FlyBase Allele Report: Dmel\Abl[2]

Expression of Abl^{N.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^exex-Gal4 exacerbates the ISNb stalling phenotypes found in Abl² mutant embryos.

(O'Donnell and Bashaw, 2013)

Abl mutant flies are fully viable and do not display and PCP defects.

(Yanfeng et al., 2011)

Approximately 9% of Abl² mutant embryos display a duplication of the RP2 neuron in one hemisegment and have one missing in the contralateral segment. RP2 neurons in embryos mutant for the maternal as well as the zygotic Abl gene product (derived from females containing homozygous germline clones mated to homozygous males) fail to migrate completely, remaining in the location where the parent GMC-1 forms. This phenotype is almost fully penetrant.

(Zhu and Bhat, 2011)

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)

90% of Abl¹/Abl² embryos hatch.

Abl² homozygous embryos have intact commissures but show mild discontinuities in the longitudinal tracts.

Instead of forming an even plexus of growth cones at the lamina, photoreceptor axons in Abl¹/Abl² larvae fasciculate aberrantly to produce an irregular pattern of gaps and thickenings in the lamina, with a significant percentage of axon bundles failing to terminate properly at the lamina.

Whereas wild type and small Abl² photoreceptor clones (generated via MARCM) exhibit normal axon targeting, large clones exhibit aberrant fasciculation and targeting to wild type brain tissue in third instar larvae. In contrast, wild type photoreceptor clones exhibit normal targeting to Abl² brain tissue.

(Xiong et al., 2009)

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

(Yu et al., 2009)

Homozygous embryos show axons ectopically crossing the midline. Mutant embryos occasionally show premature arrest of the ISNb axon, at either the muscle 6/7 or muscle 13 cleft.

(Lee et al., 2004)

In homozygous Abl² stage 16 embryos, several axon bundles cross the midline incorrectly. Only a few embryos heterozygous for Abl² 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 Abl^KN.ftz in Abl² mutants results in all embryos exhibiting several axon bundles crossing the midline incorrectly.

(Hsouna et al., 2003)

Homozygous and Abl²/Abl⁴ embryos show ectopic crossing of the midline by axons in the central nervous system.

(Wills et al., 2002)

ISNb growth cones fail to reach the distal target (muscle 12) in 24% of hemizygous embryos, although contacts with muscles 6,7 and 13 appear grossly normal. 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)

Shows 29% viability when heterozygous with Df(3L)st-j7.

(Giniger, 1998)

l(2)gl⁴ Abl² double mutants exhibit a deformed cephalopharyngeal skeleton, defective CNS, absence of the longitudinal tract and commissures. Presence of a wild type copy of ena allows partial restoration of the CNS phenotype.

(Saha and Sinha, 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Abl² has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Hem^J4-48

(Zhu and Bhat, 2011)

Abl² has abnormal cell migration | embryonic stage phenotype, enhanceable by Hem^J4-48

(Zhu and Bhat, 2011)

Abl²/Abl¹ has partially lethal - majority live phenotype, enhanceable by eya[+]/eya^A188

(Xiong et al., 2009)

Abl²/Abl¹ has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by eya[+]/eya^A188

(Xiong et al., 2009)

Abl²/Abl¹ has partially lethal - majority live phenotype, enhanceable by eya^G130/eya[+]

(Xiong et al., 2009)

Abl² has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by eya[+]/eya^A188

(Xiong et al., 2009)

Abl² has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by eya^A188/eya^A188

(Xiong et al., 2009)

Abl² has abnormal neuroanatomy phenotype, enhanceable by chb⁴

(Lee et al., 2004)

Abl² has abnormal neuroanatomy phenotype, enhanceable by chb^P4

(Lee et al., 2004)

Abl²/Df(3L)st-j7 has lethal phenotype, enhanceable by N^l1N-ts1

(Giniger, 1998)

Abl² has lethal phenotype, enhanceable by pros^m4

(Gertler et al., 1989)

Abl² has lethal phenotype, enhanceable by Nrt^M2

(Gertler et al., 1989)

Abl² has lethal phenotype, enhanceable by Nrt^M29

(Gertler et al., 1989)

NOT Enhanced by

Statement

Reference

Abl² has abnormal neuroanatomy phenotype, non-enhanceable by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Suppressed by

Statement

Reference

Abl²/Abl¹ has abnormal neuroanatomy | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl²/Abl¹ has abnormal cell size | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl² has abnormal neuroanatomy | P-stage | somatic clone - tissue specific phenotype, suppressible | partially by ena²³

