FB2024_03 , released June 25, 2024
Allele: Dmel\Arpc1Q25sd
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General Information
Symbol
Dmel\Arpc1Q25sd
Species
D. melanogaster
Name
FlyBase ID
FBal0135790
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
sop2Q25sd
Key Links
Genomic Maps

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

A mutation in the conserved splice donor dinucleotide after Q25 (C/gt->C/at).

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

G13829027A

Reported nucleotide change:

GT?AT

Amino acid change:

W108term | Arpc1-PA; W108term | Arpc1-PB

Comment:

A mutation in the conserved splice donor dinucleotide after Q25 (C/gt->C/at).

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

Arpc1Q25sd heterozygous mutant third instar larvae display increased number of boutons on neuromuscular junctions. The number of dendritic branches as well as the total dendrite length in class IV dendritic arborizing neurons in heterozygous larvae is comparable to controls but severely reduced in MARCM somatic clones homozygous for Arpc1Q25sd.

Homozygous SCARΔ37 mutant eye clones lack interommatidial bristles. They also show an irregular ommatidia array and crater-like intrusions. Rhabdomeres appear short and bulky and photoreceptors have fallen through the fenestrated membrane, retinal depth is reduced and defects are seen in cytoskeletal architecture.

Cultured primary neurons derived from Sop21/Sop2Q25sd embryos show a significant reduction in the number of filopodia compared to control neurons.

Ring canals between nurse cells mutant for Sop2Q25sd first begin to look different from wild-type ring canals at stage 5-6 of oogenesis: actin incorporation in mutant ring canals is less robust, and ring canals are smaller in diameter. These defects are more clear by stage 8, when some ring canals also become misshapen. By stage 10, mutant ring canals are severely deformed. In later stages, ring canals are sometimes detached from the nurse cell membranes, nurse cell subcortical actin becomes destabilized, and some nurse cells become multinucleate. This latter phenotype is not due to an inhibition of cell division, as nurse cell numbers remain normal.

When homozygous mutant clones are made in the head, a pronounced loss of external sensory organ structures is seen, including both the bristle-shafts and the socket structures from which they emanate.

CNS axon morphology in Sop2Q25sd homozygous embryos is normal. Extensive bristle loss and a rough-eye phenotype are apparent in heads carrying somatic clones of Sop2Q25sd. The abnormal eye facet pattern of these mosaic eyes is characterized by irregularly shaped ommatidia, craters of missing lens material, and a bristle-loss phenotype.

External Data
Interactions
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Phenotypic Class
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Phenotype Manifest In
Suppressed by
Enhancer of
NOT Enhancer of
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Reference
Suppressor of
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Reference
NOT Suppressor of
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Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The increased number of boutons on neuromuscular junctions observed in third instar larvae mutant for any of the following alleles: Arpc1Q25sd (in heterozygous state), Pldndel (homozygous), Dysbe01028 (either homozygous or heterozygous) or Blos1ex65 (heterozygous) is restored to wild-type levels in Arpc1Q25sd/+;Pldndel/+, Arpc1Q25sd/+;Dysbe01028/+ or Arpc1Q25sd/+;Blos1ex65/+ double heterozygotes.

The reduced number of dendritic branches as well as the total dendrite length in class IV dendritic arborizing neurons characteristic for Dysbe01028 heterozugous larvae is not modified by combination with a single copy of Arpc1Q25sd. The reduced number of branches observed in Blos1ex65 heterozygotes is mildly enhanced in Blos1ex65;Arpc1Q25sd double heterozygotes but the total dendrite length per neuron remains unchanged.

An Arpc1Q25sd 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.

Only 20% of cultured primary neurons derived from DAAMEx1/DAAMEx68 Sop21/Sop2Q25sd embryos have neurites.

In Sop2Q25sd/Df(2L)b84a9; Arp66BEP3640/+ embryos, commissural axons are severely reduced.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (12)