Abelson tyrosine kinase, Abelson, dAbl, D-abl, Abelson kinase
Low-frequency RNA-Seq exon junction(s) not annotated.
Stop-codon suppression (UAA) postulated; FBrf0216885.
Gene model reviewed during 5.44
Gene model reviewed during 5.45
Gene model reviewed during 5.56
6.0, 5.5-6.0 (northern blot)
Studies of mutated Abl proteins reveal that sequences in the carboxy terminus mediate axonal localization. Disruption of proper subcellular localization correlates with lack of Abl biological function. A novel kinase-independent function of the Abl protein has been identified.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Abl using the Feature Mapper tool.
Abl protein isobserved in axons in the CNS and in the cytoplasm of epithelial cells.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Abl in GBrowse 2
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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.
The N/Abl interaction may promote the turning of ISNb axons by attenuating Abl-dependant adhesion of ISNb axons to their substratum, thus releasing the axons to respond to attraction from target muscles.
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 retracted (unspread but flat). Kc167 cells are unaffected.
dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.
Identification: Enhancer trap expression pattern survey for loci expressed in the ring gland.
Phylogenetic analysis of the PTK family.
Abl gene product may play a role in establishing and maintaining cell-cell interactions.
In vitro modified Abl constructs are used to investigate the Abl function in axonal localization. Fusion proteins with analogous regions of the human, murine or viral abl genes were expressed and tested for their ability to provide function for Abl mutants that would normally die as pupae.
Drosophila Abl and murine v-abl chimeric protein was constructed to assess functional conservation. Results imply that the transforming function of Abl tyrosine protein kinases are only partially conserved through evolution.
Structural and biochemical evidence suggest the gene encodes a protein tyrosine kinase.
The Abl gene product participates in the process of forming and/or maintaining axonal connections in the nervous system.
The transcription pattern of Abl was analyzed in neuroblasts derived from tumorous larval brain of l(2)gl larvae and S2 tissue culture cells. Abl expresses constitutive as well as maternal/embryonic-specific transcripts.
The highest level of transcript hybridization for Abl, Btk29A and Src64B was found during embryogenesis and metamorphosis, suggesting that the transcripts are of maternal origin. Adult females carry three to four times the amount of transcript males do, the major site of expression in the females is the ovary.
Considered to be the Drosophila sequence homologous to mammalian c-abl based both on its origin and amino acid sequence as inferred from its nucleotide sequence. ABL protein detected at the time of germ-band shortening in the axons of the central nervous system in a bilateral symmetrical series of points that correspond to the positions of neuromeres; later, protein appears in the axons growing across the midline, but not in the cell bodies of the CNS nor in the PNS. As development proceeds, staining of the longitudinal fascicles and to a lesser extent the commissural fascicles becomes intense; staining also seen in association with axonal outgrowth of neural cells in the eye imaginal disk (Bennett and Hoffmann). Recessive alleles in combination with Df(3L)st-j7 either die as late pupae or pharate adults with complete cuticle and roughened eyes, Abll1, or as short lived (5-6 days), rough-eyed adults, Abll2 and Abll3. Surviving females lay few eggs, some of which develop into adults; surviving males have motile sperm, but do not mate and produce no progeny. The rough eye is a reflection of some loss of photoreceptor cells plus ommatidial fusion. In combination with a deficiency extending further to the left, e.g., In(3L)std11 to include the locus of Dab, Abll1/Abl- genotypes die as late embryos or early first-instar larvae with disrupted axonal organization in the ventral nerve cord (Henkemeyer, Gertler, Goodman and Hoffmann, 1987). CNS of doubly deficient embryos, i.e., Abl- Dab-, fails to form commissures and is defective in axonal outgrowth, although the PNS develops normally.