Open Close
General Information
Symbol
Dmel\vas1
Species
D. melanogaster
Name
FlyBase ID
FBal0017845
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
vasPD, vasaPD, vasPD23, vasaPD23
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

Sequencing revealed that there is no amino acid replacement in the coding sequence.

Expression Data
Reporter Expression
Additional Information
Statement
Reference

Oocytes from vas1 females express vas protein only at the germarium stage.

 
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

Embryos from vas1 homozygous mothers fail to form pole cells and show impaired dorsal patterning (assessed by no. of ftz stripes).

vas1/vasPH165 egg chambers are similar to wild-type, consisting of 15 nurse cells and an oocyte surrounded by a layer of follicle cells.

100% of eggs laid by vas1/vas15, vas1/vas6 or vas1/vas7 females appear wild-type.

Strong abdominal defects.

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

Normal eggs. Embryos lack polar granules, pole cells and abdominal segments.

Reduced posterior vas localization in the oocyte. vas protein is only detectable at the germarium stage of ovarian development. Females lay wild type numbers of eggs that develop into embryos lacking abdominal segments and pole cells.

Homozygous embryos derived from homozygous females have no polar granules, fail to form pole cells and have deletions of abdominal structures. Posterior localization of vas and CycB transcripts is completely abolished.

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.

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.

maternal-effect lethal. Embryos from homozygous mothers exhibit a so-called 'grandchildless-knirps' phenotype: all eggs lack polar granules and no pole cells are formed; most of the embryos show large deletions of abdominal segments, whereby anterior parts of segment A1 become fused to posterior parts of segment A8. Telson elements are always present and relatively normal. Eggs have abnormal shape. Analysis of germ-line clones indicates that the mutation is germ-line autonomous (Schupbach and Wieschaus, 1986). Homozygous vasa males cannot be distinguished from wild-type males in viability and fertility.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
NOT suppressed by
Statement
Reference

vas1 has phenotype, non-suppressible by nosαTub84B.UTR.virTCE.Tag:HA

vas1 has phenotype, non-suppressible by nosnos.+1.Hsp83

vas1 has primordial germ cell phenotype, non-suppressible by osk+t8

Enhancer of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The failure to form pole cells as well as the impaired dorsal patterning (assessed by no. of ftz stripes) observed in embryos from vas1 homozygous mothers is partially rescued in progeny from vas1;bel::vasvas.C.bel.T:Avic\GFP-EGFP females.

vas1/+ enhances the primordial germ cell phenotype resulting from the overexpression of Scer\GAL4nos.UTR.T:Hsim\VP16>FsnScer\UAS.T:Ivir\HA1.

More than 50% of vas1/vasPH165 ; mei-P261/mei-P26fs1 egg chambers are tumorous and fail to differentiate nurse cells and oocytes. The double mutant egg chambers contain mostly early-stage cystocytes as they contain either punctate spectrosomes or branched fusomes.

nosnos.+2'ME-3X.T:Ivir\HA1 partially rescues the abdominal segmentation defect of embryos derived from vas1/vas3 females; 2% of the embryos develop no abdominal segments, 53% develop 1-3 abdominal segments, 43% develop 4-6 abdominal segments and 2% develop 7-8 abdominal segments. The embryos do not have anterior defects. nosnos.+1.+2' or nosnos.+2RO.T:Ivir\HA1 fail to rescue the abdominal segmentation defect of embryos derived from vas1/vas3 females; 100% of the embryos develop no abdominal segments. The embryos do not have anterior defects.

The lack of abdominal segments seen in embryos derived from vas1/vas3 females is rescued if the females also carry nosαTub84B.UTR.T:Ivir\HA1, but not if they carry nosαTub84B.UTR.virTCE.T:Ivir\HA1 or nosnos.+1.Hsp83.

Embryos derived from vas1/vas3 females carrying nosnos.+2.Hsp83 or nosnos.+2-3X.T:Ivir\HA1 do not produce any abdominal segments. 98% of embryos derived from vas1/vas3 females carrying nosnos.+2'.Hsp83 produce 7-8 abdominal segments and 58% of these embryos show loss of head or thorax structures. Embryos derived from vas1/vas3 females carrying nosnos.+2'-2X.T:Ivir\HA1 develop 0-3 abdominal segments in 16% of cases, 4-6 abdominal segments in 51% of cases and 7-8 abdominal segments in 34% of cases. Embryos derived from vas1/vas3 females carrying nosnos.+2'-3X.T:Ivir\HA1 develop 0-3 abdominal segments in 72% of cases and 4-6 abdominal segments in 28% of cases.

vas1;6xP{osk+108} embryos exhibit a vas cuticular phenotype, deletion of most abdominal segments. Embryos also fail to form pole cells.

Does not interact with RpII140wimp maternal effect.

Injection of nosN5 RNA into vas1/vas3 embryos completely rescues the abdominal phenotype.

torhb1+hb2 transcripts fully rescue posterior and anterior development in vas1 embryos.

In double mutants vas1, fs(1)N12 all abdominal segments are transformed to the eighth abdominal segment.

vas1 mutant embryos can develop into larvae and adults with a normal abdominal pattern, provided that they lack functional maternal transcripts of hb.

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

The loss of pole cells and patterning defects (assessed by no. of ftz stripes) characteristic for embryos from vas1 homozygous mothers is rescued in progeny from vas1;vasΔ15-75.T:Avic\GFP-EGFP females, almost fully rescued in the progeny from vas1;vasΔ15-75.T:Avic\GFP-EGFP females and partially rescued in embryos from vas1;vasΔ15-75.T:Avic\GFP-EGFP mothers: the loss of pole cells is not restored but the patterning defects are ameliorated.

Expression of vasDQAD.Scer\UAS.T:Avic\GFP using Scer\GAL4nos.UTR.T:Hsim\VP16 fails to rescue the infertility phenotype of vas1/vas3 mutants.

When vasScer\UAS.T:Avic\GFP is expressed using Scer\GAL4nos.UTR.T:Hsim\VP16 in a vas1/vas3 mutant background, it rescues infertility. The rescued embryos show normal segmentation patterns, very similar to those hatched from eggs laid by wild-type females.

Maternal expression of vas5xAla.T:Avic\GFP rescues the viability and primordial germ cell formation defect in vas1/vasPH165 embryos.

Maternal expression of vascKa.T:Avic\GFP rescues the viability and primordial germ cell formation defect in vas1/vasPH165 embryos.

vasαTub67C.T:Avic\GFP rescues the abdominal and germ-line defects of vas1/vas3 mutant embryos.

Images (0)
Mutant
Wild-type
Stocks (7)
Notes on Origin
Discoverer
Comments
Comments

Germline mosaic analysis shows that vas 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 (6)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (73)