FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Abl4
Open Close
General Information
Symbol
Dmel\Abl4
Species
D. melanogaster
Name
FlyBase ID
FBal0028710
Feature type
allele
Associated gene
Dmel\Abl
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Progenitor genotype
    Cytology
    Description

    23bp deletion at the 3' end of exon 2 that extends into the intron between exons 2 and 3. The deleted sequence is 5'TTTGAGGTGCGTAGATGG3' (the TTTGAG at the 5' end of the deleted sequence is that which comprises part or all of codons 291-293). RNA analysis has not been undertaken to investigate the effect of the mutation on splicing, but conceptual translation of residues 1-290 results in a protein of 29.4kD molecular weight, which is in good agreement with the previously reported molecular weight of 25-35kD for the Abl4 protein (obtained by immuno-blotting).

    (Smith and Liebl, 2005)
    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    deletion
    3L:16,628,646..16,628,668 [-]
    Comment:

    A 23 bp deletion.

    (Smith and Liebl, 2005)
    Variant Molecular Consequences
    Associated Sequence Data
    DDBJ / EMBL / GenBank
    DNA sequence
    Protein sequence
     
    UniProtKB/Swiss-Prot
      UniProtKB/TrEMBL
        Expression Data
        Reporter Expression
        Additional Information
        Statement
        Reference
         
        Marker for
        Reflects expression of
        Reporter construct used in assay
        Human Disease Associations
        Disease Ontology (DO) Annotations
        Models Based on Experimental Evidence ( 0 )
        Disease
        Evidence
        References
        Modifiers Based on Experimental Evidence ( 0 )
        Disease
        Interaction
        References
        Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
         
        Disease-implicated variant(s)
         
        Phenotypic Data
        Phenotypic Class

        abnormal cell shape | embryonic stage

        (Rogers et al., 2021)

        abnormal mitotic cell cycle | maternal effect

        (Grevengoed et al., 2003)

        abnormal neuroanatomy

        (Andrews et al., 2008, Bhat et al., 2007, Lee et al., 2004)

        abnormal neuroanatomy (with Abl1)

        (Forsthoefel et al., 2005, Liebl et al., 2003)

        abnormal neuroanatomy | embryonic stage 15

        (Spracklen et al., 2019)

        abnormal neuroanatomy | embryonic stage 16

        (Hsouna et al., 2003)

        abnormal neuroanatomy | embryonic stage, with AblKN.ftz

        (Hsouna et al., 2003)

        abnormal neuroanatomy | embryonic stage (with Abl1)

        (Lin et al., 2009)

        abnormal neuroanatomy | embryonic stage (with Abl2)

        (Song et al., 2010)

        abnormal neuroanatomy | larval stage (with Abl1)

        (Lin et al., 2009)

        abnormal neuroanatomy | larval stage (with AblEP3101)

        (Lin et al., 2009)

        abnormal neuroanatomy | larval stage (with Df(3L)st-j7)

        (Lin et al., 2009)

        abnormal neuroanatomy | recessive

        (Wills et al., 2002)

        abnormal neuroanatomy | somatic clone | third instar larval stage

        (Sterne et al., 2015, Li et al., 2005)

        abnormal neuroanatomy | third instar larval stage (with Abl1)

        (Kim et al., 2019)

        abnormal neurophysiology | larval stage (with Abl1)

        (Lin et al., 2009)

        lethal (with Abl1)

        (Lin et al., 2009, Liebl et al., 2003)

        lethal - all die before end of pupal stage (with Abl1)

        (Liebl et al., 2000)

        lethal - all die during embryonic stage | germline clone | maternal effect

        (Rogers et al., 2021)

        lethal - all die during embryonic stage | recessive | rescuable maternal effect

        (Grevengoed et al., 2001)

        majority die during embryonic stage | maternal effect

        (Rogers et al., 2016)

        majority die during embryonic stage | maternal effect (with Df(3L)st-j7)

        (Rogers et al., 2016)

        partially lethal - majority die (with Abl2)

        (Hsouna et al., 2003)

        partially lethal - majority die (with Df(3L)st7)

        (Rogers et al., 2021)

        partially lethal - majority die (with Df(3L)st-j7)

        (Rogers et al., 2016)

        some die during embryonic stage | rescuable maternal effect

        (Grevengoed et al., 2001)

        some die during pupal stage (with Abl1)

        (Liebl et al., 2000)

        visible (with Abl2)

        (Hsouna et al., 2003)

        visible | recessive

        (Bennett and Hoffmann, 1992)
        Phenotype Manifest In

        actin cytoskeleton | embryonic stage | maternal effect

        (Grevengoed et al., 2003)

        actin filament & egg chamber | germ-line clone

        (Gates et al., 2009)

        axon | embryonic stage 15

        (Spracklen et al., 2019)

        dendrite | somatic clone

        (Li et al., 2005)

        egg | germline clone | maternal effect

        (Gates et al., 2009)

        embryo

        (Rogers et al., 2021)

        embryo | dorsal closure stage

        (Grevengoed et al., 2001)

        embryonic/first instar larval cuticle | dorsal

        (Grevengoed et al., 2001)

        embryonic/first instar larval cuticle | embryonic stage

        (Rogers et al., 2021)

        embryonic/larval neuromuscular junction (with Abl1)

        (Lin et al., 2009)

        embryonic/larval neuromuscular junction | larval stage (with Abl1)

        (Kim et al., 2024)

        embryonic/larval neuromuscular junction | third instar larval stage (with Abl1)

        (Kim et al., 2019)

        embryonic leading edge cell

        (Rogers et al., 2021)

        embryonic midline of ventral nerve cord | embryonic stage 15

        (Spracklen et al., 2019)

        eye (with Abl2)

        (Hsouna et al., 2003)

        eye photoreceptor cell

        (Bennett and Hoffmann, 1992)

        follicle cell & actin filament | somatic clone

        (Baum and Perrimon, 2001)

        follicle cell | somatic clone

        (Baum and Perrimon, 2001)

        interommatidial bristle

        (Bennett and Hoffmann, 1992)

        larval anterior commissure

        (Andrews et al., 2008)

        larval dorsal multidendritic neuron ddaE | somatic clone

        (Li et al., 2005)

        larval intersegmental nerve (with Abl1)

        (Kraut et al., 2001)

        larval intersegmental nerve (with Abl2)

        (Wills et al., 1999)

        larval intersegmental nerve branch ISNb of A1-7 (with Abl2)

        (Song et al., 2010)

        larval intersegmental nerve branch ISNb of A1-7 | embryonic stage

        (Kannan et al., 2017)

        larval longitudinal connective

        (Bhat et al., 2007)

        larval longitudinal connective (with Abl1)

        (Lin et al., 2009, Liebl et al., 2000)

        larval longitudinal connective (with Abl2)

        (Wills et al., 1999)

        larval longitudinal connective (with AblEP3101)

        (Lin et al., 2009)

        larval longitudinal connective (with Df(3L)st-j7)

        (Lin et al., 2009)

        larval longitudinal connective | embryonic stage 16

        (Hsouna et al., 2003)

        larval longitudinal connective | embryonic stage, with AblKN.ftz

        (Hsouna et al., 2003)

        larval multidendritic class IV neuron | somatic clone | third instar larval stage

