FlyBase Allele Report: Dmel\Abl[1]

Abl¹/Abl⁴ third instar larvae display supernumerary mature and satellite NMJ boutons. A significant increase in the number of synaptic boutons containing microtubule loops points towards an increase in microtubule stability.

(Kim et al., 2019)

The class IV dendritic arborizing neurons in Abl¹/Abl¹ MARCM somatic clones display slightly but significantly decreased presynaptic terminal lengths than controls but dendritic length or morphology is unchanged.

(Sterne et al., 2015)

Abl¹ mutants exhibit minor midline crossing defects.

(Al-Anzi and Wyman, 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 Abl¹/Abl⁴ and Abl¹/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)

90% of Abl¹/Abl² embryos hatch.

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.

(Xiong et al., 2009)

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)

In homozygous Abl¹ stage 16 embryos, several axon bundles cross the midline incorrectly.

(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)

Homozygous embryos show ectopic crossing of the midline by axons in the central nervous system. The most lateral Fas2-positive fascicle is often thin or missing.

(Wills et al., 2002)

Abl¹ embryos derived from homozygous Abl¹ female germline clones (lacking both maternal and zygotic Abl function) die at the end of embryogenesis, while embryos derived from homozygous Abl¹ female germline clones that receive a wild-type paternal copy of Abl survive to adulthood. Abl¹ mutant embryos derived from homozygous Abl¹ female germline clones show a range of defects. 1% are "U-shaped", showing a complete failure of germband retraction. 13% have a "tail-up" phenotype, showing strong defects in germband retraction and also often have defects in dorsal closure. 67% have defects in dorsal closure ranging from dorsal holes to defects in the dorsal pattern. 1% have severe defects in head involution, most in this class also show defects in dorsal closure and/or germband retraction.

(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 63% of hemizygous embryos, although contacts with muscles 6,7 and 13 appear grossly normal. 53% of ISNb growth cones terminate before reaching muscle 12 in homozygous embryos. The Fas2-positive longitudinal fascicles of the central nervous system are disorganised in hemizygous embryos, with breaks in the most lateral fascicle being common.

(Wills et al., 1999)

Shows 41% viability when heterozygous with Df(3L)st-j7.

(Giniger, 1998)

Homozygous embryos have a normal central nervous system.

(Loureiro and Peifer, 1998)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

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)

Abl⁴/Abl¹ has abnormal neuroanatomy phenotype, enhanceable by Ama^M109/Ama[+]

(Liebl et al., 2003)

Abl⁴/Abl¹ has lethal phenotype, enhanceable by Ama^M109/Ama[+]

(Liebl et al., 2003)

Abl⁴/Abl¹ has abnormal neuroanatomy phenotype, enhanceable by Df(3R)ama/Ama^M109

(Liebl et al., 2003)

Abl⁴/Abl¹ has abnormal neuroanatomy phenotype, enhanceable by Df(3R)ama/Ama^R1

(Liebl et al., 2003)

Abl⁴/Abl¹ has lethal | prepupal stage phenotype, enhanceable by Nrt^M221/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 fax^M7/fax[+]

(Liebl et al., 2000)

Abl⁴/Abl¹ has lethal | prepupal stage phenotype, enhanceable by trio[+]/trio^M89

(Liebl et al., 2000)

Abl¹/Df(3L)st-j7 has lethal phenotype, enhanceable by N^l1N-ts1

(Giniger, 1998)

Abl¹ has lethal phenotype, enhanceable by Nrt^M2

(Gertler et al., 1989)

Abl¹ has lethal phenotype, enhanceable by Nrt^M29

(Gertler et al., 1989)

Abl¹ has lethal phenotype, enhanceable by pros^m4

(Gertler et al., 1989)

NOT Enhanced by

Statement

Reference

Abl⁴/Abl¹ has abnormal neuroanatomy phenotype, non-enhanceable by Ama^R1/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

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)

Abl⁴/Abl¹ has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^elav-C155/Abi^{4YE.UAS.Tag:HA}

(Kim et al., 2019)

Abl⁴/Abl¹ has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by wit^A12

(Kim et al., 2019)

Abl⁴/Abl¹ has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by wit^B11

(Kim et al., 2019)

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

(Lin et al., 2009)

Abl⁴/Abl¹ has lethal phenotype, suppressible | partially by Abi[+]/Abi^P1

(Lin et al., 2009)

