wing/haltere identity selector gene - transcription factor - when bound to Scalloped , Vg activates several genes in the wing field, for example activation of Serum response factor intervein promoter - muscle specification
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.40
Gene model reviewed during 5.49
Gene model reviewed during 6.43
453 (aa); 46 (kD)
The Ser-rich protein domain within the C-terminal region interacts with the C-terminus of sd to form a complex which acts as a selector for wing development. Interacts with Dhfr.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\vg using the Feature Mapper tool.
Expression is strongly enriched in the ventral midline at embryonic stage 16.
In addition to the previously reported expression in wing and haltere discs, vg transcripts are detected in third larval instar brain by RT-PCR.
vg transcripts are first detected in embryos at stage 10. They are found in lateral stripes from T1 to A7 and in ventrolateral clusters that correspond to the presumptive wing and haltere discs. They are also expressed in a segmentally repeated pattern in the CNS. The vg transcript is expressed at low levels throughout the wing and haltere discs. It is expressed in elevated levels in a broad stripe across the wing and haltere discs in a region that demarcates the wing and haltere forming subregions of the discs. The identification of the presumptive humeral disc as a site of expression is tentative.
Embryonic expression and low level wing and haltere disc expression are normal while the high level restricted expression in wing and haltere discs is absent in vg83b27 mutants.
vg transcripts are expressed at maximal levels in embryos and pupae and are also detected in adults on northern blots. vg transcripts are present at very low levels in 0-4 and 4-8hr embryos, increase substantially in 8-12hr embryos and are expressed through the remainder of embryogenesis before declining in first instar larvae. A 2kb transcript is also detected with one of the probes used but it is not clear if it is vg-specific.
vg is expressed in the ventral longitudinal muscles 1-4 starting in embryonic stage 11 and in dorsal acute muscles 1-3 from stage 13 until stage 17. It is also detected in some neuronal cells.
vg is expressed in a subset of cells in the ventral nerve cord including interneurons descending from neuroblasts NB1-2, NB5-1, and NB5-6. vg-positive cells are first detected at embryonic stage 12 (10-12 cells). By stage 16, each thoracic segment contains 41-43 vg-positive cells that divide into six clusters, three located in a dorsal plane and three located in a ventral plane. Each abdominal segment contains fewer vg-positive cells in both the dorsal and ventral planes. Some of these are interneuron descendending from NB1-2, NB5-1, and NB5-6. vg is also expressed in all three midline ventral unpaired median motorneurons (mVUMSs) and in cells that may be progeny of the median neuroblast (MNB).
vg protein expression decreases in presumptive notum of early to mid second instarvg protein is expressed in a band centered on the DV boundary in early third instarvg protein expression is restricted to the distal wing pouch during late third instar
Protein can be detected in a subset of myoblasts in the region between the presumptive wing and leg discs in stage 12 and greater embryos. In the larval wing disc myoblasts in the proximal region of the notum of the developing wing disc express protein while distal myoblasts do not. In pupae protein is detected in the dorsal longitudinal muscles of the developing wings, while it is rarely detected in direct flight muscles.
GBrowse - Visual display of RNA-Seq signalsView Dmel\vg in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
Analysis of distinct mutant phenotypes of molecularly similar P-element mutant alleles suggests that their response to the P-element repressor invokes a critical RNA secondary structure in the vg transcript, the formation of which is hindered by a read-through transcript initiated at the P-element promoter.
Activation of the N receptor in the wing disc induces the expression of vg and wg, and induces strong mitotic activity. The effect of N on cell proliferation is not simply due to the upregulation of either vg or wg. On the contrary, vg and wg proteins show synergistic effects with N signaling, resulting in the stimulation of cell proliferation in imaginal discs.
The roles of N, wg and vg during the initial stages of wing development are investigated. vg is involved in the specification of the wing primordia under the combined control of N and wg signalling. Once cells are assigned to the wing fate, their development relies on a sequence of regulatory loops that involve N, wg and vg. During this process, cells that are exposed to the activity of both wg and vg will become wing blade and those that are continuously under the influence of wg alone develop as hinge. The growth of the cells in the wing blade results from a synergistic effect of the three genes N, wg and vg on the cells that have been specified as wing blade.
Ectopic wg expression non-cell autonomously induces vg expression in leg discs and activated arm (a cytosolic transducer of wg signalling) cell-autonomously induces vg expression, indicating that vg expression is directly activated by wg signalling.
Genetic combinations with mutants of nub cause additive phenotypes.
Factors, in addition to Su(H), must exist to confer tissue-specific expression of vg and to regulate the spatial and temporal features of vg expression within the wing pouch. Ser determines vg expression domains in the wing pouch. Su(H) represses the vg quadrant enhancer at the wing D/V boundary.
vg is selectively required for wing-cell proliferation and is sufficient to induce outgrowths of wing tissue from eyes, legs and antennae. Different signals (N, dpp) activate separate enhancers to control vg expression. vg integrates positional signals in more than one axis and regulates wing formation and identity.
