Gene: Dmel\tor
splc
transmembrane - receptor tyrosine kinase - membrane receptor for Trunk - crucial for establishment of anterior and posterior cell identity of the embryo - required for ecdysone synthesis in the prothoracic gland at pupariation
Please see the JBrowse view of Dmel\tor for information on other features
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Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.49
5.5, 3.6 (northern blot)
None of the polypeptides share 100% sequence identity.
923 (aa); 105 (kD predicted)
May be auto-phosphorylated on tyrosine residues.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\tor using the Feature Mapper tool.
Comment: maternally deposited
Comment: rapidly degraded
tor transcripts are detected mainly in early embryos and in adult females on northern blots. They are detected throughout development at a much lower level. The 5.5kb transcript is present at a significantly lower level than the 3.6kb transcript.
tor transcripts are detected at the earliest stages of oogenesis. They accumulate in the nurse cells until stage S10 after which they are transported to the oocyte. They become evenly distributed between the nurse cells and the oocyte. In early embryos, they are uniformly distributed. During syncytial blastoderm, the RNA moves toward the periphery of the embryos and is mainly situated in the cytoplasm underneath the nuclei. No signal is detected after cellularization.
tor protein is ubiquitously distributed over the cell surface.
The tor protein is expressed in the central portion of the embryo.
tor protein is first detected in embryos around the 9th nuclear division at which stage the nuclei have just arrived at the periphery. Protein levels increase over the next several nuclear division cycles prior to the cellularization of the blastoderm. tor protein then decreases over the next couple of hours after which it is no longer detected.
GBrowse - Visual display of RNA-Seq signals
View Dmel\tor 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.
polyclonal
Source for identity of: tor CG1389
When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, a decrease in the ratio of cells in prometaphase and metaphase versus the total number of mitotic cells seen.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
In tor gain-of-function embryos, primordial germ cells migrate out of the posterior midgut prematurely. They appear more abundant and motile than in wild-type embryos.
Mutating all the tyrosine residues in the kinase insert results in a complete loss of function phenotype. Both phosphorylated tyrosine sites in the kinase domain activation loop are necessary for tor catalytic activity - mutation of these sites also leads to a complete tor loss of function phenotype.
In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
Phylogenetic analysis of the PTK family.
Terminal structure development is regulated by the compensatory activities of positive and negative phosphotyrosine signaling sites on the tor receptor tyrosine kinase.
ksr functions in multiple receptor tyrosine kinase pathways.
The Tl signalling pathway generates a dl nuclear gradient which initiates the differentiation of the mesoderm, neuroectoderm and dorsal ectoderm by activating and repressing gene expression in the early embryo. A second signalling pathway controlled by the tor receptor kinase also modulates dl activity. The tor pathway selectively masks the ability of dl to repress gene expression but only has a slight effect on activation.
The failure to accumulate tor protein at one or both of the poles leads to spatially inappropriate activity of more centrally located tor receptor: ectopic activity depends on the same gene functions normally required for activating tor. Ectopic activity reflects inappropriate diffusion of the ligand to more central regions of the body, and therefore concluded that the tor receptor not only transduces the spatial signal imparted by the tor ligand, but sequesters the ligand, ensuring its correct localization.
In its anterior domain (labral primordia) cnc is activated by bicoid and torso maternal pathways.
An artificial bcd responder gene composed of three bcd consensus binding sites driving Ecol\lacZ is activated by bcd and repressed by tor. This repression does not require tll or hkb. Phosphorylation resulting from the tor signal transduction pathway down-regulates transcriptional activation by the bcd morphogen. The normal phosphorylation changes that affect bcd during development do not occur in tor mutant embryos.
Biochemical analysis of the signal transduction pathway determining terminal structure development.