Abl⁴/Abl¹ has abnormal neuroanatomy | embryonic stage phenotype, suppressible | partially by Abi[+]/Abi^P2

(Lin et al., 2009)

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

(Lin et al., 2009)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has abnormal neuroanatomy phenotype, suppressible | partially by ena[+]/ena^GC10

(Forsthoefel et al., 2005)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has abnormal neuroanatomy phenotype, suppressible | partially by ena[+]/ena^GC10

(Forsthoefel et al., 2005)

Abl¹/Abl[+], Khc¹⁶ has paralytic | dominant | larval stage phenotype, suppressible by ena[+]/ena²¹⁰

(Martin et al., 2005)

Abl¹/Abl[+], Khc¹⁶ has abnormal neuroanatomy | dominant | larval stage phenotype, suppressible by ena[+]/ena²¹⁰

(Martin et al., 2005)

Abl¹ has abnormal neuroanatomy phenotype, suppressible by Lar^13.2/Lar^13.2

(Wills et al., 2002)

Abl⁴/Abl¹ has lethal phenotype, suppressible by ena[+]/ena^GC10

(Liebl et al., 2000)

Abl⁴/Abl¹, Nrt^M221/Nrt[+] has lethal | prepupal stage phenotype, suppressible by ena[+]/ena^GC10

(Liebl et al., 2000)

Abl⁴/Abl¹, fax^M7/fax[+] has lethal | prepupal stage phenotype, suppressible by ena[+]/ena^GC10

(Liebl et al., 2000)

Abl⁴/Abl¹, trio[+]/trio^M89 has lethal | prepupal stage phenotype, suppressible by ena[+]/ena^GC10

(Liebl et al., 2000)

Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible | partially by Scer\GAL4³¹/Abl^UAS.cFa

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible | partially by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^P210.UAS

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible | partially by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^P185.UAS

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7 has lethal phenotype, suppressible by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^P185.UAS

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7 has lethal phenotype, suppressible by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^P210.UAS

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible | partially by Scer\GAL4³¹/Abl^K417N.UAS

(Fogerty et al., 1999)

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)

Abl⁴/Abl¹ has abnormal neuroanatomy | larval stage phenotype, non-suppressible by ena[+]/ena^GC5

(Lin et al., 2009)

Abl⁴/Abl¹ has abnormal neuroanatomy | larval stage phenotype, non-suppressible by Hem[+]/Hem^C3-20

(Lin et al., 2009)

Abl⁴/Abl¹ has abnormal neuroanatomy | larval stage phenotype, non-suppressible by SCAR^Δ37/SCAR[+]

(Lin et al., 2009)

Enhancer of

Statement

Reference

Abl¹/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Abl¹/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)

Abl¹/Abl[+] is an enhancer of abnormal neuroanatomy phenotype of fra⁴

(Forsthoefel et al., 2005)

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

(Forsthoefel et al., 2005)

Abl¹/Abl[+] is an enhancer of lethal phenotype of trio^M89/trio^S036810

(Liebl et al., 2000)

NOT Enhancer of

Statement

Reference

Abl¹/Abl[+] is a non-enhancer of abnormal neuroanatomy phenotype of Df(2R)BSC3/fra³

(O'Donnell and Bashaw, 2013)

Suppressor of

Statement

Reference

Abl¹/Abl[+] is a suppressor | partially of visible | adult stage phenotype of Hsap\ABL1::Hsap\BCR^UAS.cBa, Scer\GAL4^GMR.PU

(Bernardoni et al., 2019)

Abl¹/Abl¹ is a suppressor | somatic clone of abnormal neuroanatomy | somatic clone | third instar larval stage phenotype of Dscam1^{exon17.2.UAS.GFP}, Scer\GAL4^ppk.PG

(Sterne et al., 2015)

Abl¹/Abl[+] is a suppressor of abnormal neuroanatomy | somatic clone | third instar larval stage phenotype of Fmr1^Δ50M

(Sterne et al., 2015)

Abl¹/Abl[+] is a suppressor | partially of abnormal neuroanatomy | embryonic stage phenotype of EndoGI^cwk

(O'Keefe et al., 2011)

Abl¹/Abl[+] is a suppressor of abnormal neuroanatomy phenotype of Hsap\APP^UAS.Tag:MYC, Scer\GAL4^P2.4.Pdf

