FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\vasPH165
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General Information
Symbol
Dmel\vasPH165
Species
D. melanogaster
Name
FlyBase ID
FBal0090073
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
vasaPH165
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Caused by aberration
Cytology
Description

Imprecise excision of P{PZ}vasLYG2, resulting in a 7343bp deletion which removes the entire vas coding region (the first, non-coding, exon is not deleted). This deletion also removes nested coding sequence located within the third intron of vas (FlyBase curator comment: this nested coding sequence corresponds to the coding exons specific to the solo gene).

7343bp deletion that removes the entire coding regions of vas and solo. The deletion removes the second and third of the three exons common to vas and solo, plus all of the solo-specific and vas-specific exons (see FBrf0102626).

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

CATGATGAAATAACAT

Comment:

Deletion in which 7343bp are removed including the entire vas coding region and replaced with 16bp from the P element.

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
ameliorates  brain cancer
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

vasPH165 mutant females lay significantly fewer eggs than controls and those eggs display severe dorsal appendage defects.

Embryos from vasW660E/vasPH165 transheterozygous mothers fail to form pole cells or have only drastically reduced number of them. The number of eggs produced by either the females is comparable to wild-type but the eggs display frequent dorsal appendage defects.

Eggs laid by vasPH165/vasRG53 females display a range of ventralisation phenotypes, ranging from fusion at the base of the dorsal appendages through to complete lack of the appendages. This phenotype can be suppressed by feeding the females rapamycin.

Progression of chromosome condensation appears delayed in germline stem cells (GSCs) and cystoblasts (CBs) of vasPH165/Df(2L)BSC299 ovaries. The mutant ovaries show an increased percentage of GSCs and CBs in prometaphase compared to controls, with a concomitant drop in the number of GSCs and CBs in metaphase. 56.7% of the mutant GSCs and CBs have lagging chromosomes during anaphase.

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

vasPH165 mutant flies produce few mature eggs. In 3-4 day old females the number of stage 14 eggs per ovary ranges widely from 0-32 with an average of nine. Most mature eggs either lack or have fused dorsal appendages, and sometimes have an ectopic micropyle at the posterior end. Mature eggs from these mothers can be fertilised, but the resulting embryos have posterior segmentation defects and do not hatch. Fewer than 1% of fertilised embryos from vasPH165 mutant mothers have pole cells at cellular blastoderm.

10-30% of embryos produced by heterozygous females at 29oC fail to hatch and show variable and minor patterning defects which affect both the anteroposterior and dorsoventral axes.

Homozygous females show defects in oogenesis. The ovaries contain fewer developing cysts than normal. This phenotype shows high expressivity and increases in severity with the age of the female. Region 1 of the germaria of 7 day old females often consists of only a few stem cells and developing cysts. Posterior to these there is often what appears to be an extended interfollicular stalk, which is probably formed by follicle cells in the absence of cystocyte clusters. Approximately 1% of homozygous ovaries have defects in germline differentiation and oocyte determination, including tumorous egg chambers, egg chambers with 16 nurse cells and no oocyte, egg chambers with two oocytes, and egg chambers with a mislocalised oocyte. The oocytes produced by homozygous egg chambers are not fully differentiated; the oocyte nucleus appears more diffuse than in wild-type females. Approximately 70% of homozygous egg chambers appear normal until about stage 6, whereupon all the nuclei undergo pycnosis and further development ceases. Approximately 20% of oocytes continue beyond stage 6, most of these are blocked at stage 9-10, after which the oocyte often loses its integrity at the anterior end, and nurse cell nuclei invade the region of the egg chamber normally occupied by the oocyte. A small number of oocytes complete oogenesis, but frequently have duplicated micropyles at both the anterior and posterior ends. These eggs also often have dorsal appendage defects; 19% lack dorsal appendages, 66% have a single fused appendage and only 15% have two dorsal appendages. Homozygotes are rescued to fertility by vasT:Avic\GFP.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
NOT suppressed by
Statement
Reference
Suppressor of
Statement
Reference

vasPH165/Df(2L)A267 is a suppressor of neoplasia phenotype of l(3)mbtts1

Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The very low number of eggs laid by vasPH165 homozygous females is not rescued by maternal combination with bel::vasvas.C.bel.T:Avic\GFP-EGFP and the few embryos produced by the vasPH165;bel::vasvas.C.bel.T:Avic\GFP-EGFP females display severe defects in dorsal-ventral patterning.

The delay in prometaphase and the chromosome segregation defects which are seen in the germline stem cells and cystoblasts of vasPH165/Df(2L)BSC299 ovaries are rescued by expression of barrScer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.

The frequency with which l(3)mbtts1 larval brain tissue develops into tumours after allograft into adult host flies (taking over the entire abdomen of the host) is markedly reduced if the transplanted tissue is also carrying vasPH165/Df(2L)A267.

vasPH165/+ 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.

The frequency of unhatched embryos produced by vasPH165/+ females at 29oC is increased by addition of one copy of eIF5BΔ1 or Df(3L)G5. Many embryos from vasPH165/+ ; eIF5BΔ1/+ mothers show severe segmentation defects and 26% show a vas-like phenotype in which the 4th abdominal segment is completely or partially deleted (partial or total deletion of A4 is never seen in the progeny of either single heterozygote). There is a marked reduction in the number of pole cells in embryos derived from double heterozygotes, and occasionally pole cells are completely absent. The pole cells are often interspersed with or positioned beneath somatic cells. No reduction in pole cell number is seen in the progeny of either vasPH165/+ ; eIF-4a02439/+, vasPH165/+ ; eIF-4a1013/+ or vasPH165/+ ; eIF-4ES058911/+ females.

The eggshell patterning defects of eggs derived from vasRG53/vasPH165 females are not suppressed if the females also carry mei-41D3/mei-41D3.

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

The reduced number of eggs laid by vasPH165 homozygous females as well as the dorsal appendage defects in the eggs produced are strongly improved by maternal combination with either vasΔ15-75.T:Avic\GFP-EGFP or vasW660F.T:Avic\GFP-EGFP and to a lesser degree by vasW660E.T:Avic\GFP-EGFP.

The mitotic delay which is seen in the germline stem cells and cystoblasts of vasPH165 ovaries is rescued by vasT:Avic\GFP-EGFP and by vasΔ617.T:Avic\GFP-EGFP.

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.

vasT:Avic\GFP-EGFP rescued the oogenesis defects and the maternal effect embryonic defects due to vasPH165. vasΔ617.T:Avic\GFP-EGFP does not rescue the oogenesis defects or the maternal effect elimination of pole cells in the embryo due to vasPH165. However, posterior segmentation defects are partly rescued, and embryos hatch into viable larvae.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (36)