a secreted neuregulin-like EGFR ligand - EGF domain and Ig domain - an intrinsically weaker ligand for EGF-receptor than Spitz - Vein is the major ligand for activating EGF-R in intervein regions - has roles in growth and patterning of tissues including muscle, midgut, ovary, trachea, glia, eye and leg .
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.45
None of the polypeptides share 100% sequence identity.
622, 621 (aa); 70 (kD observed); 71 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\vn using the Feature Mapper tool.
In the wing pouch, vn is expressed as a broad discontinuous stripe straddling the A/P boundary in the L3 and L4 intervein region and also in the hinge and the notum. No transcript is observed in the haltere disc.
vn expression starts at 72 AEl in a small eliptical domain at the center of the leg disc. This is the presumptive pretarsus region. At 96 hr AEL, the domain evolves with expression in two isolated cells and a proximal domain in the dorsal pleura. Between 96 and 120 hr, the early central domain disappears, whereas the two isolated cells give rise to two symmetrical clusters in the presumptive pretarsus. Concentric rings of weak expression in tarsus 1, and near the tibia/femur and proximal femur/trochanter boundaries are apparent at this stage. Strong sub-epidermal staining in the pretarsus and weak expression in the tarsal segments is seen at 8 hr APF.
Transcripts are detected in pioneer MP2 neurons in the CNS, first appearing at stage 11 and persisting at least through stage 14. Transcript is detected in the dMP2 neurons throughout this time, however, expression in the vMP2 neuron only persists through stage 12 in many cases. Transcript is also detected in VUMs and two more cells in each hemisegment.
vn transcripts are expressed inblastoderm embryos in two ventrolateral stripes that come to the midlineas gastrulation proceeds. Expression persists in the midline but isincreasingly restricted to single cells. Expression is seen in the CNS andepidermis at germ band retraction. vn is also expressed in theamnioserosa precursors in the blastoderm and in the amnioserosa properuntil the end of germ band extension. Late in germ band extension,expression is seen in some PNS precursors which include Keilin's organprecursors and a subset of cells of the chordotonal organs. vn is alsoexpressed in the head throughout development; in the clypeolabrum, themaxillary and labial lobes and around the stomodeum. In late embryos,expression occurs in the segmental muscles and gut wall. Transientexpression is observed in the tracheal pits at stage 10.
vn transcripts are expressed in a complex and dynamic pattern in the wing, haltere, leg and eye-antenna discs. The pattern in the wing is described in detail. vn transcripts are first expressed in the presumptive notum and then in the wing pouch and hinge regions. Later, transcripts localize to intervein regions. This begins as a stripe of expression stradling the AP boundary in late larval discs and develops into all intervein regions after puparium formation.
GBrowse - Visual display of RNA-Seq signalsView Dmel\vn 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.
Source for identity of: vn CG10491
Vein-dominant1 (previously 'Vn') may be a dominant negative allele of vn, because expressing vn without the EGF domain gives a vein loss phenotype. So Vein-dominant (previously 'Vn') and vn may refer to the same gene.
Map position and phenotype suggest of "vn1" suggests a possible relationship to "Vn1", but allelism has not been tested as "Vn1" is no longer available.
Six alleles (Diaz-Benjumea et al., 1989). Not tested for allelism with Vn, a dominant mutant of similar map position and phenotype which has been lost.
vn has a minor role in the embryo and does not induce Egfr target genes such as argos and pnt in the embryo. vn has a major role in wing development and vn/Egfr signal is a potent inducer of Egfr target genes in the wing disc.
vn is the activating ligand of Egfr in the midgut. vn plays a permissive role in the induction of the endoderm by dpp and wg, which in turn up-regulate vn expression in the midgut mesoderm in two regions overlapping the dpp sources.
Genetic combinations with mutants of nub cause additive phenotypes.
In vivo culture of mutant discs from genotypes that are normally embryonic lethal demonstrates vn is essential for wing disc growth.
The molecular signal for terminal differentiation of tendon cells is secreted vn protein produced by the myotubes.
Phenotype and expression analysis show vn has an early role in global proliferation of the wing disc and specific roles in the development of the notum, hinge, longitudinal vein 4 and all intervein regions.
Mutant embryos have a phenotype similar to that seen in sr, with abnormal direction of myotubule filopodia.
Genetic mosaics demonstrate that cell proliferation is reduced in all regions of the wing blade in a local autonomous way, the effects are more extreme when clones occupy intervein regions bordering veins. Clones also have nonautonomous effects in the proliferation of wild type cells in the same wing, these effects are more extreme in double mutants with rho.
Mutations in vn cause pleiotropic phenotypes in embryonic patterns and affect several longitudinal veins.
ve, vn, ci, cg, svs, ast, H, Vno and vvl belong to the vein phenotypic group (Puro, 1982, Droso. Info. Serv. 58:205--208 ) within the 'lack-of-vein' mutant class. Loss-of-function alleles at these loci remove stretches of veins in two or more longitudinal veins. Double mutations within members of this group remove all veins, have smaller, slightly lanceolate wings, no sensilla and extra chaetae. Some alleles are embryonic lethal.
Homozygous ddd larvae perish between the first larval instar and the prepupal stage; dorsal thoracic imaginal discs, i.e. of the pronotum, mesonotum and metanotum reduced to 3% or less of normal size; all other imaginal discs develop normally. Mutant larvae support the growth of wild-type wing discs; mutant wing discs show very little development in wild-type larval. Mutant cells develop normally in wing discs that contain mixtures of mutant and wild-type cells, as produced by nuclear or cellular transplantation into blastoderms or by somatic exchange. Mutant leg discs transplanted into wild-type hosts can transdetermine to wing development. Studies of temperature-sensitive genotypes indicate that vn+ product is not required for normal wing development during embryogenesis. No evidence for a maternal effect in either conditional mutants raised under permissive conditions and switched to restrictive temperatures or in germ-line-transplants of mutant cells into wild-type hosts.