(Sun et al., 2024)

Abl² has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by robo1^UAS.cKa/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

Abl² has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by robo1^Y-F.UAS/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

Abl² has abnormal neuroanatomy phenotype, suppressible by Lar^bypass/Lar^bypass

(Wills et al., 2002)

NOT suppressed by

Statement

Reference

Abl²/Abl¹ has abnormal neuroanatomy | P-stage phenotype, non-suppressible by ena^KK107752/Scer\GAL4^LL54

(Sun et al., 2024)

Abl²/Abl^{R297K.UAS.GFP} has abnormal neuroanatomy phenotype, non-suppressible by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl² has abnormal neuroanatomy phenotype, non-suppressible by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl²/Abl⁴ has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Dab^UAS.cWa/Scer\GAL4^elav.PU

(Song et al., 2010)

Enhancer of

Statement

Reference

Abl²/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Abl² is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of Hem^J4-48

(Zhu and Bhat, 2011)

Abl² is an enhancer of abnormal cell migration | embryonic stage phenotype of Hem^J4-48

(Zhu and Bhat, 2011)

Abl²/Abl[+] is an enhancer of abnormal planar polarity phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

Abl² is an enhancer of abnormal neuroanatomy phenotype of chb⁴

(Lee et al., 2004)

Abl² is an enhancer of abnormal neuroanatomy phenotype of chb^P4

(Lee et al., 2004)

Abl²/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of sli²

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of robo1^unspecified, robo2⁴

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of robo1^unspecified, robo2⁵

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of robo1^unspecified, robo3¹

(Wills et al., 2002)

NOT Enhancer of

Statement

Reference

Scer\GAL4^eg-Mz360, Abl², Abl^{K417N.UAS.GFP}, Abl[+] is a non-enhancer of abnormal neuroanatomy phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Suppressor of

Statement

Reference

Abl², dsh^Y473F.EGFP, Abl[+] is a suppressor of lethal phenotype of dsh³

(Yanfeng et al., 2011)

Other

Statement

Reference

Abl², eya^A188/eya² has lethal - all die before end of larval stage phenotype

(Xiong et al., 2009)

Abl³/Abl², eya^A188/eya² has lethal - all die before end of larval stage phenotype

(Xiong et al., 2009)

Abl²/Abl⁴, Dscam1^RNAi.UAS.19 has abnormal neuroanatomy | embryonic stage phenotype

(Yu et al., 2009)

Abl²/Abl⁴, Dscam1^{RNAi.UAS.18-20} has abnormal neuroanatomy | embryonic stage phenotype

(Yu et al., 2009)

Abl²/Abl⁴, Dscam1^RNAi.UAS.18 has abnormal neuroanatomy | embryonic stage phenotype

(Yu et al., 2009)

Abl², capt¹⁰ has abnormal neuroanatomy phenotype

(Wills et al., 2002)

Abl², capt^k01217 has abnormal neuroanatomy phenotype

(Wills et al., 2002)

Abl², capt¹⁰/capt[+] has abnormal neuroanatomy phenotype

(Wills et al., 2002)

Abl², capt^k01217/capt[+] has abnormal neuroanatomy phenotype

(Wills et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

Abl² has larval RP2 motor neuron | embryonic stage phenotype, enhanceable by Hem^J4-48

(Zhu and Bhat, 2011)

Abl²/Abl¹ has lamina | third instar larval stage phenotype, enhanceable by eya[+]/eya^A188

(Xiong et al., 2009)

Abl² has larval ventral nerve cord | embryonic stage phenotype, enhanceable by eya[+]/eya^A188

(Xiong et al., 2009)

Abl² has larval ventral nerve cord | embryonic stage phenotype, enhanceable by eya^A188/eya^A188

(Xiong et al., 2009)

Abl² has larval intersegmental nerve phenotype, enhanceable by chb⁴

(Lee et al., 2004)

Abl² has embryonic/larval neuron phenotype, enhanceable by chb⁴

(Lee et al., 2004)

Abl² has embryonic/larval neuron phenotype, enhanceable by chb^P4

(Lee et al., 2004)

NOT Enhanced by

Statement

Reference

Abl² has larval EW neuron phenotype, non-enhanceable by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl² has symmetrical commissure phenotype, non-enhanceable by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Suppressed by