(Leyssen et al., 2005)

Abl¹/Abl[+] is a suppressor of visible phenotype of CycE^JP

(Brumby et al., 2004)

NOT Suppressor of

Statement

Reference

Abl⁴/Abl¹ is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of wit^B11/wit^A12

(Kim et al., 2019)

Abl⁴/Abl¹ is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Fmr1^UAS.cZa, Scer\GAL4^elav-C155

(Kim et al., 2019)

Abl¹/Abl[+] is a non-suppressor of abnormal neuroanatomy phenotype of Df(2R)BSC3/fra³

(O'Donnell and Bashaw, 2013)

Other

Statement

Reference

Abl¹, Df(3R)su(Hw)7/+ has abnormal neuroanatomy | dominant | third instar larval stage phenotype

(Kim et al., 2019)

Abi⁵, Abl¹/Abl[+] has abnormal neuroanatomy | dominant | third instar larval stage phenotype

(Kim et al., 2019)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has abnormal neuroanatomy phenotype

(Forsthoefel et al., 2005)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has abnormal neuroanatomy phenotype

(Forsthoefel et al., 2005)

Abl¹/Abl[+], Khc¹⁶ has paralytic | dominant | larval stage phenotype

(Martin et al., 2005)

Abl¹/Abl[+], Khc¹⁶ has abnormal neuroanatomy | dominant | larval stage phenotype

(Martin et al., 2005)

Abl⁴/Abl¹, Nrt^M100 has abnormal neuroanatomy phenotype

(Liebl et al., 2003)

Abl¹/Df(3L)st-j7, Nrt^M54/Nrt^M2 has abnormal neuroanatomy phenotype

(Liebl et al., 2003)

Abl⁴/Abl¹, Nrt^M54 has abnormal neuroanatomy phenotype

(Liebl et al., 2003)

Abl¹, shg² has lethal | embryonic stage phenotype

(Grevengoed et al., 2001)

Abl¹, shg^R69 has lethal | embryonic stage phenotype

(Grevengoed et al., 2001)

Abl¹, shg[+]/shg^R69 has lethal | embryonic stage phenotype

(Grevengoed et al., 2001)

Abl¹, shg[+]/shg² has lethal | embryonic stage phenotype

(Grevengoed et al., 2001)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹, Scer\GAL4³¹ has viable phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹, Scer\GAL4³¹ has visible phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹, Scer\GAL4³¹ has viable phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹, Scer\GAL4³¹ has visible phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has visible phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has visible phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has visible phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has visible phenotype

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype

(Fogerty et al., 1999)

Abl¹, N^55e11, Nrt^M54 has visible | dominant phenotype

(Giniger, 1998)

Abl¹, Df(1)N-8, Nrt^M54 has visible | dominant phenotype

(Giniger, 1998)

Abl¹/Df(3L)st-j7, N^l1N-ts1 has partially lethal - majority die phenotype

(Giniger, 1998)

Abl¹/Df(3L)st-j7, N^l1N-ts1 has abnormal neuroanatomy | embryonic stage phenotype

(Giniger, 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

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

(Xiong et al., 2009)

Abl⁴/Abl¹ has larval ventral nerve cord commissure phenotype, enhanceable by Ama^M109/Ama[+]

(Liebl et al., 2003)

Abl⁴/Abl¹ has larval ventral nerve cord commissure phenotype, enhanceable by Df(3R)ama/Ama^M109

(Liebl et al., 2003)

Abl⁴/Abl¹ has larval ventral nerve cord commissure phenotype, enhanceable by Df(3R)ama/Ama^R1

(Liebl et al., 2003)

Abl⁴/Abl¹ has larval posterior commissure phenotype, enhanceable by trio[+]/trio^M89

(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)

Abl⁴/Abl¹ has larval anterior commissure phenotype, enhanceable by trio[+]/trio^M89

(Liebl et al., 2000)

Abl⁴/Abl¹ has larval longitudinal connective phenotype, enhanceable by trio[+]/trio^M89

(Liebl et al., 2000)

Abl¹ has phenotype, enhanceable by fax^M12

(Hill et al., 1995)

Abl¹ has phenotype, enhanceable by fax^M34

(Hill et al., 1995)

