Allele Dmel\Abl^Scer\UAS.cFa

General Information
Symbol	Dmel\Abl^Scer\UAS.cFa	Species	D. melanogaster
Name	Saccharomyces cerevisiae UAS construct a of Fogerty	FlyBase ID	FBal0095895
Feature type	allele	Created / Updated	2006-08-20/2006-08-20
Associated gene	Dmel\Abl

Allele class
Mutagen	in vitro construct \| regulatory fusion
Nature of the Allele
Allele class
Mutagen	in vitro construct \| regulatory fusion (Fogerty et al., 1999)
Mapped Features and Mutations
Type Symbol & 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 Construct: Abl is expressed under the control of Scer\UAS regulatory sequences. (Fogerty et al., 1999)
Assay mode	In transgenic Drosophila (intraspecific) (Wills et al., 1999, Fogerty et al., 1999)
Carried in construct	P{UAS-Abl.F} (Maurel-Zaffran et al., 2001, Leyssen et al., 2005, Baum and Perrimon, 2001, Wills et al., 2002, Lee et al., 2004, Bashaw et al., 2000, Wills et al., 1999, Fogerty et al., 1999, Crowner et al., 2003)
Cytology
Phenotypic Data
Phenotypic Class
	viable, with Scer\GAL4^hs.2sev (Fogerty et al., 1999) visible, with Scer\GAL4^hs.2sev (Fogerty et al., 1999) visible, with Scer\GAL4^GMR.PF (Wills et al., 2002) fertile, with Scer\GAL4^hs.2sev (Fogerty et al., 1999) neuroanatomy defective, with Scer\GAL4^elav.PLu (Lee et al., 2004) neuroanatomy defective, with Scer\GAL4^elav-C155 (Wills et al., 2002) neuroanatomy defective, with Scer\GAL4^P2.4.Pdf (Leyssen et al., 2005)
Phenotype Manifest In
	interommatidial bristle, with Scer\GAL4^hs.2sev (Fogerty et al., 1999) eye, with Scer\GAL4^hs.2sev (Fogerty et al., 1999) ommatidium, with Scer\GAL4^hs.2sev (Fogerty et al., 1999) embryonic neuron, with Scer\GAL4^elav.PLu (Lee et al., 2004) anterior fascicle, with Scer\GAL4^elav.PLu (Lee et al., 2004, Wills et al., 1999) longitudinal connective, with Scer\GAL4^elav.PLu (Bashaw et al., 2000) anterior fascicle, with Scer\GAL4^elav-C155 (Wills et al., 2002) ommatidium, with Scer\GAL4^GMR.PF (Wills et al., 2002) ventral adult lateral neuron & axon, with Scer\GAL4^P2.4.Pdf (Leyssen et al., 2005) follicle cell, with Scer\GAL4^hs.PB (Baum and Perrimon, 2001) longitudinal connective, with Scer\GAL4^sca-537.4 (Bashaw et al., 2000) anterior fascicle, with Scer\GAL4^unspecified (Crowner et al., 2003) anterior fascicle, with Scer\GAL4¹⁴⁰⁷ (Wills et al., 1999)
Detailed Description
	Statement Reference Embryos expressing Abl^Scer\UAS.cFa under the control of Scer\GAL4³¹ have no visible defects in the central nervous system. Flies expressing Abl^Scer\UAS.cFa under the control of Scer\GAL4^hs.2sev are viable and fertile and have a mild rough eye phenotype; ommatidia are often fused and mechanosensory bristles are occasionally misplaced. Ommatidia are irregular in shape and size and show an altered trapezoid orientation of photoreceptor cells. The arrangement of the ommatidia is disrupted. Most, but not all, ommatidia contain the correct number of photoreceptor cells. (Fogerty et al., 1999) ISNb axons often show a bypass phenotype in embryos expressing Abl^Scer\UAS.cFa under the control of Scer\GAL4¹⁴⁰⁷ or Scer\GAL4^elav.PLu. (Wills et al., 1999) When Abl^Scer\UAS.cFa is expressed under the control if Scer\GAL4^elav.PLu or Scer\GAL4^sca-537.4, the bundles of longitudinal connectives of the medial pathway ectopically crosses the midline, in a dose dependant manner. (Bashaw et al., 2000) Expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^hs.PB