FB2024_03 , released June 25, 2024
Allele: Dmel\fra1
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General Information
Symbol
Dmel\fra1
Species
D. melanogaster
Name
FlyBase ID
FBal0057436
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Caused by aberration
Cytology
Description
Mutations Mapped to the Genome
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Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
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Marker for
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Disease-implicated variant(s)
 
Phenotypic Data
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Additional Comments
Genetic Interactions
Statement
Reference

Approximately 68% of fra1/Df(2R)en-SFX31 double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Nearly all the segments are affected in these embryos. Approximately 91% of the axons that project through the posterior commissures of fra1/Df(2R)en-SFX31 transheterozygotes do not grow properly, whereas only 12% of the axonal projections through the anterior commissures are affected.

Approximately 60% of fra1/enE double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Nearly all the segments are affected in these embryos.

Approximately 60.5% of fra1/en54 double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Nearly all the segments are affected in these embryos.

Approximately 34% of fra1/inv30 double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Approximately 87% of the segments are affected in these embryos.

Approximately 49% of fra1/Df(2R)en-SFX31 double mutants are adult lethal.

Approximately 33% of fra1/en54 double mutants are adult lethal.

Approximately 15% of fra1/inv30 double mutants are adult lethal.

Expression of fraScer\UAS.cKa in the early stages of axon pathfinding under the control of Scer\GAL4prd.RG1 rescues axonal defects in even segments of fra1/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra1/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fraScer\UAS.cKa in later stages of development, under the control of Scer\GAL4elav.PLu does not rescue the the defects in ventral nerve cord architecture seen in fra1/Df(2R)en-SFX31 mutants.

Xenogenetic Interactions
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Complementation and Rescue Data
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Synonyms and Secondary IDs (1)
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    References (2)