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General Information
Symbol
Dmel\vn10567
Species
D. melanogaster
Name
FlyBase ID
FBal0009626
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
vnP1749, vein-lacZ, vn-lacZ
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

P{PZ} insertion within the first non-coding exon.

Insertion components
P{PZ}vn10567
Product class / Tool use(s)
Encoded product / tool
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

Whereas wild-type adult midgut progenitor cells (AMPs) form many large clusters, few AMP clusters are found in late larval vn10567 and vn10567/vnγ7 mutant midguts.

Most vn10567/vnγ7 mutants die as pharate adults.

Lineage analysis of marked clones reveals that vn10567/vnγ7 mutants display a failure of proliferation of AMPs during early larval stages, although the number of AMPs generated initially during embryogenesis is not different between mutants and wild-type controls. The size of the few remaining AMP clusters in vn10567/vnγ7 mutants is relatively normal, suggesting that the late phase of AMP proliferation is largely unaffected in these mutants.

Expression of vnScer\UAS.cSa in larval enterocytes driven by Scer\GAL4Myo31DF-NP0001 not only rescues the adult midgut progenitor cell phenotype of vn10567 mutants, but it also causes ectopic AMP cell proliferation.

Late stage vn10567/Df(3L)v65c embryos lack lch5 ligament attachment cells.

Border cells still migrate dorsally when all dorsal follicle cells are mutant for vn10567 in females containing homozygous clones.

Shows very mild midgut phenotype. vn10567/Df(3L)γ3 causes lack of midgut constrictions and failure of elongation of gastric caeca.

A significant number of somatic muscle fibres show multiple, mis-guided membrane extensions at their leading edges. The DA1 muscle precursor is sometimes missing.

Abnormal muscle phenotype. Myotubes of mutant embryos are elongated and continuously send filopodia in random directions.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

vn[+]/vn10567 is a non-suppressor of visible phenotype of rk1

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
Enhancer of
Suppressor of
Statement
Reference

vn[+]/vn10567 is a suppressor | partially of intestinal stem cell phenotype of rk1

vn[+]/vn10567 is a suppressor | partially of adult midgut phenotype of rk1

vn10567/vn1 is a suppressor of adult midgut phenotype of rk1

vn[+]/vn10567 is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

NOT Suppressor of
Statement
Reference

vn[+]/vn10567 is a non-suppressor of wing phenotype of rk1

Other
Additional Comments
Genetic Interactions
Statement
Reference

vn10567/+ partially suppresses the intestinal stem cell hyperproliferation seen in the midgut, but fails to rescue the wing inflation defect of rk1/rk1 mutants.

vn10567/vn1 suppresses the intestinal stem cell hyperproliferation seen in rk1/rk1 mutant midguts.

Although extra wing vein material is induced in Gug14967 clones, wing vein differentiation is blocked in vn10567 rhoPΔ5 Gug14967 triple mutant clones.

2/3 of vn10567; rhounspecified double homozygous embryo cuticles show a general loss of cuticle integrity. Of the remaining 1/3 of cuticles the percentage with >2 denticle belt fusions is increased from <10% for rhounspecified to >30%. (Note, while the authors do not name an rho allele for this analysis, they do claim to have used a null allele.)

The loss of the DA1 muscle precursor in vn10567 embryos is enhanced if they are also carrying EgfrDN.Scer\UAS expressed under the control of Scer\GAL4how-24B. The loss of the DA1 muscle precursor seen in vn10567 embryos is dominantly enhanced by spi3.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of vnScer\UAS.cSa in larval enterocytes driven by Scer\GAL4Myo31DF-NP0001 not only rescues the adult midgut progenitor cell phenotype of vn10567 mutants, but it also causes ectopic AMP cell proliferation.

Expression of vnScer\UAS.cSa in adult midgut progenitor cells (AMPs) rescues the AMP cell proliferation phenotype of vn10567 mutants.

Expression of vnScer\UAS.cSa in visceral muscle driven by Scer\GAL4how-24B rescues the adult midgut progenitor cell phenotype of vn10567 mutants.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Complements: Bre101640. Complements: l(3)0233102331. Complements: l(3)0514305143. Complements: l(3)neo111.

Precise excision of the P{PZ} insertion completely reverses the muscle phenotype and results in full viability. Results indicate the insertion is responsible for the phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (21)