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General Information
Symbol
Dmel\vls2
Species
D. melanogaster
Name
FlyBase ID
FBal0018014
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
vlsPE, vlsPE36, valPE
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G20065440A

Reported nucleotide change:

G?A

Amino acid change:

W53term | vls-PA

Reported amino acid change:

W53term

Comment:

TGG to TGA

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: G?A.

Amino acid replacement: W53term.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Prevents the posterior accumulation of G-iα65A protein.

Strong abdominal defect.

Absence of posterior pole plasm, polar granules and pole cells.

Embryos lack pole cells. Large amounts of vas protein are expressed in early stages of oogenesis. vas protein localizes to the posterior pole at the same stage of egg development as wild type, the protein disappears by early gastrulation.

Hemizygous vls2embryos derived from homozygous females have no polar granules, fail to form pole cells and have deletions of abdominal structures. vas and CycB transcripts are localized at the posterior.

Eggs derived from homozygous females form a syncytial blastoderm but 80-90% of the embryos fail to cellularise. Those that do cellularise show variable cellularisation defects. The embryos show a "grandchildless-knirps" phenotype; they lack polar granules and pole cells and show typical maternal kni-like abdominal segment deletions.

Homozygous females produce embryos that fail to form pole cells, lack polar granules normally found at the posterior pole, and have deletions of abdominal segments. There are also frequent defects in cellularisation at the blastoderm stage.

Embryos derived from mutant females completely lack pole cells and show deletions in the abdominal segments. The same phenotype is seen in embryos derived from homozygous or hemizygous females.

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

vls2/vls3 has abdomen phenotype, suppressible by nosN5

Additional Comments
Genetic Interactions
Statement
Reference

Injection of nosN5 RNA into vls2/vls3 embryos completely rescues the abdominal phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Availability

Stated to be lost.

Notes on Origin
Discoverer
Comments
Comments

Germline mosaic analysis shows that vls is required in the germline.

Cytoplasmic transplantation of wild type plasm into the abdominal region restores normal abdominal development.

Although tud protein is present in mutant embryo extracts, its localization in the embryo is altered.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (19)