Allele Dmel\Abl¹

General Information
Symbol	Dmel\Abl¹	Species	D. melanogaster
Name		FlyBase ID	FBal0028708
Feature type	allele	Associated gene	Dmel\Abl

Allele class	hypomorphic allele - genetic evidence
Mutagen
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	hypomorphic allele - genetic evidence (Saha and Sinha, 1996, Leyssen et al., 2005)
Mutagen
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: Q686@. (Smith and Liebl, 2005) Nucleotide substitution: C?T. (Smith and Liebl, 2005) Truncated Abl protein. (Henkemeyer et al., 1990)
Cytology
Phenotypic Data
Phenotypic Class
	lethal (with Abl⁴) (Liebl et al., 2003, Lin et al., 2009) lethal (with Df(3L)st-j7) (Fogerty et al., 1999) lethal \| embryonic stage \| recessive \| rescuable maternal effect (Grevengoed et al., 2001) lethal \| pupal stage (with Abl⁴) (Liebl et al., 2000) lethal \| pupal stage \| recessive (Hill et al., 1995, Gertler et al., 1989) neuroanatomy defective (Wills et al., 2002, Al-Anzi and Wyman, 2009) neuroanatomy defective (with Abl⁴) (Forsthoefel et al., 2005, Liebl et al., 2003) neuroanatomy defective \| embryonic stage (with Abl⁴) (Lin et al., 2009) neuroanatomy defective \| larval stage (with Abl⁴) (Lin et al., 2009) neuroanatomy defective \| larval stage (with Df(3L)st-j7) (Lin et al., 2009) neurophysiology defective \| larval stage (with Abl⁴) (Lin et al., 2009) viable \| reduced (with Df(3L)st-j7) (Giniger, 1998)
Phenotype Manifest In
	commissure (Hu et al., 1998) commissure (with Abl⁴) (Forsthoefel et al., 2005) embryonic/larval neuromuscular junction (with Abl⁴) (Lin et al., 2009) intersegmental nerve (Wills et al., 1999) intersegmental nerve (with Abl⁴) (Kraut et al., 2001) longitudinal connective (Hu et al., 1998, Wills et al., 2002, Wills et al., 1999) longitudinal connective (with Abl⁴) (Liebl et al., 2000, Lin et al., 2009) midline crossing tract (Al-Anzi and Wyman, 2009) NMJ bouton \| supernumerary (with Abl⁴) (Lin et al., 2009) NMJ bouton \| supernumerary (with Df(3L)st-j7) (Lin et al., 2009) presumptive embryonic/larval central nervous system (Wills et al., 2002) synaptic vesicle & NMJ bouton (with Abl⁴) (Lin et al., 2009) ventral nerve cord commissure (with Abl⁴) (Liebl et al., 2003)
Detailed Description
	Statement Reference Abl[1] mutants exhibit minor midline crossing defects. (Al-Anzi and Wyman, 2009) 37% of Abl[1]/Abl[4] 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 Abl[1]/Abl[4] and Abl[1]/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 Abl[1]/Abl[4] 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 Abl[1]/Abl[4] 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) 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) 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference 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) 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 Nrt^M221/Nrt[+] (Liebl et al., 2000) Abl⁴/Abl¹ has lethal \| prepupal stage phenotype, enhanceable by trio[+]/trio^M89 (Liebl et al., 2000) Abl⁴/Abl¹ has lethal phenotype, enhanceable by Ama^M109/Ama[+] (Liebl et al., 2003) Abl⁴/Abl¹ has neuroanatomy defective phenotype, enhanceable by Ama^M109/Ama[+] (Liebl et al., 2003) Abl⁴/Abl¹ has neuroanatomy defective phenotype, enhanceable by Df(3R)ama/Ama^M109 (Liebl et al., 2003) Abl⁴/Abl¹ has neuroanatomy defective phenotype, enhanceable by Df(3R)ama/Ama^R1 (Liebl et al., 2003)
