drifter, dfr, Cf1a, ventral veinless, Drf
transcription factor - homeodomain - pou domain - mutants display severe tracheal defects and defects in ventral midline glia migration - identities of medulla neurons are pre-determined in the larval medulla primordium, which is subdivided into concentric zones characterized by the expression of four transcription factors: Drifter, Runt, Homothorax and Brain-specific homeobox
Gene model reviewed during 5.44
Triple stop-codon suppression (UAG, UAG, UAG) postulated; FBrf0216884.
Gene model reviewed during 5.46
Gene model reviewed during 5.56
Gene model reviewed during 6.02
vvl protein is a positive regulator of Ddc gene transcription. Immunoprecipitation and crosslinking studies show that vvl protein associates with acj6 protein in vivo. When bound by acj6 protein as a heterodimer, vvl protein no longer binds DNA. Transfection experiments in CV-1 cells demonstrate that vvl protein activates transcription of a reporter gene driven by the Ddc promoter or a heterologous promoter preceded by the vvl element. This activation does not occur in the presence of acj6 protein. The vvl DNA sequence and predicted amino acid sequence is significantly different than that presented in FBrf 54626.
vvl protein encodes a sequence specific DNA-binding protein. The vvl gene product binds to a DNA region required for the expression of Ddc. A high degree of similarity was noted between the vvl protein and Human Brn-1 and Brn-2 POU-domain sequences which extends to the 17aa linker between the homeodomain and the POU domain.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\vvl using the Feature Mapper tool.
Comment: reference states transcript expressed up to 8-12 hr AEL
vvl trasnscript is expressed at early stage 10 in the tracheal placodes, and in homologous cells in segments that will not form trachea. At stage 11, vvl is also expressed in 10 dorsal epithelial patches in each trunk segment, which are displaced with respect to the tracheal primoridia. By stage 15, vvl transcript is expressed in most of the embryonic trunk epithelium
Expression assayed at stages 9, 11, 13, and 17. Expression may be continuous between assayed stages in some tissues.
vvl is expressed in the ectoderm of the anterior hindgut at embryonic stage 14.
vvl transcripts first appear at 5-6hr of development, show a peak of expression between 10hr and 13hr and decline substantially by the end of embryogenesis.
vvl transcripts are first detected in 3-6 hr embryos, are at a maximum level in 6-12 hr embryos and persist throughout development. They are first detected in the tracheal placodes of germ band extended embryos. They are later observed in cells surrounding the tracheal pits that may be chordotonal organs and in a group of cells on the roof of the stomodeal invagination. A complex pattern of expression is observed in the PNS and CNS.
vvl transcripts are initially detected in 3-6 hr embryos, progressively increase to maximum levels in late embryos, and decline thereafter. Transcripts are initially detected in the ectoderm of stage 10 embyros at regular, repeating intervals. This correlates with sites of the invaginations that are the origins of the tracheal placodes. Transcripts are also found along the midline of the CNS. vvl transcripts are found in a subset of neurons in the CNS that substantially overlap those that express acj6 transcripts.
vvl protein is expressed in the differentiated neurons of the the outermost domain of the medulla anlage from third instar larvae and in pupa until 12h APF, distal to the domain of run. Thereafter and in adults, vvl protein is found in layers 8 to 10 of the medulla. It is also observed in the adult neurons of the lobula and lobula plate and in non-neuronal cells of the lamina.
vvl is expressed in many tissues in larvae and adults including fat body, oenocytes, epidermis, tracha, proventriculus, midgut, hindgut, salivary gland, and Malpighian tubule as well as in the larval brain, some imaginal discs, gastric caecum, ring gland, and ejaculatory duct. It was not detected in the lymph gland or hemocytes, in the accessory glands, seminal vesicle, or testis, or in any part of the female reproductive tract.
vvl is first detected in a few neuroblasts of the eveloping brain anlage at embryonic stage 11. By stage 13, it is abundant in neuroblasts and their progeny in each brain neuromere. By stage 15, vvl is observed in specific clusters within all brain neuromeres. A prominent expression domain is observed in the developing tritocerebrum. The majority of cells expressing vvl in the tritocerebrum overlap the lab expression domain.