        (Sterne et al., 2015)

        larval neuron

        (Lee et al., 2004)

        larval posterior commissure

        (Andrews et al., 2008)

        larval segmental nerve branch SNa of A1-7 (with Abl2)

        (Song et al., 2010)

        larval ventral nerve cord | embryonic stage 15

        (Spracklen et al., 2019)

        larval ventral nerve cord commissure (with Abl1)

        (Liebl et al., 2003)

        larval ventral nerve cord commissure | embryonic stage 15

        (Spracklen et al., 2019)

        macropinosome | larval stage (with Abl1)

        (Kim et al., 2024)

        microtubule | third instar larval stage (with Abl1)

        (Kim et al., 2019)

        mitotic domain 1 | extended germ band stage

        (Grevengoed et al., 2001)

        NMJ bouton | increased number (with Abl1)

        (Lin et al., 2009)

        NMJ bouton | increased number (with AblEP3101)

        (Lin et al., 2009)

        NMJ bouton | third instar larval stage (with Abl1)

        (Kim et al., 2019)

        ommatidium

        (Bennett and Hoffmann, 1992)

        presumptive embryonic/larval central nervous system

        (Wills et al., 2002)

        spindle | cleavage stage | maternal effect

        (Grevengoed et al., 2003)

        symmetrical commissure (with Abl1)

        (Forsthoefel et al., 2005)

        synaptic vesicle & NMJ bouton (with Abl1)

        (Lin et al., 2009)

        ventral furrow | non-rescuable maternal effect

        (Fox and Peifer, 2007)
        Detailed Description
        Statement
        Reference

        Abl4/Abl1 (but not Abl4/+) third instar larvae display supernumerary mature and satellite NMJ boutons.

        (Kim et al., 2019)

        Maternal-zygotic stage 15 Abl4 embryos display a range of CNS defects, with roughly half showing moderate axon patterning defects with frequent loss of commissures and the other half showing more severe axon patterning defects.

        (Spracklen et al., 2019)

        Vast majority of Abl4 mutant embryos display stalling of the ISNb motor nerve at the junction of muscles 6 and 13, with failure to innervate muscle 12.

        (Kannan et al., 2017)

        Abl4/Df(3L)st-j7 mutants survive morphogenesis due to maternally loaded Abl but almost all die as pupae, both maternally (progeny of either Abl4/Df(3L)st-j7 mothers or of females whose germlines are homozygous for Abl4 - created by the FLP/FRT/DFS method) and zygotically null Abl mutants generally do not survive embryogenesis and show multiple morphogenesis defects due to incorrect cellularization (multinucleate cells) and mesoderm invagination (disrupted midline), dorsal closure (uneven leading edge, zippering defects, aberrant shapes of cells at the leading edge and decreased rate of closure) and ventral nerve cord formation (disrupted axon scaffold). Abl4/Df(3L)st-j7 maternally and zygotically mutant early larval stage escapers also show signs of defective embryogenesis: germband retraction, head involution, dorsal closure or epidermal integrity defects.

        (Rogers et al., 2016)

        The class IV dendritic arborizing neurons in Abl4/Abl4 MARCM somatic clones display slightly but significantly decreased presynaptic terminal lengths than controls.

        (Sterne et al., 2015)

        Maternally mutant embryos raised at 25[o]C show a significant reduction in axis elongation compared to wild type during germband elongation.

        (Tamada et al., 2012)

        ISNb motor axons stall and fail to innervate their most distal target in 77% of hemisegments in Abl2/Abl4 embryos. These embryos also show a "stop short" phenotype in the dorsal branch of the SNa motor nerve, with the axons stopping short and failing to reach their muscle target.

        (Song et al., 2010)

        14% of eggs derived from females carrying homozygous germline clones show a "dumpless" phenotype.

        Early to mid-stages of oogenesis in females carrying homozygous germline clones are indistinguishable from wild-type in morphology and actin localisation. The nurse cell actin structures are relatively normal in the mutant egg chambers, although stage 9 mutant egg chambers already contain cytoplasmic actin filaments, suggesting a possible acceleration in initiating filament formation. Ectopic accumulations of actin are occasionally seen in the oocyte. Late stage cytoplasmic filaments sometimes appear more robust than wild type.

        (Gates et al., 2009)

        37% of Abl1/Abl4 embryos show abnormal crossing of the midline of Fas2-positive axons.

        Bouton number per muscle area is significantly increased at the larval neuromuscular junction in AblEP3101/Abl4, Abl1/Abl4 and Abl4/Df(3L)st-j7 mutants compared to controls.

        The amplitude of both evoked excitatory junctional potentials (EJPs) and spontaneous EJPs (mEJPs) at the larval neuromuscular junction are unaffected in Abl1/Abl4 larvae, but the frequency of mEJPs is increased by 57% compared to controls.

        General features of synapse structure (including bouton morphology, active zones with T-bars and the structure of subsynaptic reticulum) appear unaffected at the neuromuscular junction of Abl1/Abl4 larvae. However, the average density of the total synaptic vesicles is decreased by 50% in the mutant boutons. In addition, enlarged, but electron-clear vesicles are often seen near the T-bar.

        (Lin et al., 2009)

        The ladder-like neuronal tracts in the embryonic ventral ganglion are grossly normal in Abl2/Abl4 embryos.

        (Yu et al., 2009)

        Abl4 embryos show defects in the commissures of the central nervous system; 1% of anterior commissures are absent, 2% of anterior commissures are thin, 1% of posterior commissures are absent and 1% of posterior commissures are thin. 50% of segments fail to separate the anterior and posterior commissures correctly.

        (Andrews et al., 2008)

        Homozygous embryos have strong axon guidance defects in the longitudinal tracts.

        (Bhat et al., 2007)

        Homozygous clones that encompass the morphogenetic furrow do not result in a defect in cell constriction in the morphogenetic furrow.

        (Corrigall et al., 2007)

        Heterozygous Abl4 stage 16 embryos do not display abnormal midline crossing axon tract projections.

        (Dorsten et al., 2007)

        Embryos derived from homozygous females have only weak cellularization defects at 25oC. These embryos show no obvious germband extension defects and the cell-cell contact rearrangements that drive germband extension occur normally. However, these embryos consistently show ventral abnormalities (since this phenotype is fully penetrant, and only half the embryos lack both maternal and zygotic Abl+ function, this indicates that the phenotype depends solely on maternal Abl). The mutant embryos show differences from wild type soon after the onset of ventral furrow formation; apical constriction is not coordinated in the mutant embryos, with some cells failing to constrict (these unconstricted cells are interspersed with constricted ones in the central domain of the ventral furrow, instead of the cells constricting to a common point). As ventral furrow formation continues, uncoordinated constriction alters the shape of ventral furrow cells so that they point towards the furrow at varying angles. Some unconstricted cells persist on the surface after most cells have internalised. Despite the defects in coordinated constriction, furrow formation in the mutant embryos occurs roughly as quickly as in wild type.

        (Fox and Peifer, 2007)

        1.2% of segments have thin/missing commissures and 5.4% of segment have commissures with pathfinding errors in Abl1/Abl4 embryos.

        (Forsthoefel et al., 2005)

        Third larval instar single cell homozygous ddaE neuron clones show a significant increase in the number of dendritic ends compared to control clones.

