FB2024_03 , released June 25, 2024
Allele: Dmel\vvldfr-B129
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General Information
Symbol
Dmel\vvldfr-B129
Species
D. melanogaster
Name
FlyBase ID
FBal0044447
Feature type
allele
Associated gene
Dmel\vvl
Associated Insertion(s)
Carried in Construct
Also Known As
dfrB129, drifterB129
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(Certel et al., 1996)
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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
      Detailed Description
      Statement
      Reference

      Expressing vvldsRNA.UAS under the control of Scer\GAL4da.G32 in a vvldfr-B129 heterozygous background results in melanized spots in the cuticle, Malpighian tubules and gastric caecum, and abnormal morphology of the fat body in third instar larvae. Expressing vvldsRNA.UAS under the control of Scer\GAL4c729 in a vvldfr-B129 heterozygous background results in melanized tissues and death prior to eclosion.

      (Junell et al., 2010)

      In vvldfr-B129/+ embryos less than 2% of muscles 12 and 13 fail to be innervated and only 4% of ISNb axons leave the ventral muscle field and target the transverse nerve (TN) fascicle. In vvldsRNA.Scer\UAS, vvldfr-B129/+ embryos with Scer\GAL4Lim3.B or Scer\GAL4ftz.ng, ISNb motor axons leave the ventral muscle field and contact or target the transverse nerve (TN) fascicle. There is also an overall decrease in muscle innervation by ISNb motor axons in these embryos.

      (Certel and Thor, 2004)

      When homozygous somatic clones are made in the lateral projection neurons, no significant change is seen in cell numbers within clones. These clones do show a decrease in the number of lateral landmark glomeruli innervated. 8/10 lateral of the glomeruli are still innervated by clones, but VA4 is never innervated. DM5 is missing about half the time.

      (Komiyama et al., 2003)

      Tracheal structures are defective in homozygotes, although some tracheal tissue is present.

      (Certel et al., 1996)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by Lim3[+]/Lim36

      (Certel and Thor, 2004)

      Lim3[+]/Lim36, vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by tupisl-1/tup[+]

      (Certel and Thor, 2004)

      tupisl-1/tup[+], vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by Lim3[+]/Lim36

      (Certel and Thor, 2004)

      Lim36, vvl[+]/vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by tupisl-1/tup[+]

      (Certel and Thor, 2004)

      tupisl-1, vvl[+]/vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by Lim3[+]/Lim36

      (Certel and Thor, 2004)

      vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by tupisl-1/tup[+]

      (Certel and Thor, 2004)

      vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by Df(2L)E71/+

      (Certel and Thor, 2004)
      NOT Enhanced by
      Statement
      Reference

      vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, non-enhanceable by exex[+]/exexKK30

      (Certel and Thor, 2004)
      Enhancer of
      Statement
      Reference

      vvl[+]/vvldfr-B129 is an enhancer of abnormal neuroanatomy | dominant phenotype of Lim36

      (Certel and Thor, 2004)

      vvl[+]/vvldfr-B129 is an enhancer of abnormal neuroanatomy | dominant phenotype of tupisl-1

      (Certel and Thor, 2004)
      Phenotype Manifest In
      Enhanced by
      NOT Enhanced by
      Statement
      Reference

      vvldfr-B129 has larval intersegmental nerve | embryonic stage 16 phenotype, non-enhanceable by exex[+]/exexKK30

      (Certel and Thor, 2004)

      vvldfr-B129 has larval transverse nerve | embryonic stage 16 phenotype, non-enhanceable by exex[+]/exexKK30

      (Certel and Thor, 2004)
      Enhancer of
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      In vvldfr-B129/+ embryos less than 2% of muscles 12 and 13 fail to be innervated and only 4% of ISNb axons leave the ventral muscle field and target the transverse nerve (TN) fascicle. The expressivity of these phenotypes is enhanced to 22% and 16.5% respectively by Df(2L)E71/+, to 21% and 16% respectively by tupisl-1/+ and to 29% and 24% respectively by Lim36/+. These phenotypes are not enhanced by exexKK30/+. In tupisl-1, Lim36/+; vvldfr-B129/+ embryos, the ISNb motoneurons fail to project to and innervate their specific target muscles, including muscles 12 and 13.

      (Certel and Thor, 2004)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Complements: sinu06524.

      (Beitel and Krasnow, 2000)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      References (9)