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General Information
Symbol
Dmel\tkvQ253D.UAS.cNb
Species
D. melanogaster
Name
FlyBase ID
FBal0050626
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-tkvQD, UAS-tkvQ253D, TkvQD, UAS-tkv*, UAS-tkvQ253D, UAS-tkvQD, tkvQ253D, UAS-tkvDN, UAS-tkvA
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
UAS regulatory sequences drive expression of a constitutively active form of tkv (carries the amino acid replacement Q253D).
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
Expressing tkvQ253D.UAS.cNb under the control of Scer\GAL4btl.PS leads to defects in the formation of the dorsal trunk of the tracheal system.
The expression of tkvQ253D.UAS.cNb under the control of Scer\GAL4ppk.PG does not lead to any obvious third instar larval C4da neuron morphology defects, as compared to controls.
Expression of tkvQ253D.Scer\UAS.cNb in Pdf-positive neurons, under the control of Scer\GAL4P2.4.Pdf does not affect circadian rhythm.
Mutant wing disc clones expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4tub.PU do not show neoplastic transformation.
Expression oftkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4n-syb.PS does not result in neuromuscular junction overgrowth in third instar larvae.
Histoblasts expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4Scer\FRT.Act5C (initiated by heat-shock) show an increased predisposition to associate with the periphery of a histoblast nest edge. Histoblasts undergo dramatic morphogenetic changes and become extremely motile and progressively replace wild-type cells at the periphery to occupy leading positions. No affect on histoblast proliferation is observed. Larval epidermal cells expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4Scer\FRT.Act5C (initiated by heat-shock) display slower delamination compared to wild-type larval epidermal cells.
tkvQ253D.Scer\UAS.cNb expression, driven by Scer\GAL4e22c induces ectopic wing vein cells. Expression of tkvQ253D.Scer\UAS.cNb after a 20 minute heat-shock at 37[o]C at 18h APF, under the control of Scer\GAL4hs.PB, results in the formation of ectopic vein cells.
Anterior overexpression of tkvQ253D.Scer\UAS.cNb by Scer\GAL4dpp.blk1 leads to ectopic apical fold formation along the anteroposterior boundary of the larval wing pouch. In the early pupal stage (5 hours after puparium formation), a small gap develops along the A/P boundary at the distal tip of the wing. By this time, A and P cells are already completely separated and form two smooth apical surfaces. This may lead to the extensive cleft between A and P compartments that forms later in pupal development and which in the adult can lead to a complete separation of anterior and posterior wing blades. In cleft wings caused by posterior bi reduction the posterior wing fragment is characteristically shorter than the anterior fragment.
Expression of tkvQ253D.Scer\UAS.cNb using Scer\GAL4salm-459.2 modifies wing size, the pattern of veins and the integrity of the wing. Expression of tkvQ253D.Scer\UAS.cNb using Scer\GAL4nub-AC-62 causes the differentiation of most wing cells as vein tissue.
Expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4GMR.PF results in large eyes with patterning defects. The ommatidia in these eyes are larger than normal.
Expression of tkvQ253D.Scer\UAS.cNb in the peripheral amnioserosa (under the control of Scer\GAL4pAS) does not affect dorsal closure, which progresses normally with a smooth outer edge of pAS and with internal AS cells being removed over the normal time course. Following completion of dorsal closure, pAS remains associated with the dorsal epidermis, which is subsequently delayed entry into apoptosis.
Expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4dpp.blk1 results in a 20.8% penetrant bifurcated wing blade phenotype.
Overexpression of tkvQ253D.Scer\UAS.cNb driven by Scer\GAL4dpp.blk1 in the AP boundary in wild-type wing discs causes mild cleft formation. In adults, defects are seen in the anterior crossvein, otherwise the wing blade is normal.
The wing discs of third instar tkvQ253D.Scer\UAS.cNb; Scer\GAL4nub-AC-62 larvae have an enlarged wing pouch. The resulting flies have enlarged, poorly patterned wings.
Expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 results in accumulation of early germ cell clusters in the testis. Freshly eclosed males show signs of massive cell death in the more distal regions of the testes, while in testes of older males, often only dead or dying tissue is detected. The somatic hub is expanded compared to wild type in larval and adult testes of males expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.
Flies expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4cad-em459 lack both analia and genitalia.
Germ line clones in the testis expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4Act5C.PI overproliferate.
tkvQ253D.Scer\UAS.cNb; Scer\GAL4vg.int2.1 flies exhibit distortion, notching and changes in bristle morphology at the anterior wing margin and supression of wing vein L5 formation.
Large mutant clones are rarely induced in wing discs.
When expression is driven by Scer\GAL4prd.RG1 embryos are dorsalized.
Embryos expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL469B show partial dorsalisation of their cuticles.
Expression driven by Scer\GAL4btl.PS in a wild type background produces an extra fusion cell per tracheal branch.
Stage 11 embryos expressing tkvQ253D.Scer\UAS.cNb under the control of both Scer\GAL4how-24B and Scer\GAL4twi.PG have enlarged clusters of pericardial cell progenitors; each cluster contains approximately 8-10 eve-expressing cells (e-PCs) compared to 3-4 cells per cluster in wild-type embryos. The number of e-PCs decreases to a normal level during early stage 12. Ectopic heart progenitors are produced in the ventrolateral areas of the mesoderm, although the dorsal vessel develops essentially normally without any increase in cell number.
Scer\GAL469B-mediated expression creates dorsalised embryos that undergo normal dorsal closure. Scer\GAL469B-mediated expression in Df(2L)flp147E embryos causes a partially dorsalised phenotype and partial rescue of the dorsal closure phenotype.
When expression is driven by Scer\GAL4vg.PM, outgrowth of wing tissue results.