NOT Enhanced by
Statement Reference Abl⁴/Abl¹ has neuroanatomy defective phenotype, non-enhanceable by Ama^R1/Ama[+] (Liebl et al., 2003) Abl⁴/Abl¹ has neuroanatomy defective phenotype, non-enhanceable by Df(3R)ama/+ (Liebl et al., 2003)
Suppressed by
Statement Reference Abl¹/Abl[+], Khc¹⁶ has neuroanatomy defective \| dominant \| larval stage phenotype, suppressible by ena[+]/ena²¹⁰ (Martin et al., 2005) Abl¹/Abl[+], Khc¹⁶ has paralytic \| dominant \| larval stage phenotype, suppressible by ena[+]/ena²¹⁰ (Martin et al., 2005) Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible \| partially by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\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^{P210.Scer\UAS} (Fogerty et al., 1999) Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible \| partially by Scer\GAL4³¹/Abl¹/Abl^{K417N.Scer\UAS}/Df(3L)st-j7 (Fogerty et al., 1999, Fogerty et al., 1999) Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype, suppressible \| partially by Scer\GAL4³¹/Abl^Scer\UAS.cFa (Fogerty et al., 1999) Abl¹/Df(3L)st-j7 has lethal phenotype, suppressible by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS} (Fogerty et al., 1999) Abl¹/Df(3L)st-j7 has lethal phenotype, suppressible by Scer\GAL4³¹/Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} (Fogerty et al., 1999) Abl¹ has neuroanatomy defective phenotype, suppressible by Lar^13.2/Lar^13.2 (Wills et al., 2002) Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has neuroanatomy defective phenotype, suppressible \| partially by ena[+]/ena^GC10 (Forsthoefel et al., 2005) Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has neuroanatomy defective phenotype, suppressible \| partially by ena[+]/ena^GC10 (Forsthoefel et al., 2005) Abl⁴/Abl¹, fax^M7/fax[+] has lethal \| prepupal stage 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, trio[+]/trio^M89 has lethal \| prepupal stage phenotype, suppressible by ena[+]/ena^GC10 (Liebl et al., 2000) 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 lethal phenotype, suppressible by ena[+]/ena^GC10 (Liebl et al., 2000) Abl⁴/Abl¹ has neuroanatomy defective \| embryonic stage phenotype, suppressible \| partially by Abi[+]/Abi^P2 (Lin et al., 2009) Abl⁴/Abl¹ has neuroanatomy defective \| larval stage phenotype, suppressible \| partially by Abi[+]/Abi^KO (Lin et al., 2009)
NOT suppressed by
Statement Reference Abl⁴/Abl¹ has neuroanatomy defective \| larval stage phenotype, non-suppressible by ena[+]/ena^GC5 (Lin et al., 2009) Abl⁴/Abl¹ has neuroanatomy defective \| larval stage phenotype, non-suppressible by Hem[+]/Hem^C3-20 (Lin et al., 2009) Abl⁴/Abl¹ has neuroanatomy defective \| larval stage phenotype, non-suppressible by SCAR^Δ37/SCAR[+] (Lin et al., 2009)
Enhancer of
Statement Reference Abl¹/Abl[+] is an enhancer of lethal phenotype of trio^M89/trio^S036810 (Liebl et al., 2000) Abl¹/Abl[+] is an enhancer of neuroanatomy defective phenotype of Df(2R)vg135/fra⁴ (Forsthoefel et al., 2005) Abl¹/Abl[+] is an enhancer of neuroanatomy defective phenotype of fra⁴ (Forsthoefel et al., 2005) Abl⁴/Abl¹ is an enhancer of neuroanatomy defective phenotype of Df(2R)vg135/fra⁴ (Forsthoefel et al., 2005) Abl⁴/Abl¹ is an enhancer of neuroanatomy defective phenotype of fra⁴ (Forsthoefel et al., 2005)