Abl¹ has phenotype, enhanceable by fax^M42

(Hill et al., 1995)

Abl¹ has phenotype, enhanceable by fax^M7

(Hill et al., 1995)

NOT Enhanced by

Statement

Reference

Abl⁴/Abl¹ has larval ventral nerve cord commissure phenotype, non-enhanceable by Ama^R1/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

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)

Abl⁴/Abl¹ has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^elav-C155/Abi^{4YE.UAS.Tag:HA}

(Kim et al., 2019)

Abl⁴/Abl¹ has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by wit^A12

(Kim et al., 2019)

Abl⁴/Abl¹ has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by wit^B11

(Kim et al., 2019)

Abl⁴/Abl¹ has NMJ bouton | third instar larval stage phenotype, suppressible by Scer\GAL4^elav-C155/Abi^{4YE.UAS.Tag:HA}

(Kim et al., 2019)

Abl⁴/Abl¹ has NMJ bouton | third instar larval stage phenotype, suppressible by wit^A12

(Kim et al., 2019)

Abl⁴/Abl¹ has NMJ bouton | third instar larval stage phenotype, suppressible by wit^B11

(Kim et al., 2019)

Abl⁴/Abl¹ has larval longitudinal connective phenotype, suppressible | partially by Abi[+]/Abi^P2

(Lin et al., 2009)

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

(Lin et al., 2009)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has symmetrical commissure phenotype, suppressible | partially by ena[+]/ena^GC10

(Forsthoefel et al., 2005)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has symmetrical commissure phenotype, suppressible | partially by ena[+]/ena^GC10

(Forsthoefel et al., 2005)

Abl¹/Abl[+], Khc¹⁶ has axon phenotype, suppressible by ena[+]/ena²¹⁰

(Martin et al., 2005)

Abl¹ has presumptive embryonic/larval central nervous system phenotype, suppressible by Lar^13.2/Lar^13.2

(Wills et al., 2002)

NOT suppressed by

Statement

Reference

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

(Sun et al., 2024)

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

(Sun et al., 2024)

Abl⁴/Abl¹ has NMJ bouton | increased number phenotype, non-suppressible by ena[+]/ena^GC5

(Lin et al., 2009)

Abl⁴/Abl¹ has NMJ bouton | increased number phenotype, non-suppressible by Hem[+]/Hem^C3-20

(Lin et al., 2009)

Abl⁴/Abl¹ has NMJ bouton | increased number phenotype, non-suppressible by SCAR^Δ37/SCAR[+]

(Lin et al., 2009)

Enhancer of

Statement

Reference

Abl¹/Abl[+] is an enhancer of larval EW neuron phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Abl¹/Abl[+] is an enhancer of symmetrical commissure phenotype of fra⁶/fra³

(O'Donnell and Bashaw, 2013)

Abl¹/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)

Abl¹/Abl[+] is an enhancer of symmetrical commissure phenotype of fra⁴

(Forsthoefel et al., 2005)

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

(Forsthoefel et al., 2005)

Abl¹/Abl[+] is an enhancer of larval longitudinal connective phenotype of trio^M89/trio^S036810

(Liebl et al., 2000)

Abl¹/Abl[+] is an enhancer of larval anterior commissure phenotype of Df(3L)Fpa1/trio^M89

(Liebl et al., 2000)

Abl¹/Abl[+] is an enhancer of larval longitudinal connective phenotype of Df(3L)Fpa1/trio^M89

(Liebl et al., 2000)

Abl¹/Abl[+] is an enhancer of larval posterior commissure phenotype of Df(3L)Fpa1/trio^M89

(Liebl et al., 2000)

Abl¹ 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

Abl¹/Abl[+] is a non-enhancer of larval EW neuron phenotype of Df(2R)BSC3/fra³

(O'Donnell and Bashaw, 2013)

Abl¹/Abl[+] is a non-enhancer of symmetrical commissure phenotype of Df(2R)BSC3/fra³

(O'Donnell and Bashaw, 2013)

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

(Forsthoefel et al., 2005)

Suppressor of

Statement

Reference

Abl¹/Abl[+] is a suppressor | partially of eye phenotype of Hsap\ABL1::Hsap\BCR^UAS.cBa, Scer\GAL4^GMR.PU

(Bernardoni et al., 2019)

