FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\cpa69E
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General Information
Symbol
Dmel\cpa69E
Species
D. melanogaster
Name
FlyBase ID
FBal0193693
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid replacement: ?180term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

C21058738T

Amino acid change:

Q180term | cpa-PA

Reported amino acid change:

?180term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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 ( 1 )
Disease
Evidence
References
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

Cultured primary neurons derived from mutant embryos show a significant increase in the number of filopodia compared to control neurons.

Early development of egg chambers in females containing homozygous germline clones is relatively normal; mutant germ cells form 16-cell cysts, are encapsulated by follicle cells relatively normally and initially grow in size at a rate relatively similar to wild type. However, as they reach stage 6, mutant egg chambers become morphologically abnormal, taking on a spindle shape. The egg chambers cease increasing in size at this point and ultimately degenerate. Overall actin levels are relatively normal through stage 6/7 in the mutant egg chambers and ring canals appear to form normally.

73% of egg chambers in females containing homozygous germline clones do not contain a properly differentiate oocyte, instead having 16 nuclei that are all larger than that expected for the oocyte (32% of these egg chambers have 16 nuclei equal in size, while 68% have one nucleus that is smaller than the others, but not as small as a normal oocyte nucleus). The oocyte is not precisely positioned at the posterior in 61% of the egg chambers.

Homozygous follicle cell clones accumulate excess actin on their apical and lateral surface in early stage egg chambers. By stages 6-8, some mutant cells begin to lose their monolayer organisation, especially in clones near the posterior end of the egg chamber.

cpa69E mutant cells within wing blade primordium clones accumulate actin filaments around the entire cell cortex. cpa69E clones become extruded from this area of the wing disc. cpa69E cells within notum primordium clones accumulate actin filaments near the apical cell membrane and are not extruded from the disc.

Adults expressing cpaScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4αTub84B.PL in a cpa43D/cpa69E background sometimes show wing, eye or bristle defects.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

A cpa69E heterozygous mutant background enhances the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.

Xenogenetic Interactions
Statement
Reference

Expression of Hsap\CAPZA2UAS.cBa under the control of Scer\GAL4αTub84B.PL in cpa107E/cpa69E background leads to mild defects in notum bristle, such as mild bending or split bristle, when compared to controls.

Expression of Hsap\CAPZA2R259L.UAS under the control of Scer\GAL4αTub84B.PL in cpa107E/cpa69E background leads to severe notum bristle defects (bending, branching, shortening, missing bristles as well as multiple defects of single bristle) in adults and disrupted F-actin organization in notum bristles at pupal stage when compared to controls.

Expression of Hsap\CAPZA2K256E.UAS under the control of Scer\GAL4αTub84B.PL in cpa107E/cpa69E background leads to disrupted F-actin organization in notum bristles at pupal stage when compared to controls.

Expression of Hsap\CAPZA2R259L.UAS under the control of Scer\GAL4αTub84B.PL in cpa69E/+ background leads to defects in notum bristles when compared to controls.

Complementation and Rescue Data
Partially rescued by
Comments

Ubiquitous expression of cpaScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4αTub84B.PL rescues the lethality of cpa43D/cpa69E mutants, although some of the rescued adults exhibit wing, eye or bristle defects.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (8)