FB2025_01 , released February 20, 2025
Allele: Dmel\robo2X123
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General Information
Symbol
Dmel\robo2X123
Species
D. melanogaster
Name
FlyBase ID
FBal0123720
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
robo2123
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Allele class
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    DNA sequence
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    Expression Data
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    Phenotypic Data
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    robo2X123/robo2x135 embryos have a mildly disorganised acon scaffold in the central nervous system, but do not show defects in crossing of the midline by EW neurons.

    leaX123 embryos show much milder defects compared to robo4, leaX123 double mutant embryos: 29% of leaX123 embryos have one or more pericardial cells that migrate too far dorsally and are found closer to the dorsal midline in front of the rows of cardioblasts. leaX123 embryos also occasionally display alignment defects in the rows of cardioblasts, although gaps between cardioblasts are not apparent.

    Ventral nerve cords from stage 16 leaX123/leaX123 embryos show a random loss of ability to take up serotonin in approximately half of hemisegments. The cell bodies of serotonergic neurons in the ventral nerve cord of stage 16 leaX123/leaX123 embryos are shifted towards the midline compared to wild-type.

    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.

    Homozygous larvae have no detectable defect in distal cell neuron positioning in the visual system.

    External Data
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    Phenotypic Class
    Enhancer of
    Statement
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    Phenotype Manifest In
    Enhanced by
    NOT Enhanced by
    Statement
    Reference

    robo2X123 has serotonin neuron & ventral nerve cord phenotype, non-enhanceable by egMz360/egMz360

    Suppressed by
    Statement
    Reference

    robo2X123 has serotonin neuron & ventral nerve cord phenotype, suppressible by egUAS.cDa/Scer\GAL4eg-Mz360

    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    Statement
    Reference

    robo2X123/robo2X123 is a non-enhancer of serotonin neuron & ventral nerve cord phenotype of egMz360

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    Genetic Interactions
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    In robo11, robo2X123 double mutant stage 17 embryos, the testes often exhibit dispersed aggregates of germline niche cells, unlike the single anterior niche position in controls.

    robo2X123/robo2x135 strongly enhances the midline crossing defects seen in fra3/fra4 embryos: approximately 70% of EW neurons fail to cross the midline in the double mutant embryos.

    Embryos mutant for both robo4 and leaX123 show defects in cardioblast and pericardial cell positioning and alignment, similar to slit2 embryos. The number of cardioblast nuclei that reach the dorsal midline in these embryos is approximately 86.2, compared to approximately 104 in wild type embryos.

    Embryos expressing leaScer\UAS.cSa under the control of Scer\GAL4Mef2.PR in a robo4, leaX123 double mutant background display gaps in rows of cardioblasts indicating a loss of adhesion between cardioblasts (as seen in robo4, leaX123 double mutants) as well as the mispositioning of these cells away from the dorsal midline (as seen in leaScer\UAS.cSa, Scer\GAL4Mef2.PR embryos).

    Embryos expressing leaScer\UAS.cSa under the control of Scer\GAL4Mef2.PR in a robo4, leaX123 double mutant background exhibit mispositioning of cardioblasts away from the dorsal midline which is more severe as compared to expression of leaScer\UAS.cSa using Scer\GAL4Mef2.PR in an otherwise wild type background; cardioblasts are displaced even more laterally, with cardioblasts and pericardial cells even being observed in somatic muscle territory.

    In the ventral nerve cords of stage 16 leaX123/leaX123 embryos, the number of hemisegments showing loss of ability to take up serotonin is not significantly increased by egMz360/egMz360. The loss of serotonin uptake activity and the serotonergic axon guidance phenotypes of leaX123/leaX123 embryos are suppressed by egScer\UAS.cDa; Scer\GAL4eg-Mz360.

    robo1 leaX123 double mutant embryos show defects in the position of the vmd1a neuron of the ventral multidendritic neuron cluster in the abdomen; in 21% of segments loss of the vmd1a neuron in a hemisegment is associated with duplication of the vmd1a neuron in the contralateral hemisegment. In addition, in 36% of segments, some vmd1a neurons are missing from the ventral vmd clusters (in most of these segments, the missing md neurons are probably located near the midline).

    87% of segments show crossing of the midline by muscles 6/7 in robo1 leaX123 double mutant embryos. This defect is rescued by expression of roboScer\UAS.cKa under the control of Scer\GAL4how-24B, but the axonal phenotype of these embryos is mutant. 1% of segments show crossing of the midline by muscles 6/7, 5% show abnormal insertion of muscle 5 and 3% show abnormal insertion of muscles 6/7 in sli2 leaX123 double mutant embryos. 15% of segments show crossing of the midline by muscles 6/7, 31% show abnormal insertion of muscle 5 and 16% show abnormal insertion of muscles 6/7 in sli2 robo1 leaX123 triple mutant embryos.

    Muscles 6 and 7 cross the midline in most segments in robo1 leaX123 double mutant embryos.

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    Synonyms and Secondary IDs (4)
    References (14)