Portion of torso gene used in P element construct to provide activated phl protein, for study of phl and Ras85D functions in sevenless signal transduction pathway.
csw functions downstream of tor.
tor loss-of-function mutants delete the terminal regions in tll embryos, gain-of-function mutants expand the terminal domains. The maternal terminal system is necessary to activate tll expression in the terminal caps.
Injecting eggs with torso mRNA revealed that torso receptor tyrosine kinase activation is governed by an extracellular molecule produced at the terminal regions of the egg early in embryogenesis. When torso is absent this ligand fails to localise. Mutant ligand-binding torso proteins can suppress telson formation in a dominant negative manner indicating that the ligand is limited in amount. Analysis of torso mutations indicates that gain of function mutations causing ligand-independent activation map to the extracellular domain.
The effect of the terminal system on the expression of 2 zygotic genes involved in dorsoventral patterning, sna and dpp, is mediated by a reduction in dl activity by the terminal system. Due to this interaction the poles adopt a more dorsalised fate than their counterparts in the middle of the embryo.
Increased tor activity compensates for the absence of run activity to activate Sxl expression in the central and terminal regions.
tor has a repressive effect posteriorly and an inductive effect anteriorly on gt expression domain.
tor is responsible for specifying terminal structures.
Mutations in maternal terminal class gene tor do not interact with RpII140wimp.
tor plays a role in the specification of the anterior and posterior pole.
Zygotically active locus involved in the terminal developmental program in the embryo.
The insertion of nos response elements (NREs) is sufficient to render maternal tor transcripts sensitive to repression by nos.
tor mutants exhibit deletion of the acron and telson.
Mature follicles are immunologically stained for asymmetric distribution of ecdysteroid-related antigen. During late oogenesis localisation of the antigen changes dramatically suggesting the antigen plays a role in early embryogenesis and, perhaps, in pattern formation.
phl acts downstream of tor.
tor protein is uniformly expressed along the surface membrane of early embryos, despite its localised activity at both poles.
Mutation in tor results in a maternal effect phenotype with defects during the early stages of gastrulation and defects in the anteroposterior axis.
The product of the tor gene has a structure similar to receptor tyrosine kinase.
Involved in functions related to that of tll.
Pattern elements from the anterior and posterior have been deleted in embryos of tor mutants.
A single dose of tll1 from a tor11D/tor11D mother can partially rescue the tor11D mutant effect in the embryo (loss of abdominal segments); complete rescue may occur when the embryo is homozygous for tll1, receiving the gene from both parents (Strecker, Halsell, Fisher and Lipschitz, 1989). Injection of tor+ cytoplasm from early cleavage embryos can partially rescue tor loss-of-function mutants. ftz expression is reduced or lost in strong gain-of-function mutants (Klingerr et al., 1988; Strecker et al., 1989). phl mutations have been found to be epistatic over tor gain-of-function alleles (Nusslein-Volhard, Frohnhofer and Lehmann, 1987).
maternal-effect lethal embryos from homozygous mothers show alterations in the anterior-posterior pattern. Hypoactivity (loss-of-function) mutant embryos lack anteriormost head structures (labrum, dorsal bridges) as well as structures posterior to the seventh abdominal segment. Hyperactivity (gain of function) mutant embryos, on the other hand, show segment defects in the middle of the embryos, but may have enlarged terminal structures (Klingler, Erdelyi, Szabad and Nusslein-Volhard, 1988; Strecker, Halsell, Fisher and Lipschitz, 1989). A large number of revertants have been obtained from dominant or semidominant hypermorphic alleles. During cellularization at the blastoderm stage, hypoactivity mutant embryos show a 'pole hole' phenotype. A funnel of yolk-free cytoplasm with a small number of nuclei (between 10 and 20) is formed at the posterior pole, extending from the egg periphery to the inner yolk mass. At gastrulation the cephalic furrow is shifted toward the anterior and the germband extends all the way to the posterior end. Analysis of germ-line clones indicates that the torso mutant is germ-line autonomous (Schupbach and Wieschaus, 1986a).
