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General Information
Symbol
Dmel\fra::robo1UAS.RF.Tag:MYC
Species
D. melanogaster
Name
FlyBase ID
FBal0098246
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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 fusion protein consisting of the extracellular, transmembrane and 67 amino acids of the cytoplasmic domain of robo1 fused to the entire cytoplasmic domain of fra. The protein is tagged at the C-terminal end with 6 Tag:MYC tags.

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 fra::roboScer\UAS.RF.T:Hsap\MYC with Scer\GAL4Cha.7.4 leads to a severe depletion or absence of cholinergic axons in the commissures, efficiently displacing cholinergic axon terminals out of the dorsal motor neuropile. Under these conditions contact of motorneuron dendrites with cholinergic interneuron terminals is severely reduced and potentially absent at 18.5 hours after egg laying, unlike in the wild-type; yet the overall organisation of the neuropile, including the distribution of Fas2-positive tracts, is not affected. Dendritic intermediate (MN-LL1) and lateral (MN-DA3) territories also remain distinct, though they appear more variable compared to controls.

Expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu results in longitudinal tracts crossing the midline in embryos.

Expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav-C155 results in Fas2-positive axon bundles ectopically crossing the midline in the embryonic central nervous system. The embryos have an average of 0.86 crossovers/segment, with an average of 9.3 defects/embryo. The penetrance of this phenotype is 100%.

Expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu results in axon guidance defects in the central nervous system and reduced viability.

When driven in the neurons by Scer\GAL4elav.PLu, fra::roboScer\UAS.RF.T:Hsap\MYC causes a robo-like phenotype; too many axons cross the midline, resulting in thick fuzzy commissures and thin longitudinal tracts. This phenotype becomes stronger with more copies of fra::roboScer\UAS.RF.T:Hsap\MYC and Scer\GAL4elav.PLu. At higher levels a phenotype is seen that is much stronger than seen in robo mutants and is approaching that seen in sli mutants; the CNS axons appear to have partially collapsed onto the midline. When driven by the pan-mesodermal Scer\GAL4 line Scer\GAL4how-24B, a number of phenotypes are seen. Muscle precursors are observed extending towards and across the midline. These cells also have abnormal morphology, sending out many long thin filopodia and flattened lamellipodial extensions towards the sli expressing midline, suggesting that they are now attracted to sli. Muscles at a distance from the midline develop quite normally.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Additional Comments
Genetic Interactions
Statement
Reference

The longitudinal tract phenotype of double mutant NetAunspecified NetBunspecified embryos is not altered by expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu.

Gef64CEP3035 dramatically enhances the axon guidance defects caused by expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu, leading to a significant increase in ectopic midline crossing.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
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
fra::robo1Scer\UAS.RF.T:Hsap\MYC
fra::robo1UAS.RF.Tag:MYC
fra::roboScer\UAS.RF.T:Hsap\MYC
Name Synonyms
Secondary FlyBase IDs
    References (5)