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General Information
Symbol
Dmel\robo13
Species
D. melanogaster
Name
FlyBase ID
FBal0032590
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
roboZ14
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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
In embryonic stage 16 robo3 mutants, the medial axonal fascicle misroutes across the midline, whereas the intermediate and lateral fascicles extend laterally, some longitudinal glia migrate over the midline whereas some retain their lateral positions (100% penetrance). In robo3 embryos the pCC/vMP2 fascicle is affected, collapsing over the midline (100% penetrance). In robo3 mutants at stage 12.1 only the dMP2/MP1 fascicle extends along its normal trajectory (with 27.7% penetrance) and curves medially slightly more than in wild-type only at the most posterior end. At stage 14, the vMP2/pCC fascicle is always collapsed over the midline in robo3, but the dMP2/MP1 fascicle can form normally.
Fas2-expressing axons are seen crossing back and forth across the midline in homozygous embryos, in contrast to wild type. Heterozygous embryos show only extremely rare midline crossing defects.
Some, but not all, interface glia migrate over the CNS midline. Longitudinal connectives are somewhat closer to the midline than in wild type, and the pCC/MP2 fascicle may cross the midline. Expression of roboScer\UAS.cKa driven by Scer\GAL4s.gcm rescues the lateral positions of the glia but does not rescue the axonal misrouting across the midline of robo3 mutants.
Fas2 positive neurons, including the pCC, cross the midline in robo3 embryos.
"Fuzzy commisure" phenotype in embryonic central nervous system.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Enhancer of
Statement
Reference
robo[+]/robo13 is an enhancer of neuroanatomy defective phenotype of lolaORE120
Phenotype Manifest In
Enhanced by
Enhancer of
Statement
Reference
robo13 is an enhancer of vMP2 neuron phenotype of gcmΔP1
robo13 is an enhancer of MP1 neuron phenotype of gcmΔP1
robo13 is an enhancer of dMP2 neuron phenotype of gcmΔP1
robo13 is an enhancer of fascicle phenotype of gcmΔP1
robo13 is an enhancer of pCC neuron phenotype of gcmΔP1
robo[+]/robo13 is an enhancer of longitudinal connective phenotype of lolaORE120
Additional Comments
Genetic Interactions
Statement
Reference
In gcmΔP1 robo3 double mutants, some embryonic central nervous system Fas2-positive fascicles collapse across the midline, with full collapse observed in 12.5% of cases and collapse from one side of the embryo (i.e. one hemisegment) in 22.6% of cases. This phenotype is never observed in either mutant alone. In gcmΔP1 robo3 double mutants, 31% of Fas2-positive axons also misroute towards the muscle, which is a phenotype observed with less frequency in gcm mutants. In gcmΔP1 robo3 double mutant stage 12.1 embryos both dMP2/MP1 and vMP2/pCC fascicles are affected, as the vMP2/pCC fascicle collapses completely over the midline (100% penetrance) and the dMP2/MP1 fascicle either does not extend or misroutes towards the muscle (89%). In gcmΔP1 robo3 double mutant stage 14 embryos there is a synergistic effect on both fascicles: the vMP2/pCC fascicle is completely collapsed over the midline (96% penetrance) and the dMP2/MP1 fascicle is missing (97% penetrance). The effect of glial loss is in severe gcmΔP1 robo3 double mutant embryos in which the longitudinal fascicles either collapse along the midline (63.3% penetrance when visualised with Avic\GFPScer\UAS.T:Hsap\Myr2) or misroute severely towards the periphery and exit the central nervous system (13.3% penetrance when visualised with Avic\GFPScer\UAS.T:Hsap\Myr2). However, when MP2 axons in these embryos misexpress leaScer\UAS.T:Hsap\MYC, under the control of Scer\GAL415J2, in the MP2 neurons, they do not extend longitudinally. Instead, they either do not grow (36.6% penetrance) and remain stunted at the base of the commissures, or they leave the central nervous system and misroute towards the muscle (30.7% penetrance). Ectopic expression of leaScer\UAS.T:Hsap\MYC under the control of Scer\GAL415J2 in a robo3 mutant embryo can displace Fas2-positive axons laterally and longitudinally.
93% of lolaORE120 robo3/lolaORE120 embryos show Fas2-expressing axons crossing the midline. There are an average of 4.4 crossovers per affected embryo.
Df(2L)ast2 robo3 double heterozygotes show little if any midline crossing defects in the embryonic central nervous system.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
The axon guidance phenotype is rescued in all segments by roboScer\UAS.cKa expressed under the control of Scer\GAL4elav.PLu. The pCC axon phenotype is also rescued by roboScer\UAS.cKa expressed under the control of Scer\GAL4ftz.ng.
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Induced on: Fas3 null chromosome.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (7)