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General Information
Symbol
Dmel\vnL6
Species
D. melanogaster
Name
FlyBase ID
FBal0050929
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
vndddL6
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

T5842762A

Reported nucleotide change:

T?A

Amino acid change:

L266term | vn-PA; L266term | vn-PC

Reported amino acid change:

L265term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

Nucleotide substitution: T?A.

Amino acid replacement: L265term.

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

sensory neuron & axon & embryo

Detailed Description
Statement
Reference

vnddd-4/vnL6 third instar larvae exhibit strongly reduced axon wrapping index (proportion of axon clusters wrapped by wrapping glia) relative to controls. In wild-type larvae, subperineurial glial cells form autocellular contacts with pronounced septate junction, the length of these autocellular contacts is significantly reduced in vnddd-4/vnL6 larvae.

vnL6/vn1 mutant wings show loss of part of longitudinal vein 4 and the anterior crossvein. Very few flies show loss of longitudinal vein 3.

vnL6/vnGAL4 mutants die as white pupae with tiny white wing discs.

vnL6/vnddd-3 wing discs fail to grow beyond a rudimentary size.

In the PNS hemisegments of vnL6 embryos there are sensory axogenesis defects and at least two of the five lateral chordotonal sensory organs are missing. Additionally, the anterior and posterior sensory fascicles are spaced further apart at the CNS-PNS transition zone compared with wild type.

The DA1 muscle precursor is missing in one or occasionally two segments in 50% of vnL6/Df(3L)XAS96 embryos. The LL1 and VA2 muscle precursors are also missing at a similar frequency.

Hemizygotes exhibit deranged differentiation of the epidermal muscle attachment (EMA) cells.

Wing discs of vnL6/Df(3L)γ3 mutants are dramatically reduced in size, and larvae are smaller and narrower than wild type.

Individuals transheterozygous with a vn deletion exhibit small wings. Transheterozygotes with vnddd-4, Df(3L)γ1, Df(3L)γ2, Df(3L)γ3, vnγ4 and vnγ6 are pupal/pharate adult lethal.

Homozygotes exhibit imaginal disc abnormalities.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

vnL6/vn1 has visible phenotype, enhanceable by Krn9/Krn27

NOT Enhanced by
Statement
Reference

vnL6/vn1 has visible phenotype, non-enhanceable by spi1/spi[+]

Suppressed by
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference

Krn27, spi1, vnL6 has denticle belt phenotype, non-enhanceable by grkHF

vnL6/vn1 has wing vein L3 phenotype, non-enhanceable by spi1/spi[+]

Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

vnL6 is an enhancer of denticle belt phenotype of spi1

vnL6 is an enhancer of denticle belt phenotype of Krn27, spi1

vnL6 is an enhancer of wing phenotype of Scer\GAL471B, ptcUAS.cJa

vnL6 is an enhancer of phenotype of spi1

Suppressor of
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

vnL6 enhances the ventral patterning defects seen in spi1 mutant embryos. The double mutants have a reduced number of denticle belts compared to controls, fusion of the denticle belts and an anterior hole. The phenotype is further exacerbated by Krn27, with embryos having no denticle belts and a large anterior hole. A zygotic grkHF mutation has no additional effect.

Krn27 enhances the ventral patterning defects seen in spi1 mutant embryos. The double mutants have a reduced number of denticle belts compared to controls, fusion of the denticle belts and an anterior hole. The phenotype is further exacerbated by vnL6, with embryos having no denticle belts and a large anterior hole. A zygotic grkHF mutation has no additional effect.

Krn27/Krn9 enhances the wing vein phenotypes seen in vnL6/vn1 mutants. A greater proportion of flies show longitudinal vein 3 loss than in vnL6/vn1 alone. The phenotype is further enhanced by one copy of spi1.

One copy of spi1 does not enhance the vein phenotypes seen in vnL6/vn1 mutant wings.

Expression of rhoScer\UAS.cUa under the control of Scer\GAL4vn.GAL4 partially suppresses the lethality seen in vnL6/vnGAL4 mutant flies. Approximately 50% of flies reach adulthood and have grossly normal wings, although the region between veins L3 and L4 is fused and some extra vein material is observed. The wing disc is of normal size and pattern.

Expression of spi::vnEGF.Scer\UAS under the control of Scer\GAL4vn.GAL4 rescues the lethality of vnL6/vnGAL4 mutants to the pharate adult stage.

The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is not suppressed if the flies also simultaneously carry vnL6 and spi1.

The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is significantly suppressed if the also simultaneously carry both vnL6 and Krn27. The suppression is more pronounced if the flies simultaneously carry spi1, Krn27 and vnL6.

Large ru1 rho7M43 vnL6 triple mutant clones in the leg can result in truncations of the tarsus region (for example only three tarsal segments may be present). Mosaic legs which have wild-type tissue at the distal tip show rescue of tarsal development.

Clones expressing rhoScer\UAS.cGa under the control of Scer\GAL4αTub84B.PZ induced in the first larval instar can stimulate proliferation in vnL6/vnddd-4 wing discs, irrespective of the position of the clone within the wing disc. Clones expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4αTub84B.PC usually do not stimulate the growth of vnL6/vnddd-4 wing discs. A few discs do show a modest increase in size, but this rescue appears to be due to a cell-autonomous rescue of proliferation within the Ras85DV12.Scer\UAS expressing clone. Clones expressing apScer\UAS.cOa under the control of Scer\GAL4αTub84B.PZ induced in the first larval instar can rescue growth and differentiation vnL6/vnddd-4 wing discs.

The addition of vnL6 enhances the loss of wing vein phenotype seen in ptcScer\UAS.cJa/Scer\GAL471B flies.

The loss of the DA1 muscle precursor seen in vnL6/Df(3L)XAS96 embryos is enhanced if they are also carrying EgfrDN.Scer\UAS expressed under the control of Scer\GAL4how-24B.

Heterozygosity or homozygosity for vnddd-4 or vnL6 enhances the spi larval mutant phenotype of Df(2L)OD12/Df(2L)VA17 or spi1 mutants. Embryos collapse and extrude the head skeleton. Almost all ventral denticles are lacking.

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

Expression of vnScer\UAS.cSa under the control of Scer\GAL4vn.GAL4 partially rescues the lethality seen in vnL6/vnGAL4 mutant flies. In optimal conditions approximately 30% of flies reach adulthood and have grossly normal patterning of the wing. Some extra vein material is observed. The wing disc phenotype is partially rescues and no leg defects are observed. The extent of the rescue depends on the expression level.

Expression of vnΔIg.Scer\UAS under the control of Scer\GAL4vn.GAL4 rescues the lethality seen in vnL6/vnGAL4 mutant flies. The wings of these flies are abnormal and have deletion of wing margin bristles and notched margins, a phenotype that is also seen when this transgene is expressed in a wild type fly.

vnL6/vnddd-4 wing discs containing multiple clones expressing vnScer\UAS.cSa under the control of Scer\GAL4αTub84B.PZ appear similar in size to wild-type discs. Single clones expressing vnScer\UAS.cSa under the control of Scer\GAL4αTub84B.PZ can confer at least partial and sometimes extensive rescue of vnL6/vnddd-4 wing discs. Rescue is only seen when the clones are located in or near the prospective dorsal region of the disc.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (23)