Statement

Reference

Abl²/Abl¹ has eye photoreceptor cell | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl²/Abl¹ has apical part of cell | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl²/Abl¹ has actin cytoskeleton | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl²/Abl¹ has secondary pigment cell | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl²/Abl¹ has basal part of cell | P-stage phenotype, suppressible | partially by ena^KK107752/Scer\GAL4^elav.PLu

(Sun et al., 2024)

Abl² has rhabdomere of eye photoreceptor cell | P-stage | somatic clone - tissue specific phenotype, suppressible | partially by ena²³

(Sun et al., 2024)

Abl² has eye photoreceptor cell | P-stage | somatic clone - tissue specific phenotype, suppressible | partially by ena²³

(Sun et al., 2024)

Abl² has nucleus | P-stage | somatic clone - tissue specific phenotype, suppressible | partially by ena²³

(Sun et al., 2024)

Abl² has filamentous actin | P-stage | somatic clone - tissue specific phenotype, suppressible | partially by ena²³

(Sun et al., 2024)

Abl² has larval longitudinal connective | embryonic stage 16 phenotype, suppressible by robo1^UAS.cKa/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

Abl² has larval longitudinal connective | embryonic stage 16 phenotype, suppressible by robo1^Y-F.UAS/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

Abl² has presumptive embryonic/larval central nervous system phenotype, suppressible by Lar^bypass/Lar^bypass

(Wills et al., 2002)

NOT suppressed by

Statement

Reference

Abl²/Abl¹ has basal part of cell | P-stage phenotype, non-suppressible by ena^KK107752/Scer\GAL4^LL54

(Sun et al., 2024)

Abl²/Abl¹ has eye photoreceptor cell | P-stage phenotype, non-suppressible by ena^KK107752/Scer\GAL4^LL54

(Sun et al., 2024)

Abl²/Abl^{R297K.UAS.GFP} has larval EW neuron phenotype, non-suppressible by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl²/Abl^{R297K.UAS.GFP} has symmetrical commissure phenotype, non-suppressible by Scer\GAL4^eg-Mz360/Abl^{R297K.UAS.GFP}/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl² has larval EW neuron phenotype, non-suppressible by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl² has symmetrical commissure phenotype, non-suppressible by Scer\GAL4^eg-Mz360/fra^{ΔC.UAS.Tag:HA}

(O'Donnell and Bashaw, 2013)

Abl²/Abl⁴ has larval intersegmental nerve branch ISNb of A1-7 phenotype, non-suppressible by Dab^UAS.cWa/Scer\GAL4^elav.PU

(Song et al., 2010)

Enhancer of

Statement

Reference

Abl²/Abl[+] is an enhancer of larval EW neuron phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Abl²/Abl[+] is an enhancer of symmetrical commissure phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Abl² is an enhancer of larval RP2 motor neuron | embryonic stage phenotype of Hem^J4-48

(Zhu and Bhat, 2011)

Abl²/Abl[+] is an enhancer of ommatidium phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

Abl²/Abl[+] is an enhancer of pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

Abl²/Abl[+] is an enhancer of cone cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

Abl² is an enhancer of embryonic/larval neuron phenotype of chb^P4

(Lee et al., 2004)

Abl² is an enhancer of larval intersegmental nerve phenotype of chb⁴

(Lee et al., 2004)

Abl² is an enhancer of embryonic/larval neuron phenotype of chb⁴

(Lee et al., 2004)

Abl²/Abl[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of sli²

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of robo1^unspecified, robo2⁴

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of robo1^unspecified, robo2⁵

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of robo1^unspecified, robo3¹

(Wills et al., 2002)

Abl²/Abl[+] is an enhancer of larval longitudinal connective phenotype of chic^05205a/chic²²¹

(Wills et al., 1999)

Abl²/Abl⁴ is an enhancer of larval longitudinal connective phenotype of chic^05205a/chic²²¹

(Wills et al., 1999)

NOT Enhancer of

Statement

Reference

Scer\GAL4^eg-Mz360, Abl², Abl^{K417N.UAS.GFP}, Abl[+] is a non-enhancer of larval EW neuron phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Scer\GAL4^eg-Mz360, Abl², Abl^{K417N.UAS.GFP}, Abl[+] is a non-enhancer of symmetrical commissure phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Suppressor of

Statement

Reference

Abl² is a suppressor of larval intersegmental nerve phenotype of Lar^bypass/Lar^E55

(Wills et al., 1999)

Abl² is a suppressor of larval intersegmental nerve phenotype of Lar^OD16/Lar^13.2

(Wills et al., 1999)

