- Tools
- Downloads
- Links
- Community
- About
- Help
FB2026_01
,
released March 12, 2026
Abelson tyrosine kinase, Abelson, dAbl, D-abl, DROTKABL3
non receptor tyrosine kinase with SH2 and SH3 domains - involved in axon extension - phosphorylates cell adhesion and cytoskeletal proteins - acts as a scaffold in a signaling complex to regulate both epithelial and nervous system morphogenesis
Please see the JBrowse view of Dmel\Abl for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
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.
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)
180 (kD)
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.
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).
Abl protein isobserved in axons in the CNS and in the cytoplasm of epithelial cells.
Abl protein isexpressed in the axons of the embryonic CNS. It is also expressed in epithelial cells, with enrichment in the apical cortical cytoplasm during cellularization and early gastrulation. Expression is also observed in the epithelial cells of the imaginal discs.
JBrowse - Visual display of RNA-Seq signals
View Dmel\Abl in JBrowse3-44
3-39.3
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.
polyclonal
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.
Severe defects in CNS axonogenesis are seen in double mutants with mfas.
Phylogenetic analysis of the PTK family.
Abl mutants show phenotypes in somatic muscles and eye imaginal disks.
Abl gene product may play a role in establishing and maintaining cell-cell interactions.
Abl shows a non-additive phenotype in combination with Fas1TE89Da. Fas1 plays an important role in growth cone guidance, as seen in an Abl mutant background.
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 Abl gene promoter has been isolated and sequenced.
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.
Source for merge of: Abl l(3)04674
Source for merge of: Abl CG4032