Abl¹/Abl¹ is a suppressor | somatic clone of larval multidendritic class IV neuron | somatic clone | third instar larval stage phenotype of Dscam1^{exon17.2.UAS.GFP}, Scer\GAL4^ppk.PG

(Sterne et al., 2015)

Abl¹/Abl[+] is a suppressor of larval multidendritic class IV neuron | somatic clone | third instar larval stage phenotype of Fmr1^Δ50M

(Sterne et al., 2015)

Abl¹/Abl[+] is a suppressor | partially of larval intersegmental nerve branch ISNb of A1-7 phenotype of EndoGI^cwk

(O'Keefe et al., 2011)

Abl¹/Abl[+] is a suppressor of ventral adult lateral neuron & axon phenotype of Hsap\APP^UAS.Tag:MYC, Scer\GAL4^P2.4.Pdf

(Leyssen et al., 2005)

Abl¹/Abl[+] is a suppressor of eye phenotype of CycE^JP

(Brumby et al., 2004)

Nrt^M54/Abl¹ is a suppressor of larval intersegmental nerve | heat sensitive phenotype of N^l1N-ts1

(Crowner et al., 2003)

Abl¹/Abl[+] is a suppressor of larval intersegmental nerve | heat sensitive phenotype of N^l1N-ts1

(Crowner et al., 2003)

Abl¹/Abl[+] is a suppressor of larval longitudinal connective phenotype of robo1⁵, sli[+]/sli¹

(Bashaw et al., 2000)

robo[+], Abl¹, robo1⁵, Abl[+] is a suppressor of larval longitudinal connective phenotype of sli¹

(Bashaw et al., 2000)

Abl¹ is a suppressor of larval intersegmental nerve phenotype of Lar^bypass/Lar^5.5

(Wills et al., 1999)

Abl¹ is a suppressor of larval intersegmental nerve phenotype of Lar^bypass/Lar^13.2

(Wills et al., 1999)

Abl¹ is a suppressor of larval intersegmental nerve phenotype of Lar^bypass/Lar^E55

(Wills et al., 1999)

Abl¹ is a suppressor of larval intersegmental nerve phenotype of Lar^bypass

(Wills et al., 1999)

Abl¹/Df(3L)st-j7 is a suppressor of phenotype of arm⁴

(Loureiro and Peifer, 1998)

Abl¹ is a suppressor of phenotype of arm⁴

(Loureiro and Peifer, 1998)

NOT Suppressor of

Statement

Reference

Abl⁴/Abl¹ is a non-suppressor of NMJ bouton | third instar larval stage phenotype of wit^B11/wit^A12

(Kim et al., 2019)

Abl⁴/Abl¹ is a non-suppressor of embryonic/larval neuromuscular junction | third instar larval stage phenotype of Fmr1^UAS.cZa, Scer\GAL4^elav-C155

(Kim et al., 2019)

Abl⁴/Abl¹ is a non-suppressor of NMJ bouton | third instar larval stage phenotype of Fmr1^UAS.cZa, Scer\GAL4^elav-C155

(Kim et al., 2019)

Abl⁴/Abl¹ is a non-suppressor of embryonic/larval neuromuscular junction | third instar larval stage phenotype of wit^B11/wit^A12

(Kim et al., 2019)

Abl¹/Abl[+] is a non-suppressor of larval EW neuron phenotype of Df(2R)BSC3/fra³

(O'Donnell and Bashaw, 2013)

Abl¹/Abl[+] is a non-suppressor of symmetrical commissure phenotype of Df(2R)BSC3/fra³

(O'Donnell and Bashaw, 2013)

Other

Statement

Reference

Abl¹, Df(3R)su(Hw)7/+ has NMJ bouton | third instar larval stage phenotype

(Kim et al., 2019)

Abl¹, Df(3R)su(Hw)7/+ has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Kim et al., 2019)

Abi⁵, Abl¹/Abl[+] has NMJ bouton | third instar larval stage phenotype

(Kim et al., 2019)

Abi⁵, Abl¹/Abl[+] has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Kim et al., 2019)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has symmetrical commissure phenotype

(Forsthoefel et al., 2005)

Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has symmetrical commissure phenotype

(Forsthoefel et al., 2005)

Abl¹/Abl[+], Khc¹⁶ has axon phenotype

(Martin et al., 2005)