Other

Statement

Reference

Abl², eya[+]/eya^A188 has larval ventral nerve cord commissure | embryonic stage phenotype

(Xiong et al., 2009)

Abl², eya^A188 has larval ventral nerve cord commissure | embryonic stage phenotype

(Xiong et al., 2009)

Abl²/Abl⁴, Dscam1^RNAi.UAS.19 has larval ventral nerve cord | embryonic stage phenotype

(Yu et al., 2009)

Abl²/Abl⁴, Dscam1^{RNAi.UAS.18-20} has larval ventral nerve cord | embryonic stage phenotype

(Yu et al., 2009)

Abl²/Abl⁴, Dscam1^RNAi.UAS.18 has larval ventral nerve cord | embryonic stage phenotype

(Yu et al., 2009)

Abl², capt¹⁰ has presumptive embryonic/larval central nervous system phenotype

(Wills et al., 2002)

Abl², capt^k01217 has presumptive embryonic/larval central nervous system phenotype

(Wills et al., 2002)

Abl², capt¹⁰/capt[+] has presumptive embryonic/larval central nervous system phenotype

(Wills et al., 2002)

Abl², capt^k01217/capt[+] has presumptive embryonic/larval central nervous system phenotype

(Wills et al., 2002)

Abl², chic^05205a/chic²²¹ has larval longitudinal connective phenotype

(Wills et al., 1999)

Abl², N^l1N-ts1 has larval longitudinal connective phenotype

(Giniger, 1998)

Abl², N^l1N-ts1 has larval intersegmental nerve | lateral phenotype

(Giniger, 1998)

Abl², Fas1^TE89Da has axon phenotype

(Elkins et al., 1990)

Additional Comments

Genetic Interactions

Statement

Reference

A Abl²/+ heterozygous background increases the number of segments displaying EW axon midline crossing defects in Df(1)NetAB^Δ stage 15 embryos from approximately 40% to 45% of segments.

Expression of Abl^{R297K.Scer\UAS.T:Avic\GFP} in the EW neurons of Abl² mutant embryos fails to rescue the commissural defects found in Abl² mutant embryos expressing fra^{ΔC.Scer\UAS.T:Ivir\HA1}.

Expression of a weak transgene of fra^{ΔC.Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^eg-Mz360 has no effect on the number and severity of midline crossing defects found in Abl² homozygous mutants. The presence of Abl^{Scer\UAS.T:Avic\GFP} reduces the number of midline crossing defects (to a statistically significant level) in Abl² homozygous mutants in a fra^{ΔC.Scer\UAS.T:Ivir\HA1}-expressing background. The presence of Abl^{K417N.Scer\UAS.T:Avic\GFP} reduces (although not to a statistically significant level) the number of midline crossing defects in Abl² homozygous mutants in a fra^{ΔC.Scer\UAS.T:Ivir\HA1}-expressing background.

Expression of Abl^{ΔFABD.Scer\UAS.T:Avic\GFP} in EW neurons, under the control of Scer\GAL4^eg-Mz360 fails to rescue EW midline-crossing defects in Abl² neurons expressing fra^{ΔC.Scer\UAS.T:Ivir\HA1}.

(O'Donnell and Bashaw, 2013)

Expression of dsh^{Y473F.T:Avic\GFP-EGFP} in a Abl²/+ mutant background partially rescues the lethality seen in dsh³. The PCP defects are not rescued.

(Yanfeng et al., 2011)

Abl² Hem^J4-48 double mutant embryos show a stronger RP2 neuron migration defect compared to either single mutant. Approximately 17% of embryos display a duplication of the RP2 neuron in one hemisegment and have one missing in the contralateral segment.

(Zhu and Bhat, 2011)

The ISNb stall phenotype seen in Abl²/Abl⁴ embryos is not suppressed by expression of Dab^Scer\UAS.cWa under the control of Scer\GAL4^elav.PU.

(Song et al., 2010)

eya^A188/+ or eya^G130/+ reduces the hatch rate of Abl¹/Abl² embryos from 90% to 20%.

Abl², eya^A188/+ embryos have discontinuities along the longitudinal axon bundles with 20% of commissures lost or defective. Abl², eya^A188 embryos show severe disruptions in the longitudinal tracts and 77% of commissures are lost.

The embryonic CNS of eya^A188, Abl²/+ is indistinguishable from wild type.

eya^A188/+ enhances the Abl¹/Abl² mistargeting phenotype, resulting in a highly disorganized lamina plexus.

