FB2024_03 , released June 25, 2024
Allele: Dmel\DCTN1-p150Δ22
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General Information
Symbol
Dmel\DCTN1-p150Δ22
Species
D. melanogaster
Name
FlyBase ID
FBal0217579
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
GlΔ22
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Caused by aberration
Cytology
Description

Imprecise excision of the insertion in GlKG07739, resulting in a deletion of approximately 3.2kb that part of the Gl transcription unit (including the presumptive transcription start site) and part of the CG8833 transcription unit.

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

Cultured primary neurons derived from homozygous embryos have a significantly increased axon length compared to wild-type controls.

GlG38S/GlΔ22 larvae show normal locomotion.

GlG38S/GlΔ22 third instar larvae have a normal number of synaptic boutons per neuromuscular junction (NMJ) in proximal abdominal segments (A2 and A3) but show a small but significant increase in the number of synaptic boutons per NMJ in distal segments (A5 and A6). The terminal boutons (the distal-most synaptic boutons) are swollen at the mutant NMJ and show an approximately 2-fold increase in bouton volume in distal segments.

GlG38S/GlΔ22 larvae show a significant reduction in the amplitude of the evoked junctional potential (EJP) at the NMJ compared to controls.

GlΔ22/Gll1 and homozygous neuroblasts show centrosome and spindle formation defects. Defects include metaphase neuroblasts with curved spindles, unfocused spindle poles, spindles with one or two unattached centrosomes, spindles in which both centrosomes are attached to the same half-spindle, or occasionally neuroblasts with three or four centrosomes forming bipolar or multipolar spindles.

The mitotic index and metaphase:anaphase ratio are increased in homozygous neuroblasts compared to wild type.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference

DCTN1-p150G38S/DCTN1-p150Δ22 has phenotype, enhanceable by Khc[+]/Khc8

NOT suppressed by
Statement
Reference

DCTN1-p150Δ22 has axon phenotype, non-suppressible by CLIP-190KO/CLIP-190KO

Additional Comments
Genetic Interactions
Statement
Reference

The increase in axon length seen in cultured primary neurons derived from homozygous DCTN1-p150Δ22 embryos is unchanged if the embryos are also homozygous for CLIP-190KO.

GlG38S/GlΔ22 ; Khc8/+ animals rarely survive to pupal stages.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of GlScer\UAS.cLa under the control of Scer\GAL4T80 rescues the lethality of Gll1/GlΔ22 animals, although the rescued animals are sterile.

Expression of GlCH322-82J07 fully rescues Gll1/GlΔ22 animals (the rescued animals are viable and fertile).

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (3)