Suppressor of
Statement Reference Abl¹/Abl[+] is a suppressor \| partially of neuroanatomy defective \| embryonic stage phenotype of EndoGI^cwk (O'Keefe et al., 2011) Abl¹/Abl[+] is a suppressor of neuroanatomy defective phenotype of Hsap\APP^{Scer\UAS.T:Hsap\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) Scer\GAL4³¹, Abl¹, Abl^{K417N.Scer\UAS}, Df(3L)st-j7 is a suppressor \| partially of lethal phenotype of Abl¹/Df(3L)st-j7, Nrt^M2 (Fogerty et al., 1999, Fogerty et al., 1999)
Other
Statement Reference Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹, Scer\GAL4³¹ has viable phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹, Scer\GAL4³¹ has visible phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has visible phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has visible phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹, Scer\GAL4³¹ has viable phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹, Scer\GAL4³¹ has visible phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has visible phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has visible phenotype (Fogerty et al., 1999) Abl¹, Df(1)N-8, Nrt^M54 has visible \| dominant phenotype (Giniger, 1998, Giniger, 1998) Abl¹, fax[-] has lethal \| recessive \| prepupal stage phenotype (Hill et al., 1995) Abl¹, N^55e11, Nrt^M54 has visible \| dominant phenotype (Giniger, 1998, Giniger, 1998, Giniger, 1998) Abl¹, shg[+]/shg² has lethal \| embryonic stage phenotype (Grevengoed et al., 2001) Abl¹, shg[+]/shg^R69 has lethal \| embryonic stage phenotype (Grevengoed et al., 2001) Abl¹, shg² has lethal \| embryonic stage phenotype (Grevengoed et al., 2001) Abl¹, shg^R69 has lethal \| embryonic stage phenotype (Grevengoed et al., 2001) Abl¹/Abl[+], Khc¹⁶ has neuroanatomy defective \| dominant \| larval stage phenotype (Martin et al., 2005) Abl¹/Abl[+], Khc¹⁶ has paralytic \| dominant \| larval stage phenotype (Martin et al., 2005) Abl¹/Df(3L)st-j7, N^l1N-ts1 has neuroanatomy defective \| embryonic stage phenotype (Giniger, 1998) Abl¹/Df(3L)st-j7, N^l1N-ts1 has partially lethal - majority die phenotype (Giniger, 1998) Abl¹/Df(3L)st-j7, Nrt^M2 has lethal phenotype (Fogerty et al., 1999) Abl¹/Df(3L)st-j7, Nrt^M54/Nrt^M2 has neuroanatomy defective phenotype (Liebl et al., 2003, Liebl et al., 2003) Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has neuroanatomy defective phenotype (Forsthoefel et al., 2005) Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has neuroanatomy defective phenotype (Forsthoefel et al., 2005) Abl⁴/Abl¹, Nrt^M54 has neuroanatomy defective phenotype (Liebl et al., 2003, Liebl et al., 2003) Abl⁴/Abl¹, Nrt^M100 has neuroanatomy defective phenotype (Liebl et al., 2003, Liebl et al., 2003)
Phenotype Manifest In
Enhanced by