(Xiong et al., 2009)

Scer\GAL4^tub.PU-mediated expression of Dscam1^{miRNA.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\GAL4^tub.PU-mediated expression of Dscam1^{miRNA.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\GAL4^tub.PU-mediated expression of Dscam1^{miRNA.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)

An Abl² heterozygous background enhances the patterning defects found in Scer\GAL4^GMR.PF>cindr^{dsRNA.PC.PD.Scer\UAS} mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

(Johnson et al., 2008)

The frequency of axons ectopically crossing the midline in chb^P4 Abl² double homozygous embryos is substantially increased compared to the frequency seen in either single homozygote. The frequency of axons ectopically crossing the midline in chb⁴ Abl² double homozygous embryos is substantially increased compared to the frequency seen in either single homozygote. chb⁴ Abl² double homozygous embryos show an increased frequency of premature arrest of the ISNb axon compared to either single homozygote, with the arrest being seen at both the muscle 6/7 and the muscle 13 choice points.

(Lee et al., 2004)

Overexpression of robo^Scer\UAS.cKa under the control of Scer\GAL4^ftz.ng in Abl² homozygous mutants suppresses the frequency of abnormal crossovers observed in Abl² mutants.

Overexpression of robo^Y-F.Scer\UAS under the control of Scer\GAL4^ftz.ng in Abl² homozygous mutants suppresses the frequency of abnormal crossovers observed in Abl² mutants.

(Hsouna et al., 2003)

Central nervous system axons are seen to cross the midline in Abl² capt^k01217 double heterozygous embryos. Central nervous system axons are seen to cross the midline in Abl² capt¹⁰ double heterozygous embryos. Central nervous system axons are seen to cross the midline in Abl² capt^E636 double heterozygous embryos. Expression of capt^Scer\UAS.cBa under the control of Scer\GAL4^elav.PLu completely rescues the midline crossing defects seen in capt^E636 Abl² double heterozygotes. Expression of capt^C.Scer\UAS under the control of Scer\GAL4^elav.PLu partially rescues the midline crossing defects seen in capt^E636 Abl² double heterozygotes. The midline crossing errors seen in the central nervous system of Abl²/Abl² embryos are suppressed by Lar^bypass/Lar^bypass. The frequency of ectopic crossing of the midline by axons in the central nervous system seen in sli² heterozygous embryos is increased if they are also heterozygous for Abl². The frequency of ectopic crossing of the midline by axons in the central nervous system seen in robo^unspecified lea^robo2-4 embryos is increased by Abl²/+. The frequency of ectopic crossing of the midline by axons in the central nervous system seen in robo^unspecified lea^robo2-5 embryos is increased by Abl²/+. The frequency of ectopic crossing of the midline by axons in the central nervous system seen in robo^unspecified robo3¹ embryos is increased by Abl²/+.

(Wills et al., 2002)

chic^05205a/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 Lar^OD16/Lar^13.2 or Lar^bypass/Lar^E55 embryos.

(Wills et al., 1999)

Viability of Abl²/Df(3L)st-j7 animals reduced to <1.0% when combined with N^l1N-ts1 at 18^oC. Affected embryos do not show a neurogenic or antimyogenic phenotype. The gross morphology of the embryos is normal but they show axonal defects in all axon tracts known to require N function: CNS longitudinal tracts between neuromeres and the lateral portion of the ISN. Defects are evident from stage 13, in the combined MP fascicle. The nerve frays and stalls precisely as it attempts to grow along the trachea. The LG5 glial cell is present. Neurons aCC MP1 pCC dMP2 and vMP2 are all present. Pioneer neuron identity is unaffected (as assayed by ftz, eve, odd, Fas2 and pros expression).

(Giniger, 1998)

The pupal lethality of hemizygous flies is not affected if the flies are also mutant for Ptp99A (Ptp99A^HA64/Ptp99A^R3.

(Hamilton et al., 1995)

Abl², Fas1^TE89Da mutant embryos exhibit gross defects in the developing CNS axon guidance and the morphogenesis of CNS axon tracts: an allele specific interaction.

