Gene model reviewed during 6.03
Gene model reviewed during 5.46
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.44
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 6.05
None of the polypeptides share 100% sequence identity.
The extracellular domain (1-1412) is sufficient to inhibit bdl function.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Lar using the Feature Mapper tool.
Lar transcripts are detected throughout embryogenesis on northern blots and are most abundant in 9-15hr embryos. Lar transcripts are first detected by in situ hybridization in late stage 11 embryos. They are localized to segmentally repeated clusters of cell bodies in the neuronal layer. After germband retraction, Lar transcripts are more homogeneously distributed. High level expression is observed in a pair of cells or cell clusters located near the midline in each segment with lower level expression in many other cell bodies.
In male germline stem cells, Lar immunofluorescence is localized to the membrane at the interface between the hub and the germline stem cells. Lar was also detected in two- and four-cell spermatogonial cysts, with only a weak signal in eight-cell spermatogonial cysts, where it localized to the membrane between mitotic sister cells of a germline cyst. Lar signal was below detection in cyst progenitor cells, somatic cyst cells, and in germ cells in later stages of differentiation.
Localized Lar protein is first observed in the axonal layer in stage 12 embryos. By stage 14 uniform expression is seen along the commissures and longitudinal connectives. Weaker staining is seen on peripheral axon tracts near the edges of the CNS. Weak tracheal staining is sometimes observed.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Lar 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.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a phenotype when assayed in S2R+ cells: cells become round and detached. Kc167 cells are unaffected.
All detectable in vitro PTPase catalytic activity resides in the membrane-proximal of the two PTPase domains of Lar, PTPase D1. However, function of this domain is not required in transgenes to rescue lethal Lar mutants to viability. One important function of PTPase D2 may be to regulate the PTPase activity of PTPase D1. Both the Ig-like domains and FnIII domains of Lar serve important non-redundant functions. The Ig like domains are required for embryonic neural development and the FnIII domains are essential during oogenesis.
dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.
Lar cooperates with integrins to coordinate actin filaments at the basal surface to the follicular epithelium.
Lar is required for photoreceptor cell target specificity in the optic lobe.
Lar is required in posterior follicle cells to maintain osk localisation in the oocyte. In addition Lar plays an important role in aligning follicle cells actin relative to the polar cells to promote egg elongation along the anterior-posterior axis. lar may interact closely with the extracellular matrix to facilitate the planar polarisation of epithelial layers.
In Lar mutants, R7 cells initially project to their correct layer, but then retract to the R8 target layer in the optic lobe. This defect can be fully rescued by expression of Lar in R7 and partially rescued by expression of Lar in R8.
Lar is required for the correct targeting of R7 cell axons. It can act autonomously in R7 and nonautonomously in R8. The phosphatase domains of Lar are required for its activity in R7, but not in R8. This suggests that Lar can act both as a receptor in R7 and as a ligand provided by R8.
Requirements of Lar, Ptp69D and Ptp99A in growth cone guidance decisions along the ISN and SNb motor pathways demonstrates relationships among the tyrosine phosphatases are complex and dependent on cellular context. At growth cone choice points along one nerve, two phosphatases cooperate, while along another nerve these same phosphatases can act in opposition to one another. Lar is central to ISN guidance, Ptp69D and Ptp99A are not essential but do participate in guidance processes involving Lar.
The product of the Lar gene plays a key role during motoneuron growth cone guidance. Lar controls the ability of certain motor axons to navigate specific choice points in the developing nervous system.
Spatial and temporal transcript accumulation pattern in ovaries is determined by in situ hybridisation.
Receptor linked PTPases may be involved in axon outgrowth and guidance during embryonic development.
Lar is a member of a family of receptor linked protein tyrosine phosphatases.