Abl⁴/Abl¹, Nrt^M100 has larval ventral nerve cord commissure phenotype

(Liebl et al., 2003)

Abl¹/Df(3L)st-j7, Nrt^M54/Nrt^M2 has larval ventral nerve cord commissure phenotype

(Liebl et al., 2003)

Abl⁴/Abl¹, Nrt^M54 has larval ventral nerve cord commissure phenotype

(Liebl et al., 2003)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has eye phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has ommatidium phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has eye phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P185.UAS, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has ommatidium phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has eye phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has ommatidium phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has eye phenotype

(Fogerty et al., 1999)

Abl::Hsap\ABL1::Hsap\BCR^P210.UAS, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has ommatidium phenotype

(Fogerty et al., 1999)

Abl¹, N^55e11, Nrt^M54 has eye phenotype

(Giniger, 1998)

Abl¹, Df(1)N-8, Nrt^M54 has eye phenotype

(Giniger, 1998)

Abl¹, N^l1N-ts1 has larval longitudinal connective phenotype

(Giniger, 1998)

Abl¹, N^l1N-ts1 has larval intersegmental nerve | lateral phenotype

(Giniger, 1998)

Abl¹, Df(3R)T-47/Df(3R)kar-D1 has larval longitudinal connective phenotype

(Hu et al., 1998)

Abl¹, Df(3R)T-47/Df(3R)kar-D1 has symmetrical commissure phenotype

(Hu et al., 1998)

Abl¹, arm³ has larval longitudinal connective phenotype

(Loureiro and Peifer, 1998)

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)

Abl¹/Df(3L)st-j7, Nrt^M2 has symmetrical commissure phenotype

(Gertler et al., 1993)

Abl¹/Df(3L)st-j7, Nrt^M2 has axon phenotype

(Gertler et al., 1993)

Abl¹, Fas1^TE89Da has central nervous system phenotype

(Elkins et al., 1990)

Abl¹, Fas1^TE89Da has axon phenotype

(Elkins et al., 1990)

Additional Comments

Genetic Interactions

Statement

Reference

Df(3R)su(Hw)7/+ ; Abl¹/+ third instar larvae display supernumerary mature and satellite NMJ boutons. A significant increase in the number of synaptic boutons containing microtubule loops points towards an increase in microtubule stability.

(Kim et al., 2019)

The increased presynaptic terminal length observed in class IV dendritic arborizing neurons in somatic MARCM clones expressing Dscam1^{exon17.2.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^ppk.PG in third instar larvae is completely abolished in clones that are also homozygous mutant for Abl¹.

The ectopic repulsion between between class I and class III dendritic arborizing neurons in third instar larvae observed upon expression of Dscam1^{exon17.2.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^109(2)80 cannot be rescued by combination with Abl¹/Abl⁴.

The increased presynaptic terminal length of class IV dendritic arborizing neurons in Fmr1^Δ50M/Fmr1^Δ50M MARCM somatic clones in third instar larvae is completely suppressed by combination with Abl¹ in heterozygous state.

(Sterne et al., 2015)

Abl¹/+ partially rescues the ISNb defasiculation defects seen in homozygous EndoGI^cwk embryos.

(O'Keefe et al., 2011)

A Abl¹ heterozygous background dominantly enhances the commissural defect seen in tutl^ex383 mutant embryos. tutl^ex383; Abl¹ double homozygous embryos exhibit commissural axon defects, with an extreme reduction in commissure formation and fragmented longitudinal connectives.

(Al-Anzi and Wyman, 2009)

The frequency of the midline crossing defect seen in Fas-expressing axons in Abl¹/Abl⁴ embryos is suppressed from 37% to 18% by Abi^P2/+.

The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl¹/Abl⁴ larvae is not suppressed by ena^GC5/+.

The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl¹/Abl⁴ larvae is significantly suppressed by Abi^KO/+. This suppression further increased if the flies are also carrying ena^GC5/+.

The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl¹/Abl⁴ larvae is not suppressed by Hem^C3-20/+.

The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl¹/Abl⁴ larvae is suppressed by SCAR^Δ37/+.

(Lin et al., 2009)

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

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

(Xiong et al., 2009)

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)

Khc¹⁶/+ ; Abl¹/+ double heterozygous larvae show posterior paralysis or "tail-flipping" and show an increase in the size and abundance of axonal swellings.