results in multilayering of the follicle epithelium. Expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^T155 has little effect on follicle cells. (Baum and Perrimon, 2001) Flies expressing Abl^Scer\UAS.cFa under the control of Scer\GAL4^GMR.PF have a mild rough eye phenotype. Expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^elav-C155 results in a low level of guidance errors in the ISNb. (Wills et al., 2002) Abl^Scer\UAS.cFa animals exhibit a ISNb bypass phenotype. (Crowner et al., 2003) Embryos expressing Abl^Scer\UAS.cFa under the control of Scer\GAL4^elav.PLu show axons ectopically crossing the midline. In addition, ISNb axons in these embryos show an " ISNb bypass" phenotype, often failing to enter their ventral target domain (muscles 7/6, 13 and 12). Once they have passed their targets, the misguided ISNb axons often make contacts with muscle 12 ("reach-back" phenotype). (Lee et al., 2004) Overexpression of Abl^Scer\UAS.cFa, under the control of Scer\GAL4^P2.4.Pdf, induces a small increase in axonal outgrowth of the sLNv. (Leyssen et al., 2005)
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Abl^Scer\UAS.cFa, Scer\GAL4^elav-C155 has neuroanatomy defective phenotype, enhanceable by robo^{ΔCC3.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^elav.PLu has neuroanatomy defective phenotype, enhanceable by chb^EP3403 (Lee et al., 2004) Abl^Scer\UAS.cFa, Scer\GAL4^elav-C155 has neuroanatomy defective phenotype, enhanceable by robo^Scer\UAS.cKa (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has visible phenotype, enhanceable by lea^Scer\UAS.cSa (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has visible phenotype, enhanceable by robo3^Scer\UAS.cSa (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has visible phenotype, enhanceable by robo^{ΔCC2.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has visible phenotype, enhanceable by robo^{ΔCC3.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has visible phenotype, enhanceable by robo^Scer\UAS.cKa (Wills et al., 2002)
Suppressed by
Statement Reference Abl^Scer\UAS.cFa, Scer\GAL4^elav.PLu has neuroanatomy defective phenotype, suppressible \| partially by chb⁴/chb⁴ (Lee et al., 2004)
NOT suppressed by
Statement Reference Abl^Scer\UAS.cFa, Scer\GAL4^P2.4.Pdf has neuroanatomy defective phenotype, non-suppressible by bsk^DN.Scer\UAS (Leyssen et al., 2005)
Enhancer of
Statement Reference Abl^Scer\UAS.cFa is an enhancer of neuroanatomy defective phenotype of Scer\GAL4^elav-C155, robo^{ΔCC3.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa is an enhancer of neuroanatomy defective phenotype of Scer\GAL4^elav.PLu, chb^EP3403 (Lee et al., 2004) Abl^Scer\UAS.cFa is an enhancer of neuroanatomy defective phenotype of Scer\GAL4^elav-C155, robo^Scer\UAS.cKa (Wills et al., 2002)
Suppressor of
Statement Reference Scer\GAL4³¹/Abl^Scer\UAS.cFa is a suppressor \| partially of lethal phenotype of Abl¹/Df(3L)st-j7, Nrt^M2 (Fogerty et al., 1999)
Phenotype Manifest In
Enhanced by
Statement Reference Abl^Scer\UAS.cFa, Scer\GAL4^elav-C155 has anterior fascicle phenotype, enhanceable by robo^{ΔCC3.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^elav.PLu has anterior fascicle phenotype, enhanceable by chb^EP3403 (Lee et al., 2004) Abl^Scer\UAS.cFa, Scer\GAL4^elav.PLu has embryonic neuron phenotype, enhanceable by chb^EP3403 (