vvl protein expression is first apparent in early stage 10 in two rows of 10-cell patches corresponding to the developing tracheal placodes. vvl expression serves as a marker for the tracheal pits as they undergo extensive morphogenetic movements in stages 10-13. Epidermal vvl expression becomes prominant from stages 13-16/17 and masks the tracheal expression at these stages. During this period, strong staining is seen in the seven laterally symmetrical oenocyte clusters in segments A1-A7. vvl is also expressed in the hindgut in stages 13-15. vvl expression is observed in the developing head region in stage 10/11 embryos in tissues of the procephalon, clypeolabrum, and labium. The most prominant labeling is seen in laterally symmetrical placodes of cells located on both the dorsal and ventral sides of the stomodeal opening. This corresponds to regions containing sensory progenitor cells derived from the clypeolabrum and labrum. Expression is seen in the cells of the mesectoderm in stages 10-12. Mesectoderm expression extends beyond stage 12 in the middle pair of midline glia (MGM). In later stages, vvl is expressed in a uniform repeated pattern of ~25 nuclei per neuromere grouped into 5 distinctive clusters: 1) a midline cluster of four nuclei containing the MGM and a pair of RP motoneurons, 2) two symmetrical mediolateral clusters that contain the paired serotonergic neurons, and 3) two symmetrical lateral clusters.
GBrowse - Visual display of RNA-Seq signalsView Dmel\vvl 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: vvl CG10037
vvl may regulate dendritic targeting and coordinate dendritic and axonal connectivity of projection neurons in the olfactory system to ensure the highly stereotypes acquisition and delivery of olfactory information by the central olfactory neurons.
vvl is required for the maintenance of btl expression during tracheal tree development. vvl is also required for the specific expression in the tracheal cells of tkv and rho. vvl makes the tracheal cells competent to further signalling through activation of its target genes.
Maintenance of high level btl expression requires wild-type vvl function. Characterisation of btl regulatory sequences identifies seven high affinity and one low affinity vvl recognition elements, implying direct transcriptional regulation of btl expression by vvl.
vvl function in CNS development is studied by misexpression of the protein both temporally and spatially. Results suggest that premature vvl expression disrupts initial mesectodermal lineage designation and therefore subsequent midline differentiation.
Two variant POU domain recognition elements, DFRE1 and DFRE2, have been identified within a 514bp vvl autoregulatory enhancer. DFRE1 and DFRE2 show separable tissue-specific functions when independently disrupted or deleted.
Examination of the mutant CNS and tracheal phenotypes suggests a requirement for vvl protein for the correct differentiation and/or migration of tracheal cells and midline glia in the CNS.
The pattern of vvl expression during embryonic development has been analysed in wild-type and mutant embryos.
Examination of CNS formation in vvl loss of function mutants suggest that the vvl gene is required for the correct differentiation of selected neurons and glia in the CNS. Ecol\lacZ reporter gene constructs suggest that vvl is capable of selectively altering mesectodermal cell fates.
vvl is required in developmental processes as diverse as tracheal tree elongation and ventral ectoderm development during embryonic stages and cell proliferation and vein differentiation in the wing imaginal disc. It is proposed that vvl integrates information from different signaling molecules and in turn regulates the expression of specific cell differentiation genes during tracheal development and vein differentiation.
vvl is required for the differentiation of dorsal and ventral veins, and for cell proliferation in internal regions of the wing.
vvl links positional information and cell differentiation during embryonic and imaginal development. During embryogenesis vvl is required for the formation of the tracheal tree and in the patterning of the ventral ectoderm. During imaginal development vvl is required for cell proliferation and the differentiation of the wing veins. vvl expression is dependent on the coordinate activities of dpp, wg and hh. vvl interacts with other genes involved in vein differentiation, including rho, tkv, Egfr, dpp and N.
One of the homeodomain loci identified in a screen for genes encoding DNA binding proteins capable of binding to a consensus Engrailed binding site.
An alternative transcript of Ipou, lacking two basic amino acids, is incapable of dimerizing with Cf1a.
vvl contains a POU domain, and is expressed at maximum levels during early development.
Cf1a is a transactivator of the Ddc gene and is coexpressed in subsets of neurons with Ipou during development. Ipou forms a highly stable heterodimeric complex with Cf1a and inhibits its ability to bind DNA and activate transcription of Ddc.
Mutations in vvl have no pleiotropic phenotypes in embryonic patterns.
ve, vn, ci, cg, svs, ast(S), 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 mutant alleles of vvl prevent ventral vein differentiation. Embryonic lethal alleles also exist.