Khc¹⁶/ena²¹⁰ ; Abl¹/+ triple heterozygous larvae do not show a tail-flipping phenotype and there is a marked reduction in axonal swellings compared to Khc¹⁶/+ ; Abl¹/+ double heterozygous larvae.

(Martin et al., 2005)

Abl¹ Ama^M109/Df(3R)MAP11 embryos develop normal cuticles. Abl¹ Ama^M109/Abl⁴ animals do not survive to the pupal stage. Ama^M109/+ 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 Ama^R1/Abl⁴ pupae are observed, while 67% of the expected number of Abl¹ Ama^R1/Abl⁴ adults are observed. 4% of segments have commissure defects in the central nervous system of Abl¹ Ama^R1/Abl⁴ embryos. 23% of segments have commissure defects in the central nervous system of Abl¹ Ama^R1/Abl⁴ Df(3R)ama embryos. 86% of segments have commissure defects in the central nervous system of Abl¹ Ama^M109/Abl⁴ Df(3R)ama embryos. 31% of segments have commissure defects in the central nervous system of Abl¹ Nrt^M54/Abl⁴ embryos. 36% of segments have commissure defects in the central nervous system of Abl¹ Nrt^M100/Abl⁴ embryos. 63% of segments have commissure defects in the central nervous system of Abl¹ Nrt^M54/Nrt^M2 Df(3L)st-j7 embryos.

(Liebl et al., 2003)

The midline crossing errors seen in the central nervous system of Abl¹/Abl¹ embryos are suppressed by Lar^13.2/Lar^13.2.

(Wills et al., 2002)

Heterozygosity for shg² results in lethality in Abl¹/+ embryos derived from homozygous Abl¹ female germline clones. Heterozygosity for shg^R69 results in lethality in Abl¹/+ embryos derived from homozygous Abl¹ female germline clones. Heterozygosity for scb² does not result in lethality in Abl¹/+ embryos derived from homozygous Abl¹ female germline clones.

(Grevengoed et al., 2001)

Dominantly suppresses the "bypass" phenotype of ISNb axons in Lar^bypass/Lar^bypass, Lar^bypass/Lar^5.5, Lar^bypass/Lar^13.2 or Lar^bypass/Lar^E55 embryos. The ISNd bypass phenotype of Lar^bypass/Lar^E55 embryos is also suppressed by Abl¹.

(Wills et al., 1999)

Viability of Abl¹/Df(3L)st-j7 flies is reduced to <1.5% 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). Heterozygotes of Df(1)N-8 or N^55e11 with Abl¹, Nrt^M54 or In(3L)std11 show defects in eye development leading to rough eyes with high penetrance.

(Giniger, 1998)

Mutants exhibit a relatively normal axon scaffold with minor defects: thin connectives and commissures. In combination with Df(3R)T-47/Df(3R)kar-D1 mutants exhibit severe axonal defects in which the longitudinals and commissures are thin or absent. Axons are disorganised and bulging.

(Hu et al., 1998)

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. arm³; Abl¹/Abl¹ embryos show disruptions in axonogenesis, including segmental gaps along the longitudinal nerves. Abl^+mTnabl significantly reduces the central nervous system defects of arm⁴; Abl¹/In(3L)std11 embryos. Abl¹/Df(3L)st-j7 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 (Ptp99A^HA64/Ptp99A^R3.

(Hamilton et al., 1995)

fax mutations dominantly enhance the mutant phenotype, shift the lethal phase to a prepupal stage. This phenotype can be moderately rescued by Abl^+mTnabl-lys and completely rescued by Abl^+mTnabl.

(Hill et al., 1995)

Abl¹/Df(3L)st-j7 Nrt^M2 double mutant causes absence of most intersegmental longitudinal axon bundles and most commissural axon bundles. The loss of pros has an additive effect on the mutant phenotype. Loss of Abl function does not detectably alter pros mutant phenotype.

(Gertler et al., 1993)

Abl¹, 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

Heterozygosity for Abl¹suppresses the Scer\GAL4^P2.4.Pdf>Hsap\APP^{Scer\UAS.T:Hsap\MYC}-induced increase in axonal arborization of the sLNv.