Expression of wg and vg in the wing margin are direct and parallel responses to the activation of N. wg is not required for the activation of vg, wg activation does not depend on vg function at the dorsoventral boundary. Expression of vg in the wing pouch depends on wg activity, suggesting that a secondary function of vg is to mediate the long-range effects of secreted wg protein in the wing pouch. wg and N cooperate to activate expression of ct, suggesting the wg and N pathways interact synergistically in the wing imaginal disc. These results illustrate that a hierarchical relationship between N, wg and vg patterns the dorsoventral axis of the wing.
Depletion of the dTMP pool by aminopterin leads to a decrease in the amount of vg transcripts. The resistance of vg1 to inhibitors of dTMP synthesis is not due to a qualitatively different effect of this drug on the vg transcript but is related to the expression of a modified vg protein encoded by a truncated transcript.
Induction of vg requires the combined activities of Ser, wg and N. Based on the patterns of expression and requirements for Ser and wg during initiation wing development it is proposed that Ser is a dorsal signal and that wg is a ventral signal. Their combination at the dorso-ventral interface activates the N receptor and leads to vg expression.
vg expression in the developing wing is regulated in at least two steps, initially in a vg-independent manner at the dorso-ventral organizer, and, subsequently, in a broader domain during wing growth.
Ectopic expression of vg causes extensive overgrowth of imaginal discs including the leg, eye and antennal discs.
Deletion analysis within the vg locus demonstrates that loss of exon 3 or exon 4 correlates with wing phenotype and female sterility.
Phenotypic variation of the genetic components underlying oviposition behaviour is analysed using the complete diallel mating design.
vg wild type gene product plays a key role in the regulation of nucleotide metabolism, sensitivity to chemicals is due to the dosage of vg+ alleles. Intron 2 sequences are involved in a second function of vg in dTMP regulation.
The wg product is required to restrict the expression of the apterous gene to dorsal cells in the developing wing and to promote the expression of the vestigial and scalloped genes that demarcate the wing primordia and are required for the development of the wing proper. The pro-wing vg and sd genes regulate each other.
3.8kb cDNA has been cloned from vg locus, and has no structural homology with known DHFR eucaryotic sequences (J.A. Williams, unpublished).
Allele-specific suppressors of a 412-insertion allele of vg have been isolated.
Molecular characterization of the Psc region demonstrates that aberrant vg gene expression results in abnormal bristle development.
vg is directly involved in determining which thoracic imaginal disc cells will form wings and halteres.
vg mutant embryos exhibit normal gap-junctional communication in the imaginal discs and normal membrane potentials.
An analysis of modifiers affecting the expression of the vg mutant phenotype has been carried out.
The vestigial locus seems to be mainly involved in the development of the wing margin. The mutants are recessive viable (with or without a visible phenotype), recessive lethal, or dominant (with a visible phenotype over wild type or a vg allele); some alleles complement each other; others show pleiotropic effects or homeosis (Bownes and Roberts, 1981). In the classical vg mutants, the wings of homozygotes are reduced to vestiges and usually held at right angles to the body, the wing veins still visible. Some mutants have narrow, nicked, or scalloped wings. Halteres may be reduced or absent. Postscutellar bristles are frequently held erect. Viability is somewhat reduced; null mutants are sterile. Temperatures of 29oC or greater appreciably increase wing size (Harnly, 1936; Stanley, 1935). A suppressor of vg on the third chromosome, su(vg), results in an almost normal phenotype at 28oC, an intermediate vg phenotype at 25oC and a strong vg phenotype (in wings and especially halteres) under 20oC (David, Javellot and Touze, 1970). vg/+ heterozygotes with certain Minutes show scalloping of the wings (Green and Oliver, 1940; Simpson, Lawrence and Maschat, 1981). vg/vg/+ has scalloped wings more often than vg/+ (Green, 1946). Final size of larva is smaller than in wild type and pupation occurs slightly later. Wing discs of late larva are also somewhat smaller than in wild type (Auerbach, 1936), as are haltere discs (Chen, 1929). Goldschmidt (1935; Goldschmidt, 1937) claimed that wings are more or less fully formed and subsequently eroded by degeneration during pupation. Waddington (1939; Waddington, 1940) found no evidence of erosion and concluded that the effect of the gene occurs during the larval period and involves reduction in size of prospective wing area and shift in position of line along which wing area is folded out from the imaginal disk. Fristrom (1968), Fristrom (1969), however, using both light and electron microscopy, found numerous degenerating cells in the presumptive wing blade region of the vg wing discs, as did Bryant and Girton (1980), Bownes and Roberts (1981), Bownes and Roberts (1981), James and Bryant (1981) and O'Brochta and Bryant (1983). Duplications of the mesonotum along with deficiences of wing disk material occur in a small percentage of vg mutants (Girton and Bryant, 1980; James and Bryant, 1981).