        (Li et al., 2005)

        Homozygous embryos show axons ectopically crossing the midline.

        (Lee et al., 2004)

        During embryonic syncytial divisions and cellularisation of maternal Abl4 mutants, defects are found in pseudocleavage furrows, with some furrows absent and others breaking down. This can lead to spindle collision, resulting in abnormal mitoses. Abnormal nuclei are removed into the interior of the embryo, leaving behind smaller pseudocells. Immediately after syncytial divisions, maternally-derived Abl4 mutants exhibit defects in cellularisation furrows, with multiple nuclei surrounded by a single actin ring. Abl4 is cold-sensitive, at 18oC the defects in cellularisation furrows are much more widespread, affecting many, if not most, forming cells. At 18oC, defects are observed in pseudocleavage furrows as early as prophase - some furrows are absent, while those that do form are variable in depth, and never invaginate to the depth of wild-type furrows. Furrow defects are also found in metaphase, with the absence of furrows often leading to spindle collision. Some furrows form properly but are torn apart during anaphase. Maternally-derived Abl4 mutants have similar defects during cellularisation, exhibiting excess apical actin at the expense of some cellularisation furrows.

        (Grevengoed et al., 2003)

        In homozygous Abl4 stage 16 embryos, several axon bundles cross the midline incorrectly. Only a few embryos heterozygous for Abl4 exhibit axons abnormally crossing the midline, but greater than 50% of homozygous embryos exhibit on average two abnormal crossovers.

        There are a few adult Abl2/Abl4 escapers that display a rough eye phenotype.

        Expression of two copies of AblKN.ftz in Abl4 mutants results in all embryos exhibiting several axon bundles crossing the midline incorrectly.

        Co-expression of two copies of each AblKN.ftz and Ablftz.PH in Abl4 homozygous mutants results in axonal midline crossovers in 54% of embryos, a value almost identical to that observed in Abl4 mutants alone.

        (Hsouna et al., 2003)

        96% of the expected number of Abl1/Abl4 pupae are observed, while 56% of the expected number of Abl1/Abl4 adults are observed. 3% of segments have commissure defects in the central nervous system of Abl1/Abl4 embryos.

        (Liebl et al., 2003)

        Heterozygotes do not show midline crossing errors in the central nervous system. Homozygous and Abl2/Abl4 embryos show ectopic crossing of the midline by axons in the central nervous system.

        (Wills et al., 2002)

        Mutant follicle cell clones have subtle defects in F-actin organisation; apical actin filaments are often mislocalised, appearing at elevated levels at lateral cell cortices. In addition, the epithelial sheet is disrupted, with the mutant tissue forming a multilayered epithelium close to the posterior pole of the egg chamber, and to a smaller extent, at the anterior pole.

        (Baum and Perrimon, 2001)

        Abl4 embryos derived from homozygous Abl4 female germline clones (lacking both maternal and zygotic Abl function) die at the end of embryogenesis, while embryos derived from homozygous Abl4 female germline clones that receive a wild-type paternal copy of Abl survive to adulthood. Abl4 mutant embryos derived from homozygous Abl4 female germline clones show a range of defects. Approximately 7% have head involution defects and completely fail to germband retract. About 14% partially fail to germband retract and have variable dorsal closure defects. Approximately 67% have dorsal closure defects ranging from dorsal holes to defects in the dorsal pattern.

        (Grevengoed et al., 2001)

        In Abl1/Abl4 mutant larvae the ISNb fails to innervate muscle.

        (Kraut et al., 2001)

        Abl1/Abl4 mutants show mild defects in axon pathfinding in the longitudinal connectives which may be thinned and uneven.

        (Liebl et al., 2000)

        ISNb growth cones fail to reach the distal target (muscle 12) in 35% of Abl2/Abl4 embryos. Abl2/Abl4 embryos show mild defects in the Fas2-positive longitudinal fascicles of the central nervous system.

        (Wills et al., 1999)

        Eyes rough, with slightly reduced facet number, missing and supernumerary bristles and facets irregular in shape and size. Sections reveal defects in all cell types of the retina. Photoreceptor cell clusters show defects early in ommatidial development.

        (Bennett and Hoffmann, 1992)
        External Data
        Interactions
        Show genetic interaction network for Enhancers & Suppressors
        Phenotypic Class
        Enhanced by
        Statement
        Reference

        Abl4/Abl[+], Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng

        (Dorsten et al., 2007)

        Abl4 has abnormal neuroanatomy phenotype, enhanceable by chbP4

        (Lee et al., 2004)

        Abl4 has abnormal mitotic cell cycle | maternal effect phenotype, enhanceable by dia2/dia[+]

        (Grevengoed et al., 2003)

        Abl4 has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by robo[+]/robo11

        (Hsouna et al., 2003)

        Abl4 has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by sli[+]/sli1

        (Hsouna et al., 2003)

        Abl4/Abl1 has abnormal neuroanatomy phenotype, enhanceable by AmaM109/Ama[+]

        (Liebl et al., 2003)

        Abl4/Abl1 has lethal phenotype, enhanceable by AmaM109/Ama[+]

        (Liebl et al., 2003)

        Abl4/Abl1 has abnormal neuroanatomy phenotype, enhanceable by Df(3R)ama/AmaM109

        (Liebl et al., 2003)

        Abl4/Abl1 has abnormal neuroanatomy phenotype, enhanceable by Df(3R)ama/AmaR1

        (Liebl et al., 2003)

        Abl4/Abl1 has lethal | prepupal stage phenotype, enhanceable by trio[+]/trioM89

        (Liebl et al., 2000)

        Abl4/Abl1 has lethal | prepupal stage phenotype, enhanceable by NrtM221/Nrt[+]

        (Liebl et al., 2000)

        Abl4/Abl1 has lethal | prepupal stage phenotype, enhanceable by Df(3L)Fpa1/+

        (Liebl et al., 2000)

        Abl4/Abl1 has lethal | prepupal stage phenotype, enhanceable by faxM7/fax[+]

        (Liebl et al., 2000)
        NOT Enhanced by
        Statement
        Reference

        Abl4/Abl1 has abnormal neuroanatomy phenotype, non-enhanceable by AmaR1/Ama[+]

        (Liebl et al., 2003)

        Abl4/Abl1 has abnormal neuroanatomy phenotype, non-enhanceable by Df(3R)ama/+

        (Liebl et al., 2003)
        Suppressed by
        Statement
        Reference

        Abl4/Abl1 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4elav-C155/Abi4YE.UAS.Tag:HA

        (Kim et al., 2019)

        Abl4/Abl1 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by witA12

        (Kim et al., 2019)

        Abl4/Abl1 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by witB11

        (Kim et al., 2019)

        Abl4/Abl1 has lethal phenotype, suppressible | partially by Abi[+]/AbiKO

        (Lin et al., 2009)

        Abl4/Abl1 has lethal phenotype, suppressible | partially by Abi[+]/AbiP1

        (Lin et al., 2009)

        Abl4/Abl1 has abnormal neuroanatomy | embryonic stage phenotype, suppressible | partially by Abi[+]/AbiP2

        (Lin et al., 2009)

