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General Information
Symbol
Dmel\fraUAS.cKa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Kolodziej
FlyBase ID
FBal0057431
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-fra, UAS-Frazzled, UAS-Frawt
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of a EcoRI-XbaI cDNA fragment containing nucleotides 1-5038 from the shorter isoform of fra.

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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expression of fraScer\UAS.cKa in all R cells (using Scer\GAL4GMR.long as a driver) does not result in the redirection of R7 axons to the M3 layer, with many R8 axons remaining in the temporary layer.

Expression of fraScer\UAS.cKa in a wild-type background n MN-LL1 neurons under the control of Scer\GAL4eve.CQ2 leads to a greater proportion of dendritic branches innervating the intermediate neuropile. MN-DA3 expression of fraScer\UAS.cKa leads to ectopic innervation of the intermediate neuropile in 50% of cases, converting the dendritic arbor to a MN-LL1-like morphology. Overexpression in MN-LL1 or MN-DA3 does not lead to ectopic midline targeting of dendrites.

Ventral nerve cord axon bundles of stage 16 embryos overexpressing fraScer\UAS.cKa via Scer\GAL4ftz.ng do not display any incorrect midline crossing.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4elav.PLu does not result in any axon guidance defects in embryos.

Expression of fraScer\UAS.cKa in the salivary gland, driven by Scer\GAL4prd.RG1, causes 75% of glands to aberrantly curve medially.

Embryos expressing fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng develop normally.

Scer\GAL41407 induced expression fails to cause defects in the CNS or PNS projections, viable adult flies are recovered.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

The expression of fraScer\UAS.cKa under the control of Scer\GAL4Mef2.247 partially suppresses only the reduced filopodial and lamellopodial activities, but not the reduced migration velocity, observed in robo11 homozygous embryonic heart cardioblasts; this expression also does not suppress the associated heart lumen formation defects observed in robo11 homozygotes.

Overexpression of fraScer\UAS.cKa under the control of Scer\GAL4ppk.1.9 significantly suppresses the Trim946 midline crossing defects.

Re-expression of fraScer\UAS.cKa in fra3/fra4 mutants reverts the phenotype back to that seen when AblScer\UAS.cHa is expressed alone under the control of Scer\GAL4insc-Mz1407 : normal anterior and posterior commissure formation.

Co-expression of fraScer\UAS.cKa with Rac1V12.Scer\UAS under the control of Scer\GAL4ftz.ng results in a strong synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1V12.Scer\UAS-overexpression alone.

The frequency of crossovers across the midline in embryos expressing Rho1V14.Scer\UAS driven by Scer\GAL4ftz.ng is significantly increased by co-expression of fraScer\UAS.cKa.

Co-expression of sqhT20A.S21A.Scer\UAS under the control of Scer\GAL4ftz.ng suppresses the midline crossing phenotype in embryos expressing both Rho1V14.Scer\UAS and fraScer\UAS.cKa.

Ventral nerve cord axon bundles of stage 16 embryos overexpressing fraScer\UAS.cKa via Scer\GAL4ftz.ng in a heterozygous Abl4 genetic background display few incorrect midline crossings.

Expression of fraScer\UAS.cKa in the early stages of axon pathfinding under the control of Scer\GAL4prd.RG1 rescues axonal defects in even segments of fra1/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra1/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fraScer\UAS.cKa in later stages of development, under the control of Scer\GAL4elav.PLu does not rescue the the defects in ventral nerve cord architecture seen in fra1/Df(2R)en-SFX31 mutants.

Overexpression of fraScer\UAS.cKa under the control of Scer\GAL4prd.RG1 does not suppress the abnormal pathfinding phenotype observed in Df(2R)en-SFX31 mutants.

Expression of fraScer\UAS.cKa in the early stages of axon pathfinding under the control of Scer\GAL4prd.RG1 rescues axonal defects in even segments of fra1/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra1/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fraScer\UAS.cKa in later stages of development, under the control of Scer\GAL4elav.PLu does not rescue the the defects in ventral nerve cord architecture seen in fra1/Df(2R)en-SFX31 mutants.

Expression of fraScer\UAS.cKa in elav5 mutant EW and EG neurons (under the control of Scer\GAL4eg-Mz360) does not modify the proportion of contralateral projection defects in elav5 mutant embryos. For example, EW axons fail to cross the midline in 755 of the neuromeres in such embryos.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4elav.PLu does not enhance the sliE-158 longitudinal tract phenotype.

Xenogenetic Interactions
Statement
Reference

Re-expression of fraScer\UAS.cKa in fra3/fra4 mutants reverts the phenotype back to that seen when Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is expressed alone under the control of Scer\GAL4insc-Mz1407 : fuzzy commissures.

fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraScer\UAS.cKa is co-expressed.

Co-expression of fraScer\UAS.cKa with Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng increases the frequency of axonal midline crossing abnormalities.

Heterozygous Abl4 almost completely suppresses the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.

Homozygous Abl4 enhances the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.

The frequency of neuronal crossover projections induced by Scer\GAL4ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is significantly increased by co-expression of fraScer\UAS.cKa.

The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is enhanced by coexpression of fraScer\UAS.cKa.

Complementation and Rescue Data
Comments

The expression of fraScer\UAS.cKa under the control of Scer\GAL4Mef2.247 rescues the fra3 homozygous embryonic heart cardioblast defects (i.e. migration velocity and in filopodial and lamellopodial extensions and activities) and embryonic heart lumen formation defects.

Expression of fraScer\UAS.cKa in C4da neurons under the control of Scer\GAL4ppk.PG partially rescues the axonal defects seen in fra3/fra4 mutants.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4gcm.PU rescues the defects in interface glial cell migration seen in fra3/fra4 embryos.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4MZ1580 weakly rescues the defects in interface glial cell migration seen in fra3/fra4 embryos.

The defects in interface glial cell migration seen in fra3/fra4 embryos are not rescued by expression of fraScer\UAS.cKa under the control of any one of Scer\GAL4repo, Scer\GAL4pros.PMG, Scer\GAL4elav.PU or Scer\GAL4Mz605.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4eve.CQ2 rescues dendritic targeting to the midline in fra3/fra4 mutant MN-VO4-6 and MN-VO4/5 neurons.

Expression of fraScer\UAS.cKa under the control of Scer\GAL4eve.CQ2 selectively in MN-LL1 neurons in fra3/fra4 mutant embryos efficiently rescues dendritic targeting to the intermediate neuropile. Moreover, this manipulation leads to a greater proportion of dendritic branches innervating the intermediate neuropile.

Expression of fraScer\UAS.cKa under the control of Scer\GAL415J2 does not rescue the dMP2 axonal phenotype of fra3/fra4 embryos. Expression of fraScer\UAS.cKa under the control of Scer\GAL4605 does rescue the dMP2 axonal phenotype of fra3/fra4 embryos.

Scer\GAL41407 induced expression in fra3/fra4 embryos rescues the commissure phenotype, commissures form normally in abdominal segments A1-A7. ISN motor axons also innervate their targets at near wild type levels. Scer\GAL4how-24B induced expression in fra3/fra4 embryos fails to rescue the ISN motor axon defects.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
fraScer\UAS.cKa
fraUAS.cKa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Kolodziej
Secondary FlyBase IDs
    References (18)