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General Information
Symbol
Dmel\Abl::Hsap\ABL1::Hsap\BCRP210.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0095897
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Bcr-Abl, U-BcrAbl
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 chimeric construct consisting of Hsap\BCR exons 1 to 3 (encoding 927 amino acids), Hsap\ABL1 exon 2 and the first 204 codons of Hsap\ABL1 exon 3 and Abl sequence from codon 47 to the C-terminal end of the Abl protein.

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

Ectopic expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4ppk.PG causes a robust presynaptic terminal overgrowth and significantly increases the number of connectives in class IV dendritic arborizing neurons in third instar larvae compared to controls.

Expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in embryos results in fuzzy commissures, a defect caused by extra axons crossing the midline.

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4insc-Mz1407 causes multiple Fas2-positive axon bundles to ectopically cross the midline in most segments of nearly all embryos examined.

Stage 16 embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS driven by Scer\GAL4ftz.ng display axon bundles that cross the midline inappropriately.

Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, causes a strong increase in axonal extension and arborization of the sLNv.

Limiting expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS to primarily pCC/MP2 neurons using Scer\GAL4ftz.ng is sufficient to induce on average three to four Fas2-positive axons to cross the midline incorrectly in all embryos examined.

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4elav.PLu results in axonal midline-crossing abnormalities.

Embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL431 have defects in the central nervous system (CNS); the longitudinal and commissural axons are less tightly bundled than normal and increased numbers of axons exit the CNS from the longitudinal tracts. Flies expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4hs.2sev are viable and fertile and have a severe rough eye phenotype; the eyes are small and bar-shaped with a large reduction in the number of ommatidial facets. The facets are abnormally shaped and vary in size. Multiple misplaced mechanosensory bristles and lens defects are seen. The ommatidia lack one or more retinal cells and/or have elongated or fused rhabdomeres or retinal cells. The secondary and tertiary pigment cells are disorganised.

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

The lethality of Abl1/Df(3L)st-j7 is rescued by Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS expressed under the control of Scer\GAL431. The rescued flies are variably fertile and have rough eyes. The lethality of Abl1/NrtM2 Df(3L)st-j7 is partially rescued by Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS expressed under the control of Scer\GAL431. The rescued flies are fertile and have rough eyes.

Xenogenetic Interactions
Statement
Reference

Over-expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4insc-Mz1407 enhances the degree of thinning and missing posterior commissures in fra3/fra4 embryos, and many anterior commissures disappear. Large bundles of axons are observed ectopically exiting the central nervous system (CNS), often extending beyond the CNS/PNS boundary. The anterior commissures, which are virtually unaffected in fra3/fra4 embryos, are thin or missing in 41% of segments.

Fuzzy commissures remain evident in heterozygous fra3 embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4insc-Mz1407.

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.

In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP1.Scer\UAS is able tor revert the commissure loss seen in fra3/fra4 mutants. These mutants display fuzzy commissures.

In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP2.Scer\UAS is able tor revert the commissure loss seen in fra3/fra4 mutants. These mutants display fuzzy commissures.

In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP3.Scer\UAS restores commissure formation in fra3/fra4 mutants. The frequency of fuzzy commissures is also significantly reduced.

fra3/fra4 significantly reduces the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS.

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.

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 fraΔP1.Scer\UAS is co-expressed.

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 fraΔP2.Scer\UAS is co-expressed.

fra3/fra4 significantly reduces the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP3.Scer\UAS is co-expressed.

Nearly a third of hemi-segments in fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).

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 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 fraΔP1.Scer\UAS.

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 fraΔP2.Scer\UAS.

The frequency of neuronal crossover projections induced by Scer\GAL4ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is not significantly increased by co-expression of fraΔP3.Scer\UAS.

Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, in a Appld background still induces the axonal arborization phenotype that occurs when the transgene is expressed in a wild-type background.

Compared with heterozygous robo1 mutants alone, expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4ftz.ng enhances the frequency of abnormal axonal crossovers. Almost every segment of every robo1/+ embryo expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS exhibits abnormal crossovers.

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in heterozygous sli1 mutants results in a collapse of the longitudinal connectives towards the midline.

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.

Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in a subset of neurons under the control of Scer\GAL4ftz.ng partially suppresses the comm1 commissure phenotype.

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

The part of the chimeric construct derived from human sequences corresponds to the P210 BCR-ABL1 fusion protein found in chronic myelogenous leukemia.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS
Abl::Hsap\ABL1::Hsap\BCRP210.UAS
Name Synonyms
Secondary FlyBase IDs
    References (7)