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General Information
Symbol
Dmel\Abl4
Species
D. melanogaster
Name
FlyBase ID
FBal0028710
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    deletion
    Comment:

    A 23 bp deletion.

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    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).

    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 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In

    actin filament & egg chamber | germ-line clone

    follicle cell & actin filament | somatic clone

    synaptic vesicle & NMJ bouton (with Abl1)

    Detailed Description
    Statement
    Reference

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

    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.

    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.

    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.

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

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

    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.

    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.

    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.

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

    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.

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

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

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

    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.

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

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

    Homozygous embryos show axons ectopically crossing the midline.

    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.

    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.

    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.

    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.

    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.

    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.

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

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

    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.

    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.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhanced by
    Statement
    Reference

    Abl4 has neuroanatomy defective phenotype, enhanceable by chbP4

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

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

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

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

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

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

    NOT Enhanced by
    Statement
    Reference

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

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

    Suppressed by
    Statement
    Reference

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

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

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

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

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

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

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

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

    NOT suppressed by
    Statement
    Reference

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

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

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

    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    Statement
    Reference
    Suppressor of
    NOT Suppressor of
    Other
    Statement
    Reference
    Phenotype Manifest In
    Enhanced by
    Statement
    Reference

    Abl4 has embryonic/larval neuron phenotype, enhanceable by chbP4

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

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

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

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

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

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

    NOT Enhanced by
    Statement
    Reference

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

    Suppressed by
    Statement
    Reference

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

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

    NOT suppressed by
    Statement
    Reference

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

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

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

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

    Enhancer of
    Statement
    Reference

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

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

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

    Abl4/Abl1 is an enhancer of commissure phenotype of fra4

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

    Abl4 is an enhancer of embryonic/larval neuron phenotype of chbP4

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

    Abl4 is an enhancer of phenotype of arm4

    Abl4/Abl1 is an enhancer of commissure phenotype of arm4

    NOT Enhancer of
    Statement
    Reference
    Suppressor of
    Statement
    Reference

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

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

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

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

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

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

    Abl4 is a suppressor of phenotype of arm4

    NOT Suppressor of
    Other
    Statement
    Reference
    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.

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

    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.

    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.

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

    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.

    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/+.

    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.

    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.

    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.

    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.

    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.

    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.

    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.

    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.

    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.

    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/+.

    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.

    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.

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

    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.

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

    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/+.

    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.

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

    Complementation and Rescue Data
    Partially rescued by

    Abl4 is partially rescued by Abl2kb.EGFP

    Abl4 is partially rescued by Abl2kb.EGFP

    Abl4 is partially rescued by AblKD.EGFP

    Abl4 is partially rescued by AblKD.EGFP

    Abl4 is partially rescued by AblΔFABD.EGFP

    Abl4 is partially rescued by AblΔFABD.EGFP

    Abl4 is partially rescued by AblKDΔFABD.EGFP

    Abl4 is partially rescued by AblKDΔFABD.EGFP

    Abl4 is partially rescued by AblΔCR1.EGFP

    Abl4 is partially rescued by AblΔCR1.EGFP

    Abl4 is partially rescued by AblΔCR2.EGFP

    Abl4 is partially rescued by AblΔCR2.EGFP

    Abl4 is partially rescued by AblΔCR3.EGFP

    Abl4 is partially rescued by AblΔCR3.EGFP

    Abl4 is partially rescued by AblΔCR4.EGFP

    Abl4 is partially rescued by AblΔCR4.EGFP

    Abl4 is partially rescued by Ablftz.PH

    Comments

    The near complete pupal lethality of Abl4/Df(3L)st-j7 at both at 25 and 18[o]C as well as the almost complete embryonic lethality of progeny from Abl4/Df(3L)st-j7 mothers or from females whose germlines are homozygous for Abl4 (created using the FLP/FRT/DFS system) are rescued to a varying degree by combination with any of the following: Abl2kb.T:Avic\GFP-EGFP, AblKD.T:Avic\GFP-EGFP, AblΔFABD.T:Avic\GFP-EGFP, AblKDΔFABD.T:Avic\GFP-EGFP, AblΔCR1.T:Avic\GFP-EGFP, AblΔCR2.T:Avic\GFP-EGFP, AblΔCR3.T:Avic\GFP-EGFP or AblΔCR4.T:Avic\GFP-EGFP.

    The various embryonic morphogenesis defects characteristic for progeny of either Abl4/Df(3L)st-j7 mothers or from females whose germlines are homozygous for Abl4 (created using the FLP/FRT/DFS system) are partially rescued to a varying extent by any of the following: Abl2kb.T:Avic\GFP-EGFP, AblKD.T:Avic\GFP-EGFP, AblΔFABD.T:Avic\GFP-EGFP, AblKDΔFABD.T:Avic\GFP-EGFP or AblΔCR1.T:Avic\GFP-EGFP.

    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.

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