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General Information
Symbol
Dmel\vnγ4
Species
D. melanogaster
Name
FlyBase ID
FBal0050936
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Disrupts the vn transcribed region, breaking in the major intron, intron 1.

Translocation breakpoint is in the first intron.

Caused by aberration
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

vnγ4/Df(3L)γ3 stage 13/14 embryos show a reduction in longitudinal glia proliferation compared to wild type (assayed using pHis3 expression).

vnγ4/Df(3L)γ3 embryos have various defects in dMP2 fascicles. At stage 14 this fascicle may be absent altogether, it may fuse with the pCC fascicle, or it may fasciculate with the aCC axon and exit the central nervous system (CNS). Older mutant embryos show defasciculation within the CNS particularly of the second and third longitudinal fascicles. vnγ4/Df(3L)γ3 embryos have reduced numbers of longitudinal (interface) glial cells. The frequency and extent of apoptosis of this cell type is significantly greater than that seen in wild-type measured as either: 1. the percentage of embryos with more than one apoptotic longitudinal glial cell (around 80% for wild-type and 50% for mutant (0.025>p>0.05 by ξ2)); or 2. the overall incidence of apoptosis (p>0.001, Mann-Whitney U test.).

Null allele. Shows strongest midgut phenotype of vn alleles tested. Causes lack of midgut constrictions and failure of elongation of gastric caeca.

In vnγ4/Df(3L)γ3 mutants 50% of the Keilin's organs are missing. Head region is normal. Most die as embryos or larvae, but 5% survive to pupariate, with pupal cases shorter and slimmer than wild type.

Individuals transheterozygous with a vn deletion or with a strong EMS vn mutation exhibit small wings. Transheterozygotes with vnL6 are pupal/pharate adult lethal.

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

vnγ4 has interface glial cell phenotype, enhanceable by spi1

Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The decrease in interface glial cell numbers seen in vnγ4/Df(3L)γ3 is partially suppressed by BacA\p35Scer\UAS.cHa; Scer\GAL4htl.POS, but is unaffected by BacA\p35Scer\UAS.cHa; Scer\GAL4elav.PLu. The decrease in interface glial cell numbers and increase in interface glial cell apoptosis seen in vnγ4/Df(3L)γ3 are both enhanced by spi1/spi1.

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

Interface glial cell survival in vnγ4/Df(3L)γ3 embryos is rescued by vnScer\UAS.cSa; Scer\GAL4elav.PLu.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
  • FBal0028142
References (8)