FB2025_01 , released February 20, 2025
Allele: Dmel\Cul3gft2
Open Close
General Information
Symbol
Dmel\Cul3gft2
Species
D. melanogaster
Name
FlyBase ID
FBal0008511
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Cul-3gft2, gftHG39
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

5bp deletion at nucleotide positions 2310-2314, resulting in a frameshift at amino acid 747 and a premature stop codon at amino acid 748.

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

5bp deletion resulting in a frameshift at amino acid 747 and a premature stop codon at amino acid 748. Position of mutation on reference sequence inferred by FlyBase curator.

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 ( 1 )
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

Cul3gft2 mutant clones in sensory neurons in adult wing do not display any defects in injury-induced axon degeneration (following an axotomy, the severed axons are cleared away normally).

Cul3gft2 heterozygotes do not display any obvious dominant defects in the number of primordial germ cells in the early embryo (i.e. mitotic cycles 12/13), as compared to controls.

Germline clones of cells homozygous mutant for Cul3gft2 show a ring canal phenotype in the egg chambers: the F-actin cytoskeleton is disorganized, the kel protein accumulates in the lumen and the lumen diameter is significantly smaller compared to controls.

Examination of Cul-3gft2 mutant ring canals in egg chambers reveals a small lumen phenotype and F-actin disorganization.

cul-3mds1/cul-3gft2 spermatids show defects in individualisation.

Homozygous mutant gft2 Mushroom Body clones exhibit axon terminal morphogenetic defects.

Homozygous and gft2/Df(2L)TE35D-15 animals hatch, but die during the second larval instar. Females carrying homozygous germ-line clones produce few eggs and those which are laid are about half the size of wild-type and have fused dorsal appendages. No discernible embryonic structure can be detected interior to the chorion in these eggs. Large homozygous clones in the wing show a number of defects, including defects in the overall shape of the wing and in formation and position of the wing veins. Large clones in the wing often lack trichomes in the centre of the clone. Clones that cover the L3 vein often result in it shifting posteriorly. Clones that cover wing veins are associated with loss of vein tissue. Clones in the wing also result in ectopic sensory organ formation; clones that encompass a large part of the L3 vein have ectopic campaniform sensilla, ectopic campaniform sensilla also arise between wing vein L2 and the anterior wing margin and ectopic bristles arise distally between L2 and L3. Clones in the notum are associated with significant tufting of both micro- and macrochaetae, with the tufts being made up of ectopic fully formed external sensory organs as well as individual sensory organs that contain multiple shafts within a single socket. Homozygous clones in the wing disc show a dramatic increase in the number of sensory organ precursor (SOP) cells, while SOP development outside the clone is normal.

Adult escapers have unexpanded wings and small eyes.

gft2, but not other alleles, fails to

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Other
Statement
Reference
Phenotype Manifest In
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

Cul3[+]/Cul3gft2 is a suppressor | partially of egg chamber phenotype of gclNLS

Cul-3[+]/Cul3gft2 is a suppressor of eye | somatic clone phenotype of COX5Atend

NOT Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The axon degeneration in sensory neurons clones in the adult wing expressing Ect4ΔARM.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4VGlut-OK371 can be suppressed by combination with Cul3gft2.

Cul3gft2, gclrev390 double heterozygotes present significant decreases in the number of primordial germ cells in the early embryo (i.e. mitotic cycles 12/13), as compared to wild-type and single heterozygous controls.

Heterozygosity for Cul3gft2 partially rescues the failure of gclNLS heterozygous females to develop late stage egg chambers and to lay eggs.

A Cul-3gft2 heterozygous background does not suppress the disruptions in cell division seen in CoVatend mutant eye disc clones.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Harrington.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (14)
References (31)