Scer\GAL4btl.PS-mediated expression causes many cells to move to the dorsal side of the embryo such that dorsal branches of the tracheal system (consisting of 5 to 7 cells in wild type embryos) consist of 25 cells.
Expression with Scer\GAL469B causes strong dorsalisation of the embryo. Expression with Scer\GAL4C-765 results in large overproliferating discs.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference
Co-expression of tkvQ253D.Scer\UAS.cNb and saxQ263D.Scer\UAS.T:Ivir\HA1 in Pdf-positive neurons, under the control of Scer\GAL4P2.4.Pdf results in a long period phenotype.
Expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4tub.PU in l(2)gl4 mutant wing disc mutant clones results in overproliferation and neoplastic transformation in the proximal domain. Clones in the distal domain are eliminated, even when the growth temperature is elevated.
Expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4Act.PU in Df(2L)cbtS14 clones does not rescue the low cell viability seen in single mutant Df(2L)cbtS14 clones.
Expression of tkvQ253D.Scer\UAS.cNb in motor neurons (under the control of Scer\GAL4OK6) rescues bouton number and EJP phenotypes in Ranbp1170 mutants, although mEJP frequency is not rescued. Expression of tkvQ253D.Scer\UAS.cNb in muscle (under the control of Scer\GAL4G14) does not rescue bouton number or mEJP and EJP phenotypes in Ranbp1170 mutants.
Expression of tkvQ253D.Scer\UAS.cNb enhances the neuromuscular junction overgrowth phenotype seen in nwk1 third instar larvae.
Expression of tkvQ253D.Scer\UAS.cNb under the control of either Scer\GAL4e22c, Scer\GAL4332.3 or Scer\GAL4T80 results in nearly completely penetrant rescue of the dorsal closure defects of Sec61α1 homozygous embryos.
Coexpression of tkvQ253D.Scer\UAS.cNb with EgfrDN.Scer\UAS, under the control of Scer\GAL4e22c, not only fails to induce ectopic vein cells, but also inhibits endogenous vein formation, suggesting that activation of the dpp pathway alone is not sufficient for vein differentiation. Coexpression of tkvQ253D.Scer\UAS.cNb with EgfrDN.Scer\UAS after a 20 minute heat-shock at 37[o]C at 18h APF, under the control of Scer\GAL4hs.PB, not only fails to induce ectopic vein cells, but also inhibits endogenous vein formation.
Co-expression of SnooM67 rescues the wing phenotypes caused by Scer\GAL4salm-459.2- or Scer\GAL4nub-AC-62-mediated expression of tkvQ253D.Scer\UAS.cNb.
Co-expression of SnooEP2510 completely suppresses both the overgrowth and patterning defects seen in the eyes of flies expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4GMR.PF.
The bifurcation of the wing caused by expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4dpp.blk1 is completely suppressed by co-expression of nmoScer\UAS.cUa, although wild-type wing morphology is not completely restored. The penetrance of the bifurcated wing phenotype caused by expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4dpp.blk1 is enhanced by nmoP1/+ from 20.8% to 86.3%.
Overexpression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4dpp.blk1 in coroex6 and coroex11 heterozygous backgrounds causes a severe cleft phenotype with 85% penetrance along the AP boundary of the wing disc (as compared to mild cleft formation in tkvQ253D.Scer\UAS.cNb mutants). The enhancement is more pronounced in adult wing blades.
Overexpression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4dpp.blk1 in coroex6 and coroex11 heterozygous backgrounds causes a severe cleft phenotype with 85% penetrance along the AP boundary of the wing disc. Enhancement is more pronounced in adult wing blades.
Enlargement of wings in tkvQ253D.Scer\UAS.cNb; Scer\GAL4nub-AC-62 flies is suppressed by brkScer\UAS.cJa.
Co-expression of armΔ.Scer\UAS.T:Ivir\HA1 and tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4ey.PH in the eye disc often results in ectopic morphogenetic furrow formation from the anterior margin of the disc and a reduction in posterior differentiation.
The cuticle phenotype of embryos expressing tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL469B is not altered if they are derived from homozygous shark1 female germ-line clones (and fertilised by a shark+ sperm). The dorsal closure defects of homozygous shark1 embryos derived from shark1 female germline clones are not rescued by expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL469B.
Expression driven by Scer\GAL4btl.PS in a Nl1N-ts1 background further increases the number of fusion cells.
Flies expressing wgScer\UAS.cAa under the control of Scer\GAL4ey.PH do not show photoreceptor development at the posterior of the eye disc. This phenotype is not rescued if the flies are also co-expressing tkvQ253D.Scer\UAS.cNb. Clones expressing armΔ.Scer\UAS.T:Ivir\HA1 in the eye disc under the control of Scer\GAL4Act5C.PP do not show photoreceptor differentiation within the clone. This phenotype is not rescued if the clones are also co-expressing tkvQ253D.Scer\UAS.cNb. eyg1/Df(3L)iro-2 hemizygous eye discs completely lack photoreceptors. Photoreceptor development in these discs is not rescued by tkvQ253D.Scer\UAS.cNb expressed under the control of Scer\GAL4dpp.PH. The lack of photoreceptor phenotype of eya1 eye discs is not rescued by tkvQ253D.Scer\UAS.cNb expressed under the control of Scer\GAL4ey.PH.
Partially rescues the dorsal open phenotype of msn102/msn172 embryos when expressed under the control of Scer\GAL469B.
DadScer\UAS.cTa suppresses the wing outgrowth phenotype of tkvQ253D.Scer\UAS.cNb driven by Scer\GAL4vg.PM, resulting in an almost wild type wing.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
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Mutant
Wild-type
Stocks (1)
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Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (79)