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General Information
Symbol
Dmel\vgnull
Species
D. melanogaster
Name
FlyBase ID
FBal0093753
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
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
Deletion of the eight exons of vg.
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
vgnull mutant dorsal longitudinal indirect flight muscles are reduced in number and show an abnormal tubular fibre phenotype. The mutant flies are viable and can walk. Their leg muscles are normal.
In homozygous vgnull embryos VL2 muscles are absent in at least 30% of segments. This muscle loss seems to be VL2 cell specific because VL1 muscles are present in all segments. However, the loss of vg does not seem to block initial formation of adhesions between two differentiating muscles, because, as in stage 16 wild-type embryos, homozygous vgnull exhibit tight adhesions between pairs of VL muscles between segments. The VL1 muscle is initially specified correctly in all segments in vgnull embryos.
The waves of contraction seen in newly hatched larvae are much slower than normal in sd9 hemizygotes, taking approximately 2 times as long to pass from posterior tip to anterior tip compared to wild type. The VL2 muscle is often missing in mutant embryos (there are no detectable defects in other muscles).
vgnull clones in the prospective wing blade of the larval wing disc die quickly in either a wild type or Minute genetic background.
Adult thoraces of vgnull flies show muscle degeneration.
The dorsal/ventral compartment boundary is only slightly disturbed in vgnull/vg83b27-R wing discs.
Mutants show no growth of wing blade tissue, although some hinge structures are still present.
In vgnull mutant wing discs fewer cells are observed in S-phase compared to controls, and discs are reduced in size. There is also a significant decrease in cells in the M phase. vgnull/+ flies display nicks at the wing tip when raised on a low dose of aminopterin (0.5mg/kg). High levels of cell death are observed at the dorsal/ventral boundary in vgnull/+ wing discs from animals raised on aminopterin (2mg/kg).
In homozygous vgnull flies, some dorsal medial muscles are present but no coxal tergal remotor muscles (AKA dorsoventral muscles). The level of degeneration increases in old flies. However, the site of muscle attachment to the epidermis appears normal. Dorsal medial muscle configuration is normal in 48-h APF mutant pupae, indicating that splitting occurs normally and that degeneration of these muscles occurs during late pupal stages and in the adult. Examination of degenerating muscle fibers in mutant adults shows a complete disorganization of myofibrils and nuclei showing morphological signs of apoptosis.
vgnull/vg83b27 adults show an almost complete lack of wing structures.
Significant cell death is not seen in the third larval instar wing disc (similar to wild type). Cell death is induced in the wing disc by expression vgtr.Scer\UAS under the control of Scer\GAL4ptc-559.1 in a vgnull/vgnull background.
Homozygotes show extreme reduction of the wings. Flies heterozygous for vgnull in a sdETX4 background do not show such a significant reduction in the wing as flies heterozygous for vg79d5 in a sdETX4 or sd1 background. The formation of ectopic wing-like outgrowths caused by expression of vgScer\UAS.cZa under the control of Scer\GAL4ptc-559.1 is more strongly reduced in a vgnull homozygous background than in a vgnull heterozygous background.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
vgnull has visible | conditional | dominant phenotype, enhanceable by Df(3R)P-10/+
NOT Enhanced by
Statement
Reference
vgnull has visible | conditional | dominant phenotype, non-enhanceable by E2f[+]/E2f191
Suppressed by
Enhancer of
Statement
Reference
vg[+]/vgnull is an enhancer of visible phenotype of Scer\GAL4vg.int2.1, sdUAS.cVa
vg[+]/vgnull is an enhancer of visible phenotype of Scer\GAL4vg.int2.1, dapUAS.cLa
vg[+]/vgnull is an enhancer of visible phenotype of sdETX4
vg[+]/vgnull is an enhancer of visible phenotype of Bx3
Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
vgnull has wing | conditional phenotype, enhanceable by Df(3R)P-10/+
NOT Enhanced by
Statement
Reference
vgnull has wing | conditional phenotype, non-enhanceable by E2f[+]/E2f191
Suppressed by
Enhancer of
Statement
Reference
vg[+]/vgnull is an enhancer of wing phenotype of Scer\GAL4vg.int2.1, sdUAS.cVa
vg[+]/vgnull is an enhancer of wing blade phenotype of Scer\GAL4vg.int2.1, sdUAS.cVa
vg[+]/vgnull is an enhancer of wing hinge phenotype of Scer\GAL4vg.int2.1, sdUAS.cVa
vg[+]/vgnull is an enhancer of wing phenotype of Scer\GAL4vg.int2.1, dapUAS.cLa
vg[+]/vgnull is an enhancer of wing margin phenotype of sdETX4
vg[+]/vgnull is an enhancer of wing phenotype of Bx3
Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference
Expression of salmScer\UAS.cKa under the control of Scer\GAL41151 restores the normal muscle fibre structure in dorsal longitudinal indirect flight muscles in vgnull mutants. Fibrillar transformation of leg muscles is not observed as a result of salmScer\UAS.cKa expression. Overexpression of salrScer\UAS.cSa under the control of Scer\GAL41151 results in some suppression of the vgnull-mutant dorsal longitudinal indirect flight muscle phenotype.
At early stages (15), the VL muscles show no significant migration or attachment defects in vgnull; rhea1 double mutant embryos. However, at later stages (16+) several muscles, most prevalently VL1 can be seen detaching from their normal location. This muscle detachment phenotype appears to be solely due to a lack of vg activity as it can be rescued through expression of vgScer\UAS.T:Ivir\HA1 in muscle cells. The direction of VL1 muscle migration is unaffected in vgnull; rhea1 double mutants. The development of tendon cells is not affected in vgnull; rhea1 double mutants.
Expression of pucScer\UAS.cMa (which inhibits cell death) in vgnull clones results in clone survival in the prospective wing blade of the larval wing disc. Clone survival depends on the position along the proximal-distal axis of growth, clones being recovered at a higher frequency and larger size in the proximal territories of the vg expression domain. These clones tend to be extruded during larval stages and fail to appear in the adult wing.
Adult thoraces of vgnull, Scer\GAL41151, fngScer\UAS.cKa flies show a significant rescue of muscle degeneration compared to thoraces of vgnull flies.
The severity of wing defects caused by expression of sdScer\UAS.cVa under the control of Scer\GAL4vg.int2.1 is enhanced by vgnull/+; in the double mutant flies 93% have an "extreme" phenotype (thorax flight appendages are completely missing and no hinge structures are present) and 7% have a "severe" phenotype (wing blade growth is severely impaired). The severity of the wing nicking phenotype caused by expression of dapScer\UAS.cLa under the control of Scer\GAL4vg.int2.1 is greatly enhanced by vgnull/+.
Expression of dapScer\UAS.cLa along the dorsal/ventral boundary of the wing under the control of Scer\GAL4vg.int2.1 in a vgnull/+ mutant background results in nicks at the wing tips. There is a significant decrease in mitotic cells along the dorsal/ventral boundary. Co-expression of vgScer\UAS.cZa in flies expressing dapScer\UAS.cLa at the dorsal/ventral wing boundary under the control of Scer\GAL4vg.int2.1 in a vgnull/+ mutant background rescues wing morphology, and mitotic activity of cells is restored in this region. vgnull/+, Df(3R)P-10/+ double heterozygous flies raised on a low dose of aminopterin (0.5mg/kg) display a strong notched-wing phenotype. vgnull/+, E2f91/+ flies display small notches at the wing tip when raised on a low dose of aminopterin (0.5mg/kg). Expression of thScer\UAS.cLa at the dorsal/ventral wing disc boundary under the control of Scer\GAL4vg.int2.1 rescues the strong wing margin phenotype observed in vgnull/+ flies grown on aminopterin (0.5mg/kg). sd[ETX4]/Y males display an enhanced wing phenotype in a vgnull/+ background.
Expression of apScer\UAS.cMa under the control of Scer\GAL4vg.boundary partially rescues the loss of wing tissue seen in vgnull/vg83b27 flies. The scalloped wing phenotype seen in Bx3 homozygotes is enhanced by vgnull/+.
Expression of dapScer\UAS.cLa under the control of Scer\GAL4vg.PU in a vgnull/+ background results in a mutant wing phenotype.
Xenogenetic Interactions
Statement
Reference
Co-expression of E2fScer\UAS.cNa, DpScer\UAS.cDa and BacA\p35Scer\UAS.cHa under the control of Scer\GAL4vg.int2.1 results in a wing nicking phenotype, which is partially suppressed by vgnull/+. Co-expression of E2fScer\UAS.cNa, DpScer\UAS.cDa and BacA\p35Scer\UAS.cHa under the control of Scer\GAL4vg.int2.1 does not wing blade growth in vgnull flies and only a slight increase in wing hinge growth is seen.
Expression of E2fScer\UAS.cNa and BacA\p35Scer\UAS.cHa under the control of Scer\GAL4ptc-559.1 in vgnull mutant discs results in an increase in the number of cells in S-phase.
Complementation and Rescue Data
Rescued by
Partially rescued by
Comments
Expression of vgScer\UAS.cZa under the control of Scer\GAL4ptc-559.1 in vgnull mutant discs increases the number of cells in S-phase and results in overgrowth of the disc along the anterior/posterior axis. An increase in cells in M-phase is observed.
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (17)