        Abl4/Abl1 has abnormal neuroanatomy | larval stage phenotype, suppressible | partially by Abi[+]/AbiKO

        (Lin et al., 2009)

        Abl4/Abl1, Df(3L)Fpa1/trioM89 has abnormal neuroanatomy phenotype, suppressible | partially by ena[+]/enaGC10

        (Forsthoefel et al., 2005)

        Abl4/Abl1, Df(3L)Fpa1/trioIMP159.4 has abnormal neuroanatomy phenotype, suppressible | partially by ena[+]/enaGC10

        (Forsthoefel et al., 2005)

        Abl4 has abnormal mitotic cell cycle | maternal effect phenotype, suppressible by ena[+]/ena210

        (Grevengoed et al., 2003)

        Abl4 has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by robo1UAS.cKa/Scer\GAL4ftz.ng

        (Hsouna et al., 2003)

        Abl4 has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by robo1Y-F.UAS/Scer\GAL4ftz.ng

        (Hsouna et al., 2003)

        Abl4 has abnormal neuroanatomy phenotype, suppressible by ena[+]/ena210

        (Wills et al., 2002)

        Abl4 has lethal | recessive | rescuable maternal effect | embryonic stage phenotype, suppressible by ena[+]/enaunspecified

        (Grevengoed et al., 2001)

        Abl4/Abl1 has lethal phenotype, suppressible by ena[+]/enaGC10

        (Liebl et al., 2000)

        Abl4/Abl1, NrtM221/Nrt[+] has lethal | prepupal stage phenotype, suppressible by ena[+]/enaGC10

        (Liebl et al., 2000)

        Abl4/Abl1, faxM7/fax[+] has lethal | prepupal stage phenotype, suppressible by ena[+]/enaGC10

        (Liebl et al., 2000)

        Abl4/Abl1, trio[+]/trioM89 has lethal | prepupal stage phenotype, suppressible by ena[+]/enaGC10

        (Liebl et al., 2000)
        NOT suppressed by
        Statement
        Reference

        Abl2/Abl4 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by DabUAS.cWa/Scer\GAL4elav.PU

        (Song et al., 2010)

        Abl4/Abl1 has abnormal neuroanatomy | larval stage phenotype, non-suppressible by ena[+]/enaGC5

        (Lin et al., 2009)

        Abl4/Abl1 has abnormal neuroanatomy | larval stage phenotype, non-suppressible by Hem[+]/HemC3-20

        (Lin et al., 2009)

        Abl4/Abl1 has abnormal neuroanatomy | larval stage phenotype, non-suppressible by SCARΔ37/SCAR[+]

        (Lin et al., 2009)

        Abl4 has abnormal mitotic cell cycle | maternal effect phenotype, non-suppressible by Sop2[+]/Arpc1Q25st

        (Grevengoed et al., 2003)
        Enhancer of
        Statement
        Reference

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of fra6/fra3

        (O'Donnell and Bashaw, 2013)

        Abl4 is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa

        (Dorsten et al., 2007)

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of Df(2R)vg135/fra4

        (Forsthoefel et al., 2005)

        Abl4/Abl1 is an enhancer of abnormal neuroanatomy phenotype of Df(2R)vg135/fra4

        (Forsthoefel et al., 2005)

        Abl4/Abl1 is an enhancer of abnormal neuroanatomy phenotype of fra4

        (Forsthoefel et al., 2005)

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of fra4

        (Forsthoefel et al., 2005)

        Abl4 is an enhancer of abnormal neuroanatomy phenotype of chbP4

        (Lee et al., 2004)

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of robo11

        (Hsouna et al., 2003)

        Abl4 is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of robo11

        (Hsouna et al., 2003)

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of robo11, sli[+]/sli1

        (Hsouna et al., 2003)

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of sli1

        (Hsouna et al., 2003)

        Abl4/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of robo1unspecified, robo24

        (Wills et al., 2002)

        Abl4/Abl[+] is an enhancer of lethal phenotype of trioM89/trioS036810

        (Liebl et al., 2000)
        NOT Enhancer of
        Statement
        Reference

        Abl4/Abl[+] is a non-enhancer of abnormal neuroanatomy | adult stage | dominant phenotype of tapGal4

        (Yuan et al., 2016)

        Scer\GAL4eg-Mz360, Abl4, AblK417N.UAS.GFP, Abl[+] is a non-enhancer of abnormal neuroanatomy phenotype of fra6/fra3

        (O'Donnell and Bashaw, 2013)
        Suppressor of
        NOT Suppressor of
        Other
        Statement
        Reference

        Abl4, Df(3R)su(Hw)7/+ has abnormal neuroanatomy | dominant | third instar larval stage phenotype

        (Kim et al., 2019)

        Abl4, Fmr1Δ50M has abnormal neuroanatomy | third instar larval stage phenotype

        (Kim et al., 2019)

        Abi5, Abl4/Abl[+] has abnormal neuroanatomy | dominant | third instar larval stage phenotype

        (Kim et al., 2019)

        Abl2/Abl4, Dscam1RNAi.UAS.19 has abnormal neuroanatomy | embryonic stage phenotype

        (Yu et al., 2009)

        Abl2/Abl4, Dscam1RNAi.UAS.18-20 has abnormal neuroanatomy | embryonic stage phenotype

        (Yu et al., 2009)

        Abl2/Abl4, Dscam1RNAi.UAS.18 has abnormal neuroanatomy | embryonic stage phenotype

        (Yu et al., 2009)

        Abl4/Abl[+], Scer\GAL4ftz.ng, fraUAS.cKa has abnormal neuroanatomy | embryonic stage 16 phenotype

        (Dorsten et al., 2007)

        Abl4/Abl1, Df(3L)Fpa1/trioM89 has abnormal neuroanatomy phenotype

        (Forsthoefel et al., 2005)

        Abl4/Abl1, Df(3L)Fpa1/trioIMP159.4 has abnormal neuroanatomy phenotype

        (Forsthoefel et al., 2005)

        Abl4/Abl[+], cpbM143 has abnormal neuroanatomy | embryonic stage phenotype

        (Grevengoed et al., 2003)

        Abl4, cpbM143 has lethal | embryonic stage phenotype

        (Grevengoed et al., 2003)

        Abl4, cpbM143 has abnormal neuroanatomy | embryonic stage phenotype

        (Grevengoed et al., 2003)

        Abl4, cpbM143/cpb[+] has lethal | embryonic stage phenotype

        (Grevengoed et al., 2003)

        Abl4, cpbM143/cpb[+] has abnormal neuroanatomy | embryonic stage phenotype

        (Grevengoed et al., 2003)

        Abl4, robo11 has abnormal neuroanatomy | embryonic stage 16 phenotype

        (Hsouna et al., 2003)

        Abl4/Abl1, NrtM100 has abnormal neuroanatomy phenotype

        (Liebl et al., 2003)

        Abl4/Abl1, NrtM54 has abnormal neuroanatomy phenotype

        (Liebl et al., 2003)

        Abl4, capt10/capt[+] has abnormal neuroanatomy phenotype

        (Wills et al., 2002)

        Abl4, capt10 has abnormal neuroanatomy phenotype

        (Wills et al., 2002)

        Abl4, shg2 has lethal | embryonic stage phenotype

        (Grevengoed et al., 2001)

        Abl4, shg[+]/shg2 has lethal | embryonic stage phenotype

        (Grevengoed et al., 2001)
        Phenotype Manifest In
        Enhanced by
        Statement
        Reference

        Abl4/Abl[+], Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng

        (Dorsten et al., 2007)

        Abl4/Abl[+], Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng

        (Dorsten et al., 2007)

        Abl4 has larval neuron phenotype, enhanceable by chbP4

        (Lee et al., 2004)

        Abl4 has actin cytoskeleton | embryonic stage | maternal effect phenotype, enhanceable by dia2/dia[+]

        (Grevengoed et al., 2003)

        Abl4 has spindle | cleavage stage | maternal effect phenotype, enhanceable by dia2/dia[+]

        (Grevengoed et al., 2003)

        Abl4 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by robo[+]/robo11

        (Hsouna et al., 2003)

        Abl4 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by sli[+]/sli1

        (Hsouna et al., 2003)

        Abl4/Abl1 has larval ventral nerve cord commissure phenotype, enhanceable by AmaM109/Ama[+]

        (Liebl et al., 2003)

        Abl4/Abl1 has larval ventral nerve cord commissure phenotype, enhanceable by Df(3R)ama/AmaM109

        (Liebl et al., 2003)

        Abl4/Abl1 has larval ventral nerve cord commissure phenotype, enhanceable by Df(3R)ama/AmaR1

        (Liebl et al., 2003)

        Abl4/Abl1 has larval anterior commissure phenotype, enhanceable by trio[+]/trioM89

        (Liebl et al., 2000)

        Abl4/Abl1 has larval longitudinal connective phenotype, enhanceable by trio[+]/trioM89

        (Liebl et al., 2000)

        Abl4/Abl1 has larval posterior commissure phenotype, enhanceable by trio[+]/trioM89

        (Liebl et al., 2000)

        Abl4/Abl1 has larval anterior commissure phenotype, enhanceable by Df(3L)Fpa1/+

        (Liebl et al., 2000)

        Abl4/Abl1 has larval longitudinal connective phenotype, enhanceable by Df(3L)Fpa1/+

        (Liebl et al., 2000)

        Abl4/Abl1 has larval posterior commissure phenotype, enhanceable by Df(3L)Fpa1/+

        (Liebl et al., 2000)
        NOT Enhanced by
        Statement
        Reference

        Abl4/Abl1 has larval ventral nerve cord commissure phenotype, non-enhanceable by AmaR1/Ama[+]

        (Liebl et al., 2003)

        Abl4/Abl1 has larval ventral nerve cord commissure phenotype, non-enhanceable by Df(3R)ama/+

        (Liebl et al., 2003)
        Suppressed by
        Statement
        Reference

        Abl4/Abl1 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4elav-C155/Abi4YE.UAS.Tag:HA

        (Kim et al., 2019)

        Abl4/Abl1 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by witA12

        (Kim et al., 2019)

        Abl4/Abl1 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by witB11

        (Kim et al., 2019)

        Abl4/Abl1 has NMJ bouton | third instar larval stage phenotype, suppressible by Scer\GAL4elav-C155/Abi4YE.UAS.Tag:HA

        (Kim et al., 2019)

        Abl4/Abl1 has NMJ bouton | third instar larval stage phenotype, suppressible by witA12

        (Kim et al., 2019)

        Abl4/Abl1 has NMJ bouton | third instar larval stage phenotype, suppressible by witB11

        (Kim et al., 2019)

        Abl4 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, suppressible by Scer\GAL4elav.PU/trioUAS.cBa

        (Kannan et al., 2017)

        Abl4/Abl1 has larval longitudinal connective phenotype, suppressible | partially by Abi[+]/AbiP2

        (Lin et al., 2009)

        Abl4/Abl1 has NMJ bouton | increased number phenotype, suppressible | partially by Abi[+]/AbiKO

        (Lin et al., 2009)

        Abl4/Abl1, Df(3L)Fpa1/trioM89 has symmetrical commissure phenotype, suppressible | partially by ena[+]/enaGC10

        (Forsthoefel et al., 2005)

        Abl4/Abl1, Df(3L)Fpa1/trioIMP159.4 has symmetrical commissure phenotype, suppressible | partially by ena[+]/enaGC10

        (Forsthoefel et al., 2005)

        Abl4 has larval longitudinal connective | embryonic stage 16 phenotype, suppressible by robo1UAS.cKa/Scer\GAL4ftz.ng

        (Hsouna et al., 2003)

        Abl4 has larval longitudinal connective | embryonic stage 16 phenotype, suppressible by robo1Y-F.UAS/Scer\GAL4ftz.ng

        (Hsouna et al., 2003)

        Abl4 has presumptive embryonic/larval central nervous system phenotype, suppressible by ena[+]/ena210

        (Wills et al., 2002)
        NOT suppressed by
        Statement
        Reference

        Abl2/Abl4 has larval intersegmental nerve branch ISNb of A1-7 phenotype, non-suppressible by DabUAS.cWa/Scer\GAL4elav.PU

        (Song et al., 2010)

        Abl4/Abl1 has NMJ bouton | increased number phenotype, non-suppressible by ena[+]/enaGC5

        (Lin et al., 2009)

        Abl4/Abl1 has NMJ bouton | increased number phenotype, non-suppressible by Hem[+]/HemC3-20

        (Lin et al., 2009)

        Abl4/Abl1 has NMJ bouton | increased number phenotype, non-suppressible by SCARΔ37/SCAR[+]

        (Lin et al., 2009)

        Abl4 has actin cytoskeleton | maternal effect | embryonic stage phenotype, non-suppressible by Sop2[+]/Arpc1Q25st

        (Grevengoed et al., 2003)

        Abl4 has spindle | maternal effect | embryonic stage phenotype, non-suppressible by Sop2[+]/Arpc1Q25st

        (Grevengoed et al., 2003)
        Enhancer of
        Statement
        Reference

        Abl4/Abl[+] is an enhancer of larval EW neuron phenotype of fra6/fra3

        (O'Donnell and Bashaw, 2013)

        Abl4/Abl[+] is an enhancer of symmetrical commissure phenotype of fra6/fra3

        (O'Donnell and Bashaw, 2013)

        Scer\GAL4eg-Mz360, Abl4, AblK417N.UAS.GFP, Abl[+] is an enhancer of larval EW neuron phenotype of fra6/fra3

        (O'Donnell and Bashaw, 2013)

        Scer\GAL4eg-Mz360, Abl4, AblK417N.UAS.GFP, Abl[+] is an enhancer of symmetrical commissure phenotype of fra6/fra3

        (O'Donnell and Bashaw, 2013)

        Abl4 is an enhancer of commissure | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa

        (Dorsten et al., 2007)

        Abl4 is an enhancer of larval ventral nerve cord commissure | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa

        (Dorsten et al., 2007)

        Abl4/Abl[+] is an enhancer of symmetrical commissure phenotype of Df(2R)vg135/fra4

        (Forsthoefel et al., 2005)

        Abl4/Abl1 is an enhancer of symmetrical commissure phenotype of Df(2R)vg135/fra4

        (Forsthoefel et al., 2005)

        Abl4/Abl1 is an enhancer of symmetrical commissure phenotype of fra4

        (Forsthoefel et al., 2005)

        Abl4/Abl[+] is an enhancer of symmetrical commissure phenotype of fra4

        (Forsthoefel et al., 2005)

        Abl4 is an enhancer of larval neuron phenotype of chbP4

        (Lee et al., 2004)

        Abl4/Abl[+] is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo11

        (Hsouna et al., 2003)

        Abl4 is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo11

        (Hsouna et al., 2003)

        Abl4/Abl[+] is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo11, sli[+]/sli1

        (Hsouna et al., 2003)

        Abl4/Abl[+] is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of sli1

        (Hsouna et al., 2003)

        Abl4/Abl[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of robo1unspecified, robo24

        (Wills et al., 2002)

        Abl2/Abl4 is an enhancer of larval longitudinal connective phenotype of chic05205a/chic221

        (Wills et al., 1999)

        Abl4 is an enhancer of phenotype of arm4

        (Loureiro and Peifer, 1998)

        Abl4/Abl1 is an enhancer of symmetrical commissure phenotype of arm4

        (Loureiro and Peifer, 1998)

        Abl4/Abl1 is an enhancer of presumptive embryonic/larval central nervous system phenotype of arm4

        (Loureiro and Peifer, 1998)
        NOT Enhancer of
        Statement
        Reference

        Abl4/Abl[+] is a non-enhancer of adult mushroom body alpha-lobe | adult stage phenotype of tapGal4

        (Yuan et al., 2016)

        Abl4/Abl1 is a non-enhancer of larval longitudinal connective phenotype of Df(2R)vg135/fra4

        (Forsthoefel et al., 2005)
        Suppressor of
        Statement
        Reference

        Abl4/Abl4 is a suppressor | somatic clone of larval multidendritic class IV neuron | somatic clone | third instar larval stage phenotype of Dscam1exon17.2.UAS.GFP, Scer\GAL4ppk.PG

        (Sterne et al., 2015)

        Abl4/Abl[+] is a suppressor of egg | maternal effect phenotype of Lmon\actAFP4mito.UAS.EGFP

        (Gates et al., 2009)

        Abl4/Abl[+] is a suppressor | partially of larval longitudinal connective phenotype of AbiP2/AbiKO

        (Lin et al., 2009)

        Abl4/Abl[+] is a suppressor | partially of larval longitudinal connective phenotype of Df(3R)JY19/AbiKO

        (Lin et al., 2009)

        Abl4/Abl[+] is a suppressor of eye | ectopic phenotype of Scer\GAL4dpp.blk1, eyaWT.UAS

        (Xiong et al., 2009)

        Abl4/Abl[+] is a suppressor of commissure | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng

        (Dorsten et al., 2007)

        Abl4/Abl[+] is a suppressor of larval ventral nerve cord commissure | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng

        (Dorsten et al., 2007)

        Abl4/Abl[+] is a suppressor of commissure | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa

        (Dorsten et al., 2007)

        Abl4/Abl[+] is a suppressor of larval ventral nerve cord commissure | embryonic stage 16 phenotype of Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa

        (Dorsten et al., 2007)

        Abl4/Abl[+] is a suppressor of ventral adult lateral neuron & axon phenotype of Hsap\APPUAS.Tag:MYC, Scer\GAL4P2.4.Pdf

        (Leyssen et al., 2005)

        Abl4/Abl[+] is a suppressor of larval longitudinal connective phenotype of robo15, sli[+]/sli1

        (Bashaw et al., 2000)

        robo[+], Abl4, robo15, Abl[+] is a suppressor of larval longitudinal connective phenotype of sli1

        (Bashaw et al., 2000)

        Abl4 is a suppressor of larval intersegmental nerve phenotype of Larbypass/LarE55

        (Wills et al., 1999)

        Abl4 is a suppressor of phenotype of arm4

        (Loureiro and Peifer, 1998)
        NOT Suppressor of
        Other
        Statement
        Reference

        Abl4, Vav2 has embryonic/larval neuromuscular junction | larval stage phenotype

        (Kim et al., 2024)

        Abl4, Vav2 has NMJ bouton | increased number | larval stage phenotype

        (Kim et al., 2024)

        Abl4, Vav2 has macropinosome | larval stage phenotype

        (Kim et al., 2024)

        Abl4, PDZ-GEF6 has embryonic/larval neuromuscular junction | larval stage phenotype

        (Kim et al., 2024)

        Abl4, PDZ-GEF6 has NMJ bouton | increased number | larval stage phenotype

        (Kim et al., 2024)

        Abl4, PDZ-GEF6 has macropinosome | larval stage phenotype

        (Kim et al., 2024)

        Abl4, Rap1rvB1 has embryonic/larval neuromuscular junction | larval stage phenotype

        (Kim et al., 2024)

        Abl4, Rap1rvB1 has NMJ bouton | increased number | larval stage phenotype

        (Kim et al., 2024)

        Abl4, Rap1rvB1 has macropinosome | larval stage phenotype

        (Kim et al., 2024)

        Abl4, Df(3R)su(Hw)7/+ has NMJ bouton | third instar larval stage phenotype

        (Kim et al., 2019)

        Abl4, Df(3R)su(Hw)7/+ has embryonic/larval neuromuscular junction | third instar larval stage phenotype

        (Kim et al., 2019)

        Abl4, Fmr1Δ50M has NMJ bouton | third instar larval stage phenotype

        (Kim et al., 2019)

        Abl4, Fmr1Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype

        (Kim et al., 2019)

        Abi5, Abl4/Abl[+] has NMJ bouton | third instar larval stage phenotype

        (Kim et al., 2019)

        Abi5, Abl4/Abl[+] has embryonic/larval neuromuscular junction | third instar larval stage phenotype

        (Kim et al., 2019)

        Abl2/Abl4, Dscam1RNAi.UAS.19 has larval ventral nerve cord | embryonic stage phenotype

        (Yu et al., 2009)

        Abl2/Abl4, Dscam1RNAi.UAS.18-20 has larval ventral nerve cord | embryonic stage phenotype

        (Yu et al., 2009)

        Abl2/Abl4, Dscam1RNAi.UAS.18 has larval ventral nerve cord | embryonic stage phenotype

        (Yu et al., 2009)

        Abl4/Abl[+], Scer\GAL4ftz.ng, fraUAS.cKa has commissure | embryonic stage 16 phenotype

        (Dorsten et al., 2007)

        Abl4/Abl[+], Scer\GAL4ftz.ng, fraUAS.cKa has larval ventral nerve cord commissure | embryonic stage 16 phenotype

        (Dorsten et al., 2007)

        Abl4, cta5/Df(2L)C' has ventral midline of embryo | maternal effect phenotype

        (Fox and Peifer, 2007)

        Abl4/Abl1, Df(3L)Fpa1/trioM89 has symmetrical commissure phenotype

        (Forsthoefel et al., 2005)

        Abl4/Abl1, Df(3L)Fpa1/trioIMP159.4 has symmetrical commissure phenotype

        (Forsthoefel et al., 2005)

        Abl4/Abl1, NrtM100 has larval ventral nerve cord commissure phenotype

        (Liebl et al., 2003)

        Abl4/Abl1, NrtM54 has larval ventral nerve cord commissure phenotype

        (Liebl et al., 2003)

        Abl4, capt10/capt[+] has presumptive embryonic/larval central nervous system phenotype

        (Wills et al., 2002)

        Abl4, capt10 has presumptive embryonic/larval central nervous system phenotype

        (Wills et al., 2002)

        Abl4, shgR69 has embryonic/first instar larval cuticle phenotype

        (Grevengoed et al., 2001)

        Abl4, shg2 has embryonic/first instar larval cuticle phenotype

        (Grevengoed et al., 2001)

        Abl4, chic05205a/chic221 has larval longitudinal connective phenotype

        (Wills et al., 1999)

        Abl4/Abl1, arm4 has symmetrical commissure phenotype

        (Loureiro and Peifer, 1998)

        Abl4/Abl1, arm4 has presumptive embryonic/larval central nervous system phenotype

        (Loureiro and Peifer, 1998)
        Additional Comments
        Genetic Interactions
        Statement
        Reference

        The stalling of the ISNb motor nerve at the junction of muscles 6 and 13 with failure to innervate muscle 12 characteristic for Abl4 homozygous mutant embryos is not suppressed by Scer\GAL4elav.PU-driven expression of trioScer\UAS.cBa in the mutant background.

        (Kannan et al., 2017)

        Abl4/+ does not significantly enhance frequency of mushroom body beta lobe axon overgrowth defects in tapGal4/+ brains.

        (Yuan et al., 2016)

        The increased presynaptic terminal length observed in class IV dendritic arborizing neurons in somatic MARCM clones expressing Dscam1exon17.2.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4ppk.PG in third instar larvae is completely abolished in clones that are also homozygous mutant for Abl4.

        The ectopic repulsion between between class I and class III dendritic arborizing neurons in third instar larvae observed upon expression of Dscam1exon17.2.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4109(2)80 cannot be rescued by combination with Abl1/Abl4.

        (Sterne et al., 2015)

        A Abl4/+ heterozygous background increases the nuumber of segments displaying EW axon midline crossing defects in Df(1)NetABΔ stage 15 embryos from approximately 40% to 45% of segments.

        (O'Donnell and Bashaw, 2013)

        Abl4/+ suppresses the mature stage 16 CNS axonal phenotype of Nl1N-ts1.

        (Kuzina et al., 2011)

        The ISNb stall phenotype seen in Abl2/Abl4 embryos is not suppressed by expression of DabScer\UAS.cWa under the control of Scer\GAL4elav.PU.

        (Song et al., 2010)

        The frequency of the midline crossing defect seen in Fas-expressing axons in Abl1/Abl4 embryos is suppressed from 37% to 18% by AbiP2/+.

        The frequency of the midline crossing defect seen in Fas-expressing axons in AbiKO/Df(3R)JY19 embryos is suppressed from 32% to 15% by Abl4/+.

        The frequency of the midline crossing defect seen in Fas-expressing axons in AbiKO/AbiP2 embryos is suppressed from 9.6% to 3% by Abl4/+.

        The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is not suppressed by enaGC5/+.

        The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is significantly suppressed by AbiKO/+. This suppression further increased if the flies are also carrying enaGC5/+.

        The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is not suppressed by HemC3-20/+.

        The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is suppressed by SCARΔ37/+.

        (Lin et al., 2009)

        Scer\GAL4tub.PU-mediated expression of Dscam1miRNA.Scer\UAS.18 in a Abl2/Abl4 background causes commisureless phenotypes in the ladder-like neuronal tracts in 19% of embryonic ventral ganglion segments.

        Scer\GAL4tub.PU-mediated expression of Dscam1miRNA.Scer\UAS.19 in a Abl2/Abl4 background causes commisureless phenotypes in the ladder-like neuronal tracts in 9% of embryonic ventral ganglion segments.

        Scer\GAL4tub.PU-mediated expression of Dscam1miRNA.Scer\UAS.18-20 in a Abl2/Abl4 background causes commisureless phenotypes in the ladder-like neuronal tracts in 1% of embryonic ventral ganglion segments.

        (Yu et al., 2009)

        Dscam05518 Abl4 embryos show defects in the commissures of the central nervous system; 23% of anterior commissures are absent, 33% of anterior commissures are thin, 65% of posterior commissures are absent and 26% of posterior commissures are thin. 19% of segments fail to separate the anterior and posterior commissures correctly.

        fra4 Abl4 embryos show defects in the commissures of the central nervous system; 14% of anterior commissures are absent, 24% of anterior commissures are thin, 16% of posterior commissures are absent and 24% of posterior commissures are thin. 19% of segments fail to separate the anterior and posterior commissures correctly.

        Dscam3c02826 Abl4 embryos show defects in the commissures of the central nervous system; 1% of anterior commissures are absent and 2% of posterior commissures are absent. 85% of segments fail to separate the anterior and posterior commissures correctly.

        Dscam05518 fra4 Abl4 embryos show defects in the commissures of the central nervous system; 98% of anterior commissures are absent, 2% of anterior commissures are thin and 100% of posterior commissures are absent.

        (Andrews et al., 2008)

        Ventral nerve cord axon bundles of stage 16 embryos overexpressing fraScer\UAS.cKa via Scer\GAL4ftz.ng in a heterozygous Abl4 genetic background display few incorrect midline crossings.

        (Dorsten et al., 2007)

        Mesoderm remains on the surface and the midline cells do not join in double mutant embryos derived from cta5/Df(2L)C' ; Abl4/Abl4 females. These phenotypes are not seen in either single mutant.

        (Fox and Peifer, 2007)

        The frequency of the loss of commissure phenotype seen in Abl1/Abl4 embryos is not enhanced by fra4/+, but the frequency of commissures with pathfinding errors is increased in the fra4/+; Abl1/Abl4 embryos compared to Abl1/Abl4.

        (Forsthoefel et al., 2005)

        The frequency of axons ectopically crossing the midline in chbP4 Abl4 double homozygous embryos is substantially increased compared to the frequency seen in either single homozygote.

        (Lee et al., 2004)

        Homozygous Abl4, heterozygous cpbM143 double mutants lay few eggs. The crossing of cpbM143/+ ; Abl4/+ mothers and fathers results in 20% of the progeny dying during embryogenesis. 15% of the progeny have minor defects in central nervous system (CNS) architecture, whereas 21% exhibit more severe CNS defects. As cpbM143 Abl4 double mutants are only 6.25% of the progeny, the frequency of lethality and CNS phenotypes suggest that the mutations may dominantly enhance one another. ena210 heterozygosity strongly suppresses the cellularisation phenotype of Abl4 mutants. The majority of suppressed embryos exhibit far fewer multinucleate cells and less apical actin. Heterozygosity for dia2 enhances the Abl4 phenotype. Heterozygosity for Sop2Q25st does not suppress the Abl4 phenotype.

        (Grevengoed et al., 2003)

        Heterozygous robo1 enhances the number of abnormal axon crossovers observed in Abl4 mutants.

        Heterozygous sli1 enhances the number of abnormal axon crossovers observed in Abl4 mutants.

        The addition of one mutant copy of Abl4 doubles the number of crossovers observed in heterozygous robo1 mutants. The presence of two copies of Abl4 in heterozygous robo1 mutants increases the penetrance of crossovers to 90%, with most embryos exhibiting three or more crossovers.

        In double homozygous robo1; Abl4 embryos, several axon bundles cross the midline abnormally as gaps and thinning of the longitudinal connectives become evident.

        The addition of one mutant copy of Abl4 doubles the number of crossovers observed in heterozygous sli1 mutants.

        Overexpression of roboScer\UAS.cKa under the control of Scer\GAL4ftz.ng in Abl4 homozygous mutants suppresses the frequency of abnormal crossovers observed in Abl4 mutants.

        Overexpression of roboY-F.Scer\UAS under the control of Scer\GAL4ftz.ng in Abl4 homozygous mutants suppresses the frequency of abnormal crossovers observed in Abl4 mutants.

        (Hsouna et al., 2003)

        Abl1 AmaM109/Abl4 animals do not survive to the pupal stage. AmaM109/+ increases the frequency of commissure defects in the central nervous system of Abl1/Abl4 embryos; 31% of segments have commissure defects in the double mutant embryos. Survival to pupation and the percentage of segments with commissure defects in the central nervous system in Abl1/Abl4 animals is not dramatically altered by Df(3R)ama/+. 104% of the expected number of Abl1 AmaR1/Abl4 pupae are observed, while 67% of the expected number of Abl1 AmaR1/Abl4 adults are observed. 4% of segments have commissure defects in the central nervous system of Abl1 AmaR1/Abl4 embryos. 23% of segments have commissure defects in the central nervous system of Abl1 AmaR1/Abl4 Df(3R)ama embryos. 86% of segments have commissure defects in the central nervous system of Abl1 AmaM109/Abl4 Df(3R)ama embryos. 36% of segments have commissure defects in the central nervous system of Abl1 NrtM100/Abl4 embryos.

        (Liebl et al., 2003)

        Central nervous system axons are seen to cross the midline in Abl4 capt10 double heterozygous embryos. The midline crossing errors seen in the central nervous system of Abl4/Abl4 embryos are suppressed by ena210/+. The frequency of ectopic crossing of the midline by axons in the central nervous system seen in robounspecified learobo2-4 embryos is increased by Abl4/+.

        (Wills et al., 2002)

        The embryonic lethality seen in Abl4 animals lacking both maternal and zygotic Abl function is significantly rescued if the female parents are also heterozygous for enaunspecified. Heterozygosity for shg2 results in lethality in Abl4/+ embryos derived from homozygous Abl4 female germline clones. 70% of the lethal progeny of females with homozygous Abl4 germline clones mated to shg2/+ ; Abl4/+ males have cuticles that are reduced in size with a large dorsal-anterior hole. 30% of the lethal progeny of females with homozygous Abl4 germline clones mated to shgR69/+ ; Abl4/+ males have a prominent dorsal-anterior hole.

        (Grevengoed et al., 2001)

        chic05205a/chic221 embryos show mild defects in the Fas2-positive longitudinal fascicles of the central nervous system. The severity of the defects is enhanced by Abl2/+ and further enhanced by Abl2/Abl4.

        (Wills et al., 1999)

        Dominantly suppresses the "bypass" phenotype of ISNb axons in Larbypass/LarE55 embryos.

        (Wills et al., 1999)

        arm4; Abl1/Abl4 embryos show disruptions in axonogenesis, including fused or missing commissures. The defects become more severe as development proceeds, such that, by stage 16, the central nervous system is dramatically disrupted. Suppresses the segment polarity phenotype of hemizygous arm4 embryos.

        (Loureiro and Peifer, 1998)

        The pupal lethality of hemizygous flies is not affected if the flies are also mutant for Ptp99A (Ptp99AHA64/Ptp99AR3).

        (Hamilton et al., 1995)
        Xenogenetic Interactions
        Statement
        Reference

        The penetrance of the "dumpless" phenotype seen in eggs derived from females expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP is partially suppressed by Abl4/+.

        (Gates et al., 2009)

        No embryos heterozygous for Abl4 and expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng exhibit axonal midline crossing defects.

        Heterozygous Abl4 almost completely suppresses the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.

        Homozygous Abl4 enhances the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.

        The heterozygous Abl4-dependent suppression of the axonal midline crossing phenotype in embryos expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is lost if Rho1V14.Scer\UAS is also expressed.

        (Dorsten et al., 2007)

        Heterozygosity for Abl4 suppresses the Scer\GAL4P2.4.Pdf>Hsap\APPScer\UAS.T:Hsap\MYC-induced increase in axonal arborization of the sLNv.

        (Leyssen et al., 2005)
        Complementation and Rescue Data
        Rescued by

        Abl4 is rescued by AblΔFABD.EGFP

        (Rogers et al., 2021)

        Abl4 is rescued by Abl2kb.EGFP

        (Rogers et al., 2021)

        Abl4/Df(3L)st-j7 is rescued by AblΔCR2.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is rescued by AblΔCR3.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is rescued by Abl2kb.cRa.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is rescued by Scer\GAL4elav-C155/AblUAS.cFa

        (Lin et al., 2009)

        Abl4 is rescued by Abl+mTnabl

        (Grevengoed et al., 2003)
        Partially rescued by

        Abl4 is partially rescued by AblΔCR1.EGFP

        (Rogers et al., 2021)

        Abl4 is partially rescued by AblKDΔFABD.EGFP

        (Rogers et al., 2021)

        Abl4/Df(3L)st-j7 is partially rescued by AblKD.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is partially rescued by AblΔFABD.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is partially rescued by AblKDΔFABD.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is partially rescued by AblΔCR1.EGFP

        (Rogers et al., 2016)

        Abl4/Df(3L)st-j7 is partially rescued by AblΔCR4.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblKD.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblΔFABD.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblKDΔFABD.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblΔCR1.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblΔCR2.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblΔCR3.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by AblΔCR4.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by Abl2kb.cRa.EGFP

        (Rogers et al., 2016)

        Abl4 is partially rescued by Ablftz.PH

        (Hsouna et al., 2003)
        Not rescued by

        Abl4 is not rescued by AblΔIDR.EGFP

        (Rogers et al., 2021)

        Abl4/Df(3L)st-j7 is not rescued by Scer\GAL4how-24B/AblUAS.cFa

        (Lin et al., 2009)

        Abl4 is not rescued by Abl+mTnabl-lys

        (Grevengoed et al., 2003)

        Abl4 is not rescued by AblKN.ftz

        (Hsouna et al., 2003)
        Comments

        When two copies of Ablftz.PH are introduced into Abl4 mutants, axonal crossovers are reduced from 53% in Abl4 single mutants to 39% in the presence of the transgene.

        Expression of two copies of AblKN.ftz in Abl4 mutants results in all embryos exhibiting several axon bundles crossing the midline incorrectly.

        Co-expression of two copies of each AblKN.ftz and Ablftz.PH in Abl4 homozygous mutants results in axonal midline crossovers in 54% of embryos, a value almost identical to that observed in Abl4 mutants alone.

        (Hsouna et al., 2003)
        Images (0)
        Mutant
        Wild-type
        Stocks (3)
        Notes on Origin
        Discoverer
        External Crossreferences and Linkouts ( 0 )
        Synonyms and Secondary IDs (4)
        References (53)