Statement Reference Abl¹ has phenotype, enhanceable by fax^M7 (Hill et al., 1995) 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) Abl⁴/Abl¹ has anterior commissure phenotype, enhanceable by Df(3L)Fpa1/+ (Liebl et al., 2000) Abl⁴/Abl¹ has anterior commissure phenotype, enhanceable by trio[+]/trio^M89 (Liebl et al., 2000) Abl⁴/Abl¹ has longitudinal connective phenotype, enhanceable by Df(3L)Fpa1/+ (Liebl et al., 2000) Abl⁴/Abl¹ has longitudinal connective phenotype, enhanceable by trio[+]/trio^M89 (Liebl et al., 2000) Abl⁴/Abl¹ has posterior commissure phenotype, enhanceable by Df(3L)Fpa1/+ (Liebl et al., 2000) Abl⁴/Abl¹ has posterior commissure phenotype, enhanceable by trio[+]/trio^M89 (Liebl et al., 2000) Abl⁴/Abl¹ has ventral nerve cord commissure phenotype, enhanceable by Ama^M109/Ama[+] (Liebl et al., 2003) Abl⁴/Abl¹ has ventral nerve cord commissure phenotype, enhanceable by Df(3R)ama/Ama^M109 (Liebl et al., 2003) Abl⁴/Abl¹ has ventral nerve cord commissure phenotype, enhanceable by Df(3R)ama/Ama^R1 (Liebl et al., 2003)
NOT Enhanced by
Statement Reference Abl⁴/Abl¹ has ventral nerve cord commissure phenotype, non-enhanceable by Ama^R1/Ama[+] (Liebl et al., 2003) Abl⁴/Abl¹ has ventral nerve cord commissure phenotype, non-enhanceable by Df(3R)ama/+ (Liebl et al., 2003)
Suppressed by
Statement Reference 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) Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has commissure phenotype, suppressible \| partially by ena[+]/ena^GC10 (Forsthoefel et al., 2005) Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has commissure phenotype, suppressible \| partially by ena[+]/ena^GC10 (Forsthoefel et al., 2005) Abl⁴/Abl¹ has longitudinal connective phenotype, suppressible \| partially by Abi[+]/Abi^P2 (Lin et al., 2009) Abl⁴/Abl¹ has NMJ bouton \| supernumerary phenotype, suppressible \| partially by Abi[+]/Abi^KO (Lin et al., 2009)
NOT suppressed by
Statement Reference Abl⁴/Abl¹ has NMJ bouton \| supernumerary phenotype, non-suppressible by ena[+]/ena^GC5 (Lin et al., 2009) Abl⁴/Abl¹ has NMJ bouton \| supernumerary phenotype, non-suppressible by Hem[+]/Hem^C3-20 (Lin et al., 2009) Abl⁴/Abl¹ has NMJ bouton \| supernumerary phenotype, non-suppressible by SCAR^Δ37/SCAR[+] (Lin et al., 2009)
Enhancer of
Statement Reference Abl¹/Abl[+] is an enhancer of anterior commissure phenotype of Df(3L)Fpa1/trio^M89 (Liebl et al., 2000) Abl¹/Abl[+] is an enhancer of commissure phenotype of Df(2R)vg135/fra⁴ (Forsthoefel et al., 2005) Abl¹/Abl[+] is an enhancer of commissure phenotype of fra⁴ (Forsthoefel et al., 2005) Abl¹/Abl[+] is an enhancer of longitudinal connective phenotype of Df(3L)Fpa1/trio^M89 (Liebl et al., 2000) Abl¹/Abl[+] is an enhancer of longitudinal connective phenotype of trio^M89/trio^S036810 (Liebl et al., 2000) Abl¹/Abl[+] is an enhancer of 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 commissure phenotype of arm⁴ (Loureiro and Peifer, 1998) Abl⁴/Abl¹ is an enhancer of commissure phenotype of Df(2R)vg135/fra⁴ (Forsthoefel et al., 2005) Abl⁴/Abl¹ is an enhancer of commissure phenotype of fra⁴ (Forsthoefel et al., 2005) Abl⁴/Abl¹ is an enhancer of presumptive embryonic/larval central nervous system phenotype of arm⁴ (Loureiro and Peifer, 1998)
NOT Enhancer of
Statement Reference Abl⁴/Abl¹ is a non-enhancer of longitudinal connective phenotype of Df(2R)vg135/fra⁴ (Forsthoefel et al., 2005)
Suppressor of
