FB2024_03 , released June 25, 2024
Allele: Dmel\chic05205a
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General Information
Symbol
Dmel\chic05205a
Species
D. melanogaster
Name
FlyBase ID
FBal0095483
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
chic05205
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Associated Insertion(s)
Cytology
Description

P{PZ} insertion 3.2kb downstream of the start of exon 1, within intron 3.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
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Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

In contrast to wild type, single chic05205a γ neurons (generated via MARCM) fail to properly extend their axons in the adult.

Mean filopodium length is reduced compared to wild type in cultured primary neurons derived from chic221/chic05205a and chic05205a/Df(2L)GpdhA embryos.

chic05205a/Df(2L)GpdhA embryos show stalling of motor axons compared to wild type.

Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects.

In mutant columnar follicle cells, levels of F-actin are markedly decreased at all cortices, although actin filaments are lost preferentially from the basal cortex.

Axon growth from homozygous dissected nerve cords cultured in vitro is reduced compared to wild-type. ISNb axons innervate proximal targets (muscles 6 and 7) and extend to contact muscle 13, but fail to reach the distal target (muscle 12) in hemizygous embryos. chic05205a/chic221 embryos show mild defects in the Fas2-positive longitudinal fascicles of the central nervous system.

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

Cultured primary neurons derived from chic05205a/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.

Ectopic actin filaments do not form in capt10 chic05205a double mutant follicle cell clones, and the level of F-actin in these cells appears to be similar to that in chic05205a single mutant cells. Cells in capt10 chic05205a double mutant follicle cell clones lose their columnar morphology and collapse, forming a thin squamous-like layer of cells. These clones can interfere with the migration of wild-type portions of the follicle cell epithelium. The double mutant clones maintain extensive contacts with adjacent wild-type cells.

The severity of the central nervous system defects of chic05205a/chic221 embryos is enhanced by Abl2/+ and further enhanced by Abl2/Abl4.

Xenogenetic Interactions
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Reference
Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (9)