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General Information
Symbol
Dmel\robo31
Species
D. melanogaster
Name
FlyBase ID
FBal0121547
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Mutagen
    Nature of the Allele
    Mutagen
    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
    Nucleotide substitution: G?A. Mutation is in the splice acceptor site of the 6th intron.
    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
    robo31/robo31 MARCM clones (in Scer\GAL4fru-NP0021 neurons) develop a male-specific ipsilateral ectopic neurite in female brains at a low frequency (no effect in controls or mutant male clones).
    The adult sLNv neurons of robo31 homozygotes exhibit significantly longer axonal projections compared to controls.
    Examination of the optic lobes of homozygous robo31 mutants does not reveal any defects.
    robo31/Df(2L)Exel7006 embryos exhibit gonad compaction defects and germ cell ensheathment defects.
    In robo31 mutants, the intermediate Fas2-positive tract shifts towards the midline and joins the medial pathway. Thus, only two distinct Fas2-positive bundles (medial and lateral) are detectable in these embryos. The Scer\GAL4ap-md544-expressing axons are found in their wild-type position directly adjacent to the medial Fas2-tract.
    Homozygous embryos show a highly penetrant medial shift of the intermediate Fas2-positive longitudinal fascicle.
    46% of homozygous embryos hatch into first instar larvae, 29.5% of the embryos reach the pupal stage and 27.5% of the embryos eclose into adults.
    Homozygotes have have defects in the ellipsoid body. Homozygotes show defects in the mushroom body; 100% have the dorsal lobes close to the midline, 73% show crosswise projection of the γ fiber and 48% lack the median projection.
    robo31/robo31 DM2 glomerulus innervating neurons, produced by mitotic recombination in a robo31/+ background, often project to ectopic sites in the antennal lobes, rather than to the DM2 glomerulus. The erroneously placed terminals form large, irregular "glomerular-like" structures that do not correspond in shape or position to those previously identified in wild-type animals.
    In embryonic stage 16 robo31 mutants, the medial and intermediate axonal fascicles fuse, with some longitudinal glia lining up over the fused fascicles, whereas some remain laterally together with remaining lateral axons (100% penetrance).
    Homozygous larvae have no detectable defect in distal cell neuron positioning in the visual system.
    Homozygous embryos do not show defects in lch5 or dorsal cluster sensory axon growth.
    The ch neuron projections in robo31/+ embryos are normal. The ch neuron projections in homozygous robo31 embryos are shifted to the medial, rather than the intermediate longitudinal fascicle, as are most of the Fas2 fascicles. The dbd neuron projection is unchanged. When robo3Scer\UAS.cSa is expressed in the PNS by Scer\GAL412.1 in a robo31 mutant the medial fascicle is increased at the expense of the intermediate fascicle, as for robo31, but the ch neuron projections remain with the intermediate longitudinal fascicle.
    Axonal projections in the visual system are not disrupted in mutants. Homozygous embryos show defects in the arrangement of Fas2-expressing fascicles. The intermediate fascicle shifts medially to fuse with the medial fascicle in 98.8% of embryos. 25.2% of embryos show breaks in the lateral fascicle. The axons of the "Sema2b" neurons (which express the marker Btau\MAPTSema-2b.T:Hsap\MYC), but not the cell bodies, are shifted much closer to the midline in mutant embryos.
    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhanced by
    Statement
    Reference
    NOT Enhanced by
    Statement
    Reference
    robo3[+]/robo31, robo11 has neuroanatomy defective | recessive phenotype, non-enhanceable by capt10/capt[+]
    NOT Enhancer of
    Statement
    Reference
    robo31 is a non-enhancer of neuroanatomy defective phenotype of chb4, robo11
    NOT Suppressor of
    Other
    Phenotype Manifest In
    Enhanced by
    Statement
    Reference
    robo31 has chordotonal organ & embryo & nerve terminal phenotype, enhanceable by sli2/sli[+]
    NOT Enhanced by
    NOT Enhancer of
    NOT Suppressor of
    Other
    Additional Comments
    Genetic Interactions
    Statement
    Reference
    A robo31 genetic background does not affect the ability of ectopic Scer\GAL4ap-md544>leaScer\UAS.T:Ivir\HA1,T:SS-wg to force the Scer\GAL4ap-md544-expressing axons to extreme lateral positions. In robo31, robo1 double mutants, the intermediate Fas2-positive tract fuses with the medial tract, and this thick fascicle crosses the midline. As in robo1 mutants, the Scer\GAL4ap-md544-expressing axons follow this fascicle across the midline. The lateral Fas2-positive tract remains in robo31, robo1 double mutants. Ectopic Scer\GAL4ap-md544>leaScer\UAS.T:Ivir\HA1,T:SS-wg is able to direct the Scer\GAL4ap-md544-expressing axons to extreme lateral positions even in a robo31, robo1 mutant genetic background.
    Heterozygosity for robo31 does not enhance the frequency of axons ectopically crossing the midline that is seen in robo1 chb4 double heterozygous embryos.
    robo1 robo31 double mutant embryos do not show defects in the position of the vmd1a neuron of the ventral multidendritic neuron cluster in the abdomen; a single vmd1a neuron is seen in each hemisegment.
    The ch neurons in sli2/+ robo31/+ embryos frequently show abnormal projections.
    capt10 robo31 double heterozygotes show little if any midline crossing defects in the embryonic central nervous system. One copy of capt10 does not enhance the frequency of midline crossing defects seen in robo1 robo31 double mutant heterozygotes. The frequency of ectopic crossing of the midline by axons in the central nervous system seen in robounspecified robo31 embryos is increased by Abl2/+.
    robo1/robo31 show an embryonic nervous system that is merely additive.
    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Partially rescued by
    Comments
    Images (0)
    Mutant
    Wild-type
    Stocks (1)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (1)
    References (23)