FB2024_03 , released June 25, 2024
Allele: Dmel\vnL6
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General Information
Symbol
Dmel\vnL6
Species
D. melanogaster
Name
FlyBase ID
FBal0050929
Feature type
allele
Associated gene
Dmel\vn
Associated Insertion(s)
Carried in Construct
Also Known As
vndddL6
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(Schnepp et al., 1996, Simcox et al., 1996)
Progenitor genotype
Cytology

Polytene chromosomes normal.

(Simcox et al., 1996)
Description

Nucleotide substitution: T?A.

(Donaldson et al., 2004)

Amino acid replacement: L265term.

(Donaldson et al., 2004)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
3L:5,842,762..5,842,762 [-]
Nucleotide change:

T5842762A

Reported nucleotide change:

T?A

Amino acid change:

L266term | vn-PA; L266term | vn-PC

Reported amino acid change:

L265term

(Donaldson et al., 2004)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In

      chordotonal organ | embryonic stage

      (Sepp and Auld, 2003)

      embryonic/larval CNS subperineurial glial cell | third instar larval stage (with vnddd-4)

      (Matzat et al., 2015)

      embryonic/larval wrapping glial cell | third instar larval stage (with vnddd-4)

      (Matzat et al., 2015)

      imaginal disc

      (Wurst et al., 1984)

      larva

      (Schnepp et al., 1996)

      larval intersegmental nerve sensory neuron

      (Sepp and Auld, 2003)

      larval segmental nerve sensory neuron

      (Sepp and Auld, 2003)

      muscle attachment site

      (Yarnitzky et al., 1997)

      muscle cell of abdominal 2 dorsal acute muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 2 lateral longitudinal muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 2 ventral acute muscle 2 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 3 dorsal acute muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 3 lateral longitudinal muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 3 ventral acute muscle 2 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 4 dorsal acute muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 4 lateral longitudinal muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 4 ventral acute muscle 2 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 5 dorsal acute muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 5 lateral longitudinal muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 5 ventral acute muscle 2 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 6 dorsal acute muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 6 lateral longitudinal muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 6 ventral acute muscle 2 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 7 dorsal acute muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 7 lateral longitudinal muscle 1 | precursor

      (Yarnitzky et al., 1998)

      muscle cell of abdominal 7 ventral acute muscle 2 | precursor

      (Yarnitzky et al., 1998)

      sensory neuron & axon & embryo

      (Sepp and Auld, 2003)

      wing

      (Simcox et al., 1996)

      wing disc

      (Schnepp et al., 1996)

      wing disc (with Df(3L)γ3)

      (Schnepp et al., 1996)

      wing disc (with vnddd-3)

      (Austin et al., 2014)

      wing disc (with vnddd-4)

      (Zecca and Struhl, 2002)

      wing disc (with vnGAL4)

      (Austin et al., 2014)

      wing margin (with vnGAL4), with Scer\GAL4vn-GAL4, vnΔIg.UAS

      (Austin et al., 2014)

      wing margin bristle (with vnGAL4), with Scer\GAL4vn-GAL4, vnΔIg.UAS

      (Austin et al., 2014)

      wing vein | ectopic (with vn1), with Scer\GAL4vn-GAL4, vnUAS.cSa

      (Austin et al., 2014)

      wing vein L3 (with vn1)

      (Austin et al., 2014)

      wing vein L4 (with vn1)

      (Austin et al., 2014)
      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.

      (Matzat et al., 2015)

      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.

      (Austin et al., 2014)

      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.

      (Sepp and Auld, 2003)

      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.

      (Yarnitzky et al., 1998)

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

      (Yarnitzky et al., 1997)

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

      (Schnepp et al., 1996)

      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.

      (Simcox et al., 1996)

      Homozygotes exhibit imaginal disc abnormalities.

      (Wurst et al., 1984)
      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

      (Austin et al., 2014)
      NOT Enhanced by
      Statement
      Reference

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

      (Austin et al., 2014)
      Suppressed by
      Suppressor of
      Statement
      Reference

      vnL6/Krn27 is a suppressor | partially of visible phenotype of AdamTS-BKK108644, Scer\GAL4Act5C.PU

      (Butchar et al., 2012)

      spi1, vnL6, Krn27 is a suppressor of visible phenotype of AdamTS-BKK108644, Scer\GAL4Act5C.PU

      (Butchar et al., 2012)
      NOT Suppressor of
      Statement
      Reference

      spi1/vnL6 is a non-suppressor of visible phenotype of AdamTS-BKK108644, Scer\GAL4Act5C.PU

      (Butchar et al., 2012)
      Other
      Phenotype Manifest In
      Enhanced by
      NOT Enhanced by
      Statement
      Reference

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

      (Austin et al., 2014)

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

      (Austin et al., 2014)
      Suppressed by
      Statement
      Reference

      vnL6/vnGAL4 has wing disc phenotype, suppressible by Scer\GAL4vn-GAL4/rhoUAS.cUa

      (Austin et al., 2014)

      vnL6/vnGAL4 has leg phenotype, suppressible by Scer\GAL4vn-GAL4/grkΔTC.UAS

      (Austin et al., 2014)

      vnL6/vnddd-4 has wing disc phenotype, suppressible by apUAS.cOa/Scer\GAL4αTub84B.PZ

      (Zecca and Struhl, 2002)

      vnL6/vnddd-4 has wing disc phenotype, suppressible | partially by Scer\GAL4αTub84B.PZ/rhoUAS.cGa

      (Zecca and Struhl, 2002)

      vnL6 has phenotype, suppressible by EgfrE1

      (Schnepp et al., 1996)

      vnL6 has phenotype, suppressible by EgfrE3

      (Schnepp et al., 1996)

      vnL6 has phenotype, suppressible by rlSem

      (Schnepp et al., 1996)
      Enhancer of
      Statement
      Reference

      vnL6 is an enhancer of ventral denticle belt phenotype of spi1

      (Austin et al., 2014)

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

      (Austin et al., 2014)

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

      (Wessells et al., 1999)

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

      (Wessells et al., 1999)

      vnL6 is an enhancer of phenotype of spi1

      (Schnepp et al., 1996)
      Suppressor of
      NOT Suppressor of
      Statement
      Reference

      spi1/vnL6 is a non-suppressor of wing vein | ectopic phenotype of AdamTS-BKK108644, Scer\GAL4Act5C.PU

      (Butchar et al., 2012)
      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.

      (Austin et al., 2014)

      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.

      (Butchar et al., 2012)

      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.

      (Campbell, 2002)

      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.

      (Zecca and Struhl, 2002)

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

      (Wessells et al., 1999)

      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.

      (Yarnitzky et al., 1998)

      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.

      (Schnepp et al., 1996)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      vnL6/vnGAL4 is rescued by vnΔIg.UAS/Scer\GAL4vn-GAL4

      (Austin et al., 2014)

      vnL6/vnddd-4 is rescued by Scer\GAL4αTub84B.PZ/vnUAS.cSa

      (Zecca and Struhl, 2002)
      Partially rescued by

      vnL6/vn1 is partially rescued by vnUAS.cSa/Scer\GAL4vn-GAL4

      (Austin et al., 2014)

      Df(3L)γ3/vnL6 is partially rescued by vnUAS.cSa/Scer\GAL4T80

      (Schnepp et al., 1996)
      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.

      (Austin et al., 2014)

      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.

      (Zecca and Struhl, 2002)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (4)
      References (23)