(Elkins et al., 1990)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Abl² is rescued by Scer\GAL4^exex-Gal4/Abl^UAS.GFP

(O'Donnell and Bashaw, 2013)

Abl² is rescued by Abl^{R297K.UAS.GFP}/Scer\GAL4^exex-Gal4

(O'Donnell and Bashaw, 2013)

Abl² is rescued by Abl^{ΔFABD.UAS.GFP}/Scer\GAL4^exex-Gal4

(O'Donnell and Bashaw, 2013)

Partially rescued by

Abl²/Abl¹ is partially rescued by Scer\GAL4^elav.PLu/Abl^UAS.GFP

(Sun et al., 2024)

Abl²/Abl¹ is partially rescued by Scer\GAL4^LL54/Abl^UAS.GFP

(Sun et al., 2024)

Abl² is partially rescued by Abl^ftz.PH

(Hsouna et al., 2003)

Abl² is partially rescued by Abl^+mTnabl

(Giniger, 1998)

Not rescued by

Abl² is not rescued by Abl^{K417N.UAS.GFP}/Scer\GAL4^exex-Gal4

(O'Donnell and Bashaw, 2013)

Abl² is not rescued by Scer\GAL4^eg-Mz360/Abl^UAS.GFP

(O'Donnell and Bashaw, 2013)

Abl² is not rescued by Scer\GAL4^eg-Mz360/Abl^N.UAS.GFP

(O'Donnell and Bashaw, 2013)

Abl² is not rescued by Abl^KN.ftz

(Hsouna et al., 2003)

Comments

Expression of Abl^{N.Scer\UAS.T:Avic\GFP} in the EW neurons of Abl² mutant embryos results in a dramatic increase in the number of commissural defects.

Expression of Abl^{N.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^exex-Gal4 exacerbates the ISNb stalling phenotypes found in Abl² mutant embryos.

Expression of Abl^{Scer\UAS.T:Avic\GFP} in the EW neurons of Abl² mutant embryos has no effect on the mild commissural defects found in these mutants.

Expression of Abl^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^exex-Gal4 rescues the ISNb motor axon defects found in Abl² mutants.

Expression of Abl^{ΔFABD.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^exex-Gal4 rescues the ISNb motor axon defects found in Abl² mutants.

Expression of Abl^{R297K.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^exex-Gal4 rescues the ISNb motor axon defects found in Abl² mutants.

Expression of Abl^{K417N.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^exex-Gal4 fails to rescue the ISNb motor axon defects found in Abl² mutants.

(O'Donnell and Bashaw, 2013)

When two copies of Abl^ftz.PH are introduced into Abl² mutants, axonal crossovers are reduced from 68% in Abl² single mutants to 37% in the presence of the transgene.

Expression of two copies of Abl^KN.ftz in Abl² mutants results in all embryos exhibiting several axon bundles crossing the midline incorrectly.

(Hsouna et al., 2003)

Images (0)

Mutant

Wild-type

Stocks (7)

Bloomington

8565

Abl²/TM6B, Tb¹

97271

w^*; Abl², M{10xUAS-Abl.GFP}ZH-86Fb/TM3, P{Ubx-lacZ.w⁺}TM3, Sb¹

97273

w^*; Abl², M{10xUAS-Abl.C.GFP}ZH-86Fb/TM3, P{Ubx-lacZ.w⁺}TM3, Sb¹

97275

w^*; Abl², M{10xUAS-Abl.ΔFABD.GFP}ZH-86Fb/TM3, P{Ubx-lacZ.w⁺}TM3, Sb¹

97276

w^*; Abl², M{10xUAS-Abl.R297K.GFP}ZH-86Fb/TM3, P{Ubx-lacZ.w⁺}TM3, Sb¹

97274

w^*; Abl², M{10xUAS-Abl.F1591E.GFP}ZH-86Fb/TM3, P{Ubx-lacZ.w⁺}TM3, Sb¹

97272

w^*; Abl², M{10xUAS-Abl.N.K417N.GFP}ZH-86Fb/TM3, P{Ubx-lacZ.w⁺}TM3, Sb¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

Abl²

(Marquilly et al., 2021, Cheong et al., 2020, Cheong and VanBerkum, 2017, Yoon et al., 2017, O'Donnell and Bashaw, 2013, Zhu and Bhat, 2011, Song et al., 2010, Smith and Liebl, 2005)

abl

(Yanfeng et al., 2011)

abl-2

(Gertler et al., 1989)

abl²

(Sun et al., 2024, Knox et al., 2011, Xiong et al., 2009, Yu et al., 2009, Dorsten et al., 2007, Hsouna et al., 2003, Hsouna et al., 2001, Wills et al., 1999, Wills et al., 1999, Giniger, 1998, Garcia-Alonso et al., 1995, Therianos et al., 1995)

Name Synonyms

abelson2

(Johnson et al., 2008)

Secondary FlyBase IDs

References (28)

Report Sections

Open Close