Statement Reference Abl¹/Abl[+] is a suppressor \| partially of intersegmental nerve \| heat sensitive phenotype of N^l1N-ts1 (Crowner et al., 2003) Abl¹/Abl[+] is a suppressor \| partially of intersegmental nerve branch ISNb of A1-7 phenotype of EndoGI^cwk (O'Keefe et al., 2011) Abl¹/Abl[+] is a suppressor of eye phenotype of CycE^JP (Brumby et al., 2004) Abl¹/Abl[+] is a suppressor of longitudinal connective phenotype of robo⁵, sli[+]/sli¹ (Bashaw et al., 2000) Abl¹/Abl[+] is a suppressor of ventral adult lateral neuron & axon phenotype of Hsap\APP^{Scer\UAS.T:Hsap\MYC}, Scer\GAL4^P2.4.Pdf (Leyssen et al., 2005) Abl¹/Df(3L)st-j7 is a suppressor of phenotype of arm⁴ (Loureiro and Peifer, 1998) Abl¹ is a suppressor of intersegmental nerve phenotype of Lar^bypass (Wills et al., 1999) Abl¹ is a suppressor of intersegmental nerve phenotype of Lar^bypass/Lar^5.5 (Wills et al., 1999) Abl¹ is a suppressor of intersegmental nerve phenotype of Lar^bypass/Lar^13.2 (Wills et al., 1999) Abl¹ is a suppressor of intersegmental nerve phenotype of Lar^bypass/Lar^E55 (Wills et al., 1999) Abl¹ is a suppressor of phenotype of arm⁴ (Loureiro and Peifer, 1998) Nrt^M54/Abl¹ is a suppressor \| partially of intersegmental nerve \| heat sensitive phenotype of N^l1N-ts1 (Crowner et al., 2003) robo[+], Abl¹, robo⁵, Abl[+] is a suppressor of longitudinal connective phenotype of sli¹ (Bashaw et al., 2000)
Other
Statement Reference Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has eye phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has ommatidium phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has eye phenotype (Fogerty et al., 1999, Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P185.Scer\UAS}, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has ommatidium phenotype (Fogerty et al., 1999, Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has eye phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹/Df(3L)st-j7, Nrt^M2, Scer\GAL4³¹ has ommatidium phenotype (Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has eye phenotype (Fogerty et al., 1999, Fogerty et al., 1999) Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS}, Abl¹/Df(3L)st-j7, Scer\GAL4³¹ has ommatidium phenotype (Fogerty et al., 1999, Fogerty et al., 1999) Abl¹, arm³ has longitudinal connective phenotype (Loureiro and Peifer, 1998, Loureiro and Peifer, 1998) Abl¹, Df(1)N-8, Nrt^M54 has eye phenotype (Giniger, 1998, Giniger, 1998) Abl¹, Df(3R)T-47/Df(3R)kar-D1 has commissure phenotype (Hu et al., 1998) Abl¹, Df(3R)T-47/Df(3R)kar-D1 has longitudinal connective phenotype (Hu et al., 1998) Abl¹, Fas1^TE89Da has axon phenotype (Elkins et al., 1990) Abl¹, Fas1^TE89Da has central nervous system phenotype (Elkins et al., 1990) Abl¹, N^55e11, Nrt^M54 has eye phenotype (Giniger, 1998, Giniger, 1998, Giniger, 1998) Abl¹, N^l1N-ts1 has intersegmental nerve \| lateral phenotype (Giniger, 1998) Abl¹, N^l1N-ts1 has longitudinal connective phenotype (Giniger, 1998) Abl¹/Abl[+], Khc¹⁶ has axon phenotype (Martin et al., 2005) Abl¹/Df(3L)st-j7, Nrt^M2 has axon phenotype (Gertler et al., 1993, Gertler et al., 1993) Abl¹/Df(3L)st-j7, Nrt^M2 has commissure phenotype (Gertler et al., 1993, Gertler et al., 1993) Abl¹/Df(3L)st-j7, Nrt^M54/Nrt^M2 has ventral nerve cord commissure phenotype (Liebl et al., 2003, Liebl et al., 2003) Abl⁴/Abl¹, arm⁴ has commissure phenotype (Loureiro and Peifer, 1998) Abl⁴/Abl¹, arm⁴ has presumptive embryonic/larval central nervous system phenotype (Loureiro and Peifer, 1998) Abl⁴/Abl¹, Df(3L)Fpa1/trio^IMP159.4 has commissure phenotype (Forsthoefel et al., 2005) Abl⁴/Abl¹, Df(3L)Fpa1/trio^M89 has commissure phenotype (Forsthoefel et al., 2005) Abl⁴/Abl¹, Nrt^M54 has ventral nerve cord commissure phenotype (Liebl et al., 2003, Liebl et al., 2003) Abl⁴/Abl¹, Nrt^M100 has ventral nerve cord commissure phenotype (Liebl et al., 2003, Liebl et al., 2003)
Additional Comments
Genetic Interactions
Statement Reference Abl[1]/+ partially rescues the ISNb defasiculation defects seen in homozygous EndoGI[cwk] embryos. (O'Keefe et al., 2011) A Abl[1] heterozygous background dominantly enhances the commissural defect seen in tutl[ex383] mutant embryos. tutl[ex383]; Abl[1] 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 Abl[1]/Abl[4] 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 Abl[1]/Abl[4] larvae is not suppressed by ena[GC5]/+. The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl[1]/Abl[4] 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 Abl[1]/Abl[4] larvae is not suppressed by Hem[C3-20]/+. The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl[1]/Abl[4] larvae is suppressed by SCAR[Δ37]/+. (Lin 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 & Rescue Data
Rescued by	Abl¹ is rescued by Abl^+mTnabl (Wills et al., 2002, Gertler et al., 1989, Hill et al., 1995) Abl¹ is rescued by Scer\GAL4^elav-C155/Abl^Scer\UAS.cFa (Wills et al., 2002)
Partially rescued by	Abl¹/Df(3L)st-j7 is partially rescued by Scer\GAL4³¹/Abl^{K417N.Scer\UAS} (Fogerty et al., 1999) Abl¹/Df(3L)st-j7 is partially rescued by Scer\GAL4³¹/Abl^Scer\UAS.cFa (Fogerty et al., 1999) Abl¹ is partially rescued by Abl^+mTnabl (Wills et al., 1999) Abl¹ is partially rescued by Abl^+mTnabl-lys (Hill et al., 1995) In(3L)std11/Abl¹ is partially rescued by Abl^+mTnabl (Loureiro and Peifer, 1998)
Not rescued by	Abl¹ is not rescued by Abl^+mTnabl-lys (Wills et al., 1999, Wills et al., 2002)
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)
Stocks ( 4 )
Bloomington	9568 w^; Abl¹ P{FRT(w^hs)}2A/TM6B, Tb⁺ 3554 Abl¹ kar¹ red¹ e¹/TM6B, Tb¹ 8566 w^; P{UAS-Abl.K417N}2; Abl¹ e^*/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 & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	abl-1 (Gertler et al., 1989) Abl1 (Zhu and Bhat, 2011) abl¹ (Grevengoed et al., 2001, Crowner et al., 2003, Bashaw et al., 2000, Wills et al., 1999, Wills et al., 1999, Fogerty et al., 1999, Le and Simon, 1998, Loureiro and Peifer, 1998, Giniger, 1998, Hu et al., 1998, Gertler et al., 1993, O'Keefe et al., 2011, Andrews et al., 2008, Al-Anzi and Wyman, 2009) Abl¹ (Martin et al., 2005, Lin et al., 2009, Smith and Liebl, 2005)
Name Synonym
Secondary FlyBase IDs

References ( 32 )

Generate a list of	All references relating to this allele ( 32 )

List References by type	Research paper ( 31 ) Abstract ( 1 )
Recent research papers ( 2 )
	O'Keefe et al., 2011, Mech. Dev. 128(1-2): 59--70 EndoGI modulates Notch signaling and axon guidance in Drosophila. [FBrf0213012] Zhu and Bhat, 2011, Dev. Biol. 357(2): 283--294 The Hem protein mediates neuronal migration by inhibiting WAVE degradation and functions opposite of Abelson tyrosine kinase. [FBrf0214765] Show all research papers ...

Allele Dmel\Abl1

Allele Dmel\Abl¹