FB2024_03 , released June 25, 2024
Allele: Dmel\fracΔ1
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General Information
Symbol
Dmel\fracΔ1
Species
D. melanogaster
Name
FlyBase ID
FBal0266870
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Imprecise excision of Mi{ET1}fracMB05690 results in a 1.2kb deletion, removing part of the first intron and second exon of the frac gene.

Mutations Mapped to the Genome
Curation Data
Type
Location
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Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
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Marker for
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Human Disease Associations
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Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

fracΔ1 mutants are viable and display no overt behavioral defects.

fracΔ1 mutants do not display defects in muscle size, number, or epidermal attachment.

fracΔ1 mutant embryos exhibit prominent axon guidance defects. Approximately 64% of ISNb axons in fracΔ1 mutant embryos do not stay tightly bundled and display targeting errors in which individual axons circle back or project to neighbouring nerve bundles. Further classification of these defects reveals that 51% of ISNb nerves display hypo-fasciculated or frayed axons, and 29% include axons that make connections with other nerve branches or other ISNb axons. Approximately 44% of ISNb nerves exhibit ectopic splintering of axons, and 22% display erroneous projections. The penetrance of ISNb guidance defects is not affected by maternal frac levels.

Approximately 49% of hemisegments in fracΔ1 contain axons that separate inappropriately and project ectopically. The majority of defects are hypo-fasciculation errors in which axons inappropriately branch away from SNa axons.

fracΔ1/Df(3L)pbl-X1 mutants exhibit the same guidance defects as fracΔ1 homozygotes.

External Data
Interactions
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Phenotype Manifest In
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Additional Comments
Genetic Interactions
Statement
Reference

Mmp2W307stop/+ ; fracΔ1/+ double heterozygotes exhibit elevated levels of ISNb and SNa guidance defects. The incidence of ISNb mis-projection rises from 1% and 2% in fracΔ1 and Mmp2W307stop single heterozygotes, respectively, to 18% in the double heterozygote.

A heterozygous Sema-1ak13702 background dominantly suppresses the ISNb pathfinding phenotypes from 64% in fracΔ1 homozygotes to 18% in double mutants.

A Df(2L)N22-5 background dominantly suppresses the ISNb pathfinding phenotypes from 64% in fracΔ1 homozygotes to 18% in double mutants.

A heterozygous beat-IaC163 background dominantly suppresses the ISNb pathfinding phenotypes from 64% in fracΔ1 homozygotes to 18% in double mutants.

A homozygous fracΔ1 mutant background suppresses the excess fasciculation seen in embryos ove-rexpressing Mmp2Scer\UAS.cPa under the control of Scer\GAL4repo.PU. Furthermore, these embryos display diminished motor axon bundling similar to that observed in fracΔ1 homozygotes.

Pan-neuronal expression of saxQ263D.Scer\UAS.T:Ivir\HA1 reduces the incidence of defasciculation from 64% to 30% in fracΔ1 mutants.

The ISNb of LIMK1EY08757; fracΔ1 double heterozygous mutant embryos is defasciculated and has ectopic projections. These double mutants display an increase in mis-projections relative to either heterozygote alone.

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