dab, BP106, disabled, Neur
transmembrane serine esterase homolog - Mutations in Neurotactin frequently cause defasciculation of the normally tightly associated ocellar pioneer axons
Please see the JBrowse view of Dmel\Nrt for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.46
4.25, 3.65, 3.2 (northern blot)
4.7, 3.7, 3.4 (northern blot)
846 (aa); 135 (kD observed); 93 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Nrt using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as ventral nerve cord anlage
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: DFM myoblasts
Nrt protein is expressed in myoblasts that will give rise to direct flight muscle (DFM).
Nrt-XP is excluded from the calyx of the larval mushroom body, but not from the lobes.
In situ hybridization shows that Nrt is enriched in border follicle cells relative to follicle cells in stage S9 or S10 egg chambers.
Protein is first observed in the golgi basal to the nuclei in embryonic cycle 13. At cellularization the protein becomes concentrated at the apical invaginating membrane and later is detected in the lateral membrane.
JBrowse - Visual display of RNA-Seq signals
View Dmel\Nrt in JBrowse




3-44
3-39.4
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 JBrowse 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.
monoclonal
Nrt is required during axon outgrowth, fasciculation and guidance.
In vitro fusion of the homologous extracellular domain of Egfr and Glt to the Nrt cytoplasmic domain can mediate aggregation of cells incubated with a soluble crude fraction containg Nrt ligand activity. The binding site for the Nrt ligand is localised within the extracellular domain. A stretch of 25 amino acids forms an alpha-helix located close to the pseudocatalytic site and is crucial for the adhesive function.
Induction of Nrt in transfected Schneider S2 cells is capable of mediating cell adhesion in a heterophilic manner.
Nrt has been cloned and characterised.
Embryos homozygous for either of the two Nrt- deletions used by de al Escalera et al. (1990) do not exhibit any 'extra' gross abnormalities of the CNS. Deletion of regions just distal to Nrt <up>i.e. Df(3L)st100.62 or Df(3L)st-e5</up> leads to defects in axonal patternings (because of the absence of the abl and dab genes in 73B, cf. Gertler, Bennet, Clark and Hoffman, 1989), but the further removal of Nrt+ does not make this phenotype worse (de la Escalera, Bockamp, Moya, Piovant and Jimenez, 1990).
Three monoclonal antibodies selected because of binding to presumptive imaginal neurons within the larval central nervous system (CNS) (de la Escalera, Bockamp, Moya, Piovant and Jimenez, 1990) and an additional one found by virtue of binding to neuronal surfaces in embryos (Hortsch, Patel, Bieber, Traquina and Goodman, 1990) detected the same ca. 135kD protein on Western blots of homogenates from embryos, late larva and pupae. The membrane-bound material is called neurotactin (NRT) because of its expression at points of interneuronal cell contact. Antibody staining (de la Escalera, Bockamp, Moya, Piovant and Jimenez, 1990; Hortsch, Patel, Bieber, Traquina and Goodman, 1990) shows concentration of the protein in dorsal and ventral portions of embryonic blastoderm (where staining appears cell surface-limited), all over gastrulating embryos (although Hortsch, Patel, Bieber, Traquina and Goodman, 1990 imply a somewhat more restricted expression pattern), in the 'proliferating' CNS (including neuroblasts and their progeny) of stage 10-11 embryos and in regions of contact between neuroblasts. In visceral mesoderm (stage 13), non-neuronal expression diminishes, although it is seen on fat body cells and the 'dorsal vessel'; intense staining continues in embryonic CNS (but is relatively weak in axons of motor neurons); PNS expression is evident as well (seemingly restricted to sensory cells that send out multiple dendritic projections, and, in fact, PNS cell-body signals are weaker than on dendrites); cell-surface expression apparent in the various expressing tissues during mid-embryogenesis; in early L1, NRT signals decay but reappear in CNS (in optic formation centers and in neuron clusters and associated axons in ventral cord); the protein's expression persists in imaginal neurons through mid-pupal stage, wanes as such cells complete maturation and is undetectable in adults. L3 imaginal discs are NRT positive (e.g. on developing chordotonal neurons of leg discs and in developing photoreceptor cells plus their axons, posterior to the morphogenetic furrow). Cell culture studies, including electron-microscope observations (Barthalay, Hipeau-Jacquotte, de la Escalera, Jimenez and Piovant, 1990), suggest further that NRT is a 'contact molecule' between neurons or epithelial cells; there is uniform expression along intercellular contact areas; non-adhesive Schneider-2 cells, transfected with Nrt cDNA, do not become self adhesive, but these cells bind to a subpopulation of embryonic cells.
Source for merge of: Nrt BcDNA:LD22004
All five mutations originally thought to be lesions in the Dab gene (see FBrf0049327, FBrf0058531 and FBrf0084025) are actually lesions in the Nrt gene, the alleles are: NrtM2, NrtM29, NrtM54, NrtM100 and NrtM221.
Source for merge of Nrt BcDNA:LD22004 was sequence comparison ( date:990717 ).
FlyBase curator comment: in FBrf0058531, the NrtM2 allele is stated to be due to a lesion in the Dab gene, since four copies of a rescue construct containing Dab sequences (P{Dab.G}) rescue the lethality of NrtM2 Df(3L)st-j7/Abl1 animals. However this has subsequently been shown to be an error (see FBrf0162067) - the NrtM2 allele is actually due to a lesion in the Nrt gene.
The "M2" and "M29" mutations isolated in FBrf0049327 were named "disabled" alleles to indicate their genetic interaction with Abl and the effect of the mutations, in an Abl mutant background, on the embryonic central nervous system.