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General Information
Symbol
Dmel\Vps25N55
Species
D. melanogaster
Name
FlyBase ID
FBal0194622
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C8625854T

Amino acid change:

Q93term | Vps25-PA

Reported amino acid change:

Q93term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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

Amino acid replacement: Q93term.

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

Vps25N55 mutant clones in late third instar larval eye imaginal discs causes non-autonomous overproliferation of neighbouring wild type cells.

Vps25N55 somatic clones in eye-antennal imaginal discs contain enlarged early endosomes.

Vps25N55 somatic clones in eye-antennal imaginal discs show high levels of apoptosis compared to wildtype. Non-autonomous tissue overgrowth of the eye-antennal imaginal disc, adult eye and head occurs these animals.

When the majority of cells in the eye-antennal imaginal discs are mutant for Vps25N55, striking tissue overgrowth of the disc occurs and loose cellular architecture is observed.

Vps25N55 mutant somatic clones in eye-antennal imaginal discs do not proliferate very well, however the wildtype tissue immediately adjacent to the mutant clones show increased cell proliferation rates.

Vps25N55/Vps25K2 mosaic eyes are larger than wild-type, even if homozygous mutant clones are not recovered, indicating that the mutant clones do not contribute to the adult eye tissue, but appear to be able to induce overgrowth in wild-type tissue. Third-instar eye-antennal discs are overgrown and disorganised when compared with wild-type.

TUNEL labelling, indicating the beginning of apoptosis, is increased in Vps25N55 mutant clones, consistent with the lack of mutant clones in the adult eye. Vps25N55 clones can grow to a fairly large size, suggesting that they are not growth-impaired. However, these clones are completely removed by apoptosis during pupal stages.

Cell proliferation is significantly increased in tissue adjacent to Vps25N55 clones. This non-autonomous cell proliferation is best visible in wing imaginal discs, where Vps25N55 clones appear to be the origin for the increased proliferation of the adjacent tissue.

Vps25N55 eye-antennal disc mutant clones are unable to differentiate.

Abnormal endosomal structures are found in Vps25N55 mutant clones concurrent with increased ubiquitin and N-signaling activity.

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

Vps25N55 has eye | somatic clone phenotype, suppressible by N[+]/N264-39

Vps25N55 has adult head | somatic clone phenotype, suppressible by N[+]/N264-39

Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

Atg61 suppresses the non-autonomous overgrowth seen in Vps25N55 mutant eye disc clones.

Heterozygosity for N264-39 suppresses the overgrowth of the adult eye and head that occurs in animals with somatic clones of Vps25N55 generated in the eye-antennal disc.

The eye-ablation phenotype in WGMR.PG animals is suppressed in Vps25N55 somatic clones generated in the eye-antennal imaginal disc in a non-autonomous manner.

Vps25N55 moderate-strongly suppresses the WGMR.PG eye phenotype.

In Vps25N55/Vps25K2 mosaic eyes, in a WGMR.PG background, the rescued tissue is genetically wild-type or heterozygous, suggesting that Vps25N55 and Vps25K2 mutant tissue does not contribute to the suppression of WGMR.PG.

Vps25N55/NDN.Scer\UAS mutants (using the MARCM technique) exhibit reduced or absent Stat92E activity. Cell proliferation is not significantly increased in Vps25N55/NDN.Scer\UAS mutants, with eye imaginal discs appearing normal in shape and size. These Vps25N55/NDN.Scer\UAS double mutant clones exhibit the same level of apoptosis as Vps25N55 single mutant clones.

Blocking cell death, through expression of thScer\UAS.cHa in Vps25N55 mutant clones does not affect proliferation or Stat92E activity.

Vps25N55/thScer\UAS.cHa mosaics exhibit non-autonomous cell proliferation, as do Vps25N55/ArkH16 mutants. Eye-antennal discs of Vps25N55/thScer\UAS.cHa mosaics are extremely overgrown and can be 5-times as large as wild-type discs. Cell death is completely blocked in Vps25N55/thScer\UAS.cHa mosaics. Vps25N55/ArkH16 cells undergo apoptosis. Vps25N55/ArkH16 clones cannot be recovered in the adult eye. Vps25N55/thScer\UAS.cHa and Vps25N55/ArkH16 clones occupy a large fraction of the eye discs, suggesting that these clones have no intrinsic growth disadvantage over wild-type tissue if cell death is blocked. The adult eye of Vps25N55/ArkH16 mosaics is severely overgrown and folded. Thus, inhibiting cell death in Vps25N55 clones can give rise to an even stronger overgrowth phenotype.

Vps25N55 ArkH16/pucScer\UAS.cMa mosaic eye discs are severely overgrown.

Vps25N55 hpo3D mutant clones do not undergo apoptosis.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)