FB2024_03 , released June 25, 2024
Allele: Dmel\Arpc1Q25st
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General Information
Symbol
Dmel\Arpc1Q25st
Species
D. melanogaster
Name
FlyBase ID
FBal0150605
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
sop2Q25st
Key Links
Genomic Maps

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

Amino acid replacement: Q25term.

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

C13829346T

Reported nucleotide change:

C?T

Amino acid change:

Q25term | Arpc1-PA; Q25term | Arpc1-PB

Reported amino acid change:

Q25term

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
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

Arpc1Q25st heterozygous mutant third instar larvae display increased number of boutons on neuromuscular junctions.

Arpc1Q25st/+ mutants embryos show no defects in development or survival.

Arpc1Q25st mutant follicle cell clones are apically constricted, and adherens junctions appear jagged between mutant cells and between mutant and wild type cells. The phenotypes are most pronounced in stage 11 or older egg chambers.

Arpc1Q25st mutant wings frequently show wing blisters and the morphology of the wings is grossly affected.

Arpc1Q25st clones in the adult thorax show bristle loss.

Within Arpc1Q25st pIIa-pIIb cells, an apical actin-rich structure (ARS) is formed as in wild type, but its apical area is markedly reduced and, in about 50% of cases, the stalk of the normal 'umbrella shape' is not formed properly.

Embryos homozygous for Sop2Q25st commonly display unfused myoblasts.

Single cell γ neuron mutant clones in the mushroom body do not show axon growth defects.

Germ-line clones of Sop2Q25st lead to defects in nurse cell dumping: late stage oocytes are abnormally small, while late stage nurse cells are abnormally large. By stage 10B the arrangement of actin filament bundles in the cytoplasm of mutant nurse cells is abnormally uneven, and the diameter and shape of ring canals between these cells is severely compromised. There are approximately twice as many longitudinal ridges on anterior dorso-central bristles in Sop2Q25st mutant clones as in wild-type. A similar phenotype is seen in all other mutant macrochaete.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The increased number of boutons on neuromuscular junctions observed in third instar larvae heterozygous for either Arpc1Q25st or Blos1ex65 is restored to wild-type levels in Arpc1Q25st/+;Blos1ex65/+ double heterozygotes.

Arpc1Q25st/+ fails to suppress the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background.

An Arpc1Q25st 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.

One copy of Arpc1Q25st partially suppresses the cuticle defects seen in α-Cat1 mutant embryos. The phenotype is more severe when Arpc1Q25st is introduced maternally rather than paternally.

washΔ185/+ ; Sop2Q25st/+ egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormal by stage 10b.

washΔ185/+ ; RpII140wimp/+ Sop2Q25st egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormal by stage 10b.

Heterozygosity for Sop2Q25st does not suppress the Abl4 phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments
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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (13)