(Leyssen et al., 2005)

Abl¹/Df(3L)st-j7 flies carrying Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} or Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS} expressed under the control of Scer\GAL4³¹ are variably fertile. Abl¹/Df(3L)st-j7 flies carrying Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} or Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS} expressed under the control of Scer\GAL4³¹ have rough eyes. The lethality of Abl¹/Nrt^M2 Df(3L)st-j7 is partially rescued by Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} or Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS} expressed under the control of Scer\GAL4³¹.

(Fogerty et al., 1999)

Complementation and Rescue Data

Rescued by

Abl¹ is rescued by Abl^+mTnabl

(Wills et al., 2002)

Abl¹ is rescued by Scer\GAL4^elav-C155/Abl^UAS.cFa

(Wills et al., 2002)

Abl¹ is rescued by Abl^+mTnabl

(Hill et al., 1995)

Abl¹/Df(3L)st-j7 is rescued by Abl^+mTnabl-ala

(Henkemeyer et al., 1990)

Abl¹/Df(3L)st-j7 is rescued by Abl^+mTnabl-ts

(Henkemeyer et al., 1990)

Abl¹ is rescued by Abl^+mTnabl

(Gertler et al., 1989)

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)

Abl¹/Df(3L)st-j7 is partially rescued by Scer\GAL4³¹/Abl^UAS.cFa

(Fogerty et al., 1999)

Abl¹/Df(3L)st-j7 is partially rescued by Scer\GAL4³¹/Abl^K417N.UAS

(Fogerty et al., 1999)

Abl¹ is partially rescued by Abl^+mTnabl

(Wills et al., 1999)

In(3L)std11/Abl¹ is partially rescued by Abl^+mTnabl

(Loureiro and Peifer, 1998)

Abl¹ is partially rescued by Abl^+mTnabl-lys

(Hill et al., 1995)

Abl¹/Df(3L)st-j7 is partially rescued by Abl^+mTnabl-lys

(Henkemeyer et al., 1990)

Not rescued by

Abl¹ is not rescued by Abl^+mTnabl-lys

(Wills et al., 2002)

Abl¹ is not rescued by Abl^+mTnabl-lys

(Wills et al., 1999)

Comments

Abl¹/Df(3L)st-j7 flies carrying Abl^Scer\UAS.cFa expressed under the control of Scer\GAL4³¹ have rough eyes. The lethality of Abl¹/Nrt^M2 Df(3L)st-j7 is partially rescued by Abl^Scer\UAS.cFa or Abl^{K417N.Scer\UAS} expressed under the control of Scer\GAL4³¹.

(Fogerty et al., 1999)

The phenotype seen in ISNb growth cones, is not rescued by Abl^+mTnabl-lys but is partially rescued by Abl^+mTnabl.

(Wills et al., 1999)

Images (0)

Mutant

Wild-type

Stocks (5)

Bloomington

90305

Abl¹ Ama^R1/TM6B, Tb¹

8566

P{UAS-Abl.K417N}2; Abl¹ e^*/TM6B, Tb¹

9568

w^*; Abl¹ P{FRT(w^hs)}2A/TM6B, Tb⁺

3554

Abl¹ kar¹ red¹ e¹/TM6B, Tb¹

Kyoto

107092

Abl¹ kar¹ red¹ e¹/TM6B, Tb¹

Notes on Origin

Discoverer

Comments

Protein product does not specifically localize in the axon bundles of the CNS.

(Henkemeyer et al., 1990)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

Abl1

(Zhu and Bhat, 2011)

Abl¹

(Kim et al., 2024, Marquilly et al., 2021, Bernardoni et al., 2019, Kim et al., 2019, Yoon et al., 2017, Becker et al., 2016, O'Donnell and Bashaw, 2013, Lin et al., 2009, Martin et al., 2005, Smith and Liebl, 2005)

abl-1

(Gertler et al., 1989)

abl¹

(Sun et al., 2024, Sterne et al., 2015, O'Keefe et al., 2011, Al-Anzi and Wyman, 2009, Xiong et al., 2009, Andrews et al., 2008, Crowner et al., 2003, Hsouna et al., 2003, Grevengoed et al., 2001, Bashaw et al., 2000, Fogerty et al., 1999, Wills et al., 1999, Wills et al., 1999, Giniger, 1998, Hu et al., 1998, Le and Simon, 1998, Loureiro and Peifer, 1998, Gertler et al., 1993)

Name Synonyms

Secondary FlyBase IDs

References (43)

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