc expression domain in CskIR.Scer\UAS Scer\GAL4ptc-559.1 third instar larvae.
Overexpression of pucScer\UAS.cMa and parkScer\UAS.T:Hsap\MYC in the notum of wing imaginal discs, under the regulation of Scer\GAL4ap-md544 enhances the thoracic cleft observed in each single overexpression.
When 4xdmyc and 2xdmyc clones are made in wing discs that express pucScer\UAS.cMa (driven by Scer\GAL4hh-Gal4) in the posterior compartment, 2xdmyc clones grow significantly more slowly than 4xdmyc clones in the Anterior (control) compartment. This effect is lessened in the posterior compartment. The 4xdmyc clones also grow less well in the posterior compartment.
pucScer\UAS.cMa; Scer\GAL4αTub84B.PL only partially rescues arr2 homozygous somatic clone size in the wing disc: These clones are on average 32% of twin-spot clone size, compared to 17% in the absence of pucScer\UAS.cMa.
The presence of pucScer\UAS.cMa suppresses the wing ablation phenotype seen in P{UAS-eiger.M}Av; Scer\GAL4C-765 flies and the eye ablation phenotype due to egrScer\UAS.cMa with Scer\GAL4GMR.PF. The presence of pucScer\UAS.cMa allows somatic clones expressing egrScer\UAS.cMa under the control of Scer\GAL4Ubx.PdC in the wing disc to survive for at least 60 hours after induction. In the absence of pucScer\UAS.cMa all such clones are lost by 24 hours after induction.
Co-expression of pucScer\UAS.cMa allows the survival of clones expressing brkScer\UAS.cJa under the control of Scer\GAL4Ubx.PdC in the centre of the wing disc.
Expression of pucScer\UAS.cMa under the control of Scer\GAL4elav-C155 suppresses the effect of co-expression of kayScer\UAS.cEa and JraScer\UAS.cEa (under the control of Scer\GAL4elav-C155) on bouton number and EJC amplitude (synaptic strength) at the larval neuromuscular junction.
Suppresses the extra wing vein phenotype of flies expressing rlSem.Scer\UAS under the control of Scer\GAL4455.2.
Xenogenetic Interactions
Statement
Reference
The aggressive tissue overgrowth observed in third instar larval wing discs carrying somatic (flip-out) clones simultaneously expressing Snr1HMS00363 and BacA\p35Scer\UAS.cHa driven by Scer\GAL4Act.PU is significantly suppressed by co-expression of pucScer\UAS.cMa.
Expression of pucScer\UAS.cMa enhances the reduction in eye size seen in both males and females when Zzzz\E4orf4Scer\UAS.cPa is expressed under the control of Scer\GAL4GMR.PF at any of 18[o]C, 24[o]C or 29[o]C.
Co-expression of pucScer\UAS.cMa significantly rescues the increase in cell death seen in the third larval instar eye disc of animals expressing Hsap\APPAβ42.Scer\UAS.cUa under the control of Scer\GAL4GMR.PU and also strongly rescues the neurodegenerative phenotype of the adult eye.
Inhibition of cell death, through co-expression of BacA\p35Scer\UAS.cHa and pucScer\UAS.cMa under the control of Scer\GAL4unspecified, only slightly rescues the wing growth defects seen in vgScer\UAS.cKa, Scer\GAL4unspecified flies.
Coexpression of pucScer\UAS.cMa and BacA\p35Scer\UAS.cHa, under the control of Scer\GAL4ey.PH, does not affect the eye. Coexpression of BacA\p35Scer\UAS.cHa and pucScer\UAS.cMa under the control of Scer\GAL4ey.PH rescues the ventral eye loss of L2/+ flies to a near wild-type eye in 69% of flies and pharate adults; this is a much greater suppression than that seen when either transgene is expressed without the other.
The eye neurodegeneration phenotype of Hsap\MJDQ78.Scer\UAS.T:Ivir\HA1; Scer\GAL4GMR.PF flies is not supressed by pucScer\UAS.cMa.
Complementation and Rescue Data
Comments
Expression of pucScer\UAS.cMa under the control of either Scer\GAL448Y or Scer\GAL4Gap1-NP3392 completely rescues the left-right asymmetry defects seen in the anterior midgut of pucGS16811 embryos. The defects in dorsal closure are not rescued. The lack of left-right asymmetry in the tilting of the nuclei of the circular visceral muscle which is seen in late stage 15 and 16 pucGS16811 embryos is rescued by expression of pucScer\UAS.cMa under the control of Scer\GAL4Gap1-NP3392. Expression of pucScer\UAS.cMa under the control of either Scer\GAL4dpp.PS or Scer\GAL4NP7020 does not rescue the left-right asymmetry defects seen in the anterior midgut of pucGS16811 embryos. Expression of pucScer\UAS.cMa under the control of Scer\GAL4hs.PU using heat shock for 30 minutes at 37[o]C significantly rescues the left-right asymmetry defects seen in the anterior midgut of pucGS16811 embryos when the heat shock is applied at any time during 4.5 to 9.5 AEL.
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
pucScer\UAS.cMa
pucUAS.cMa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Martin-Blanco
Secondary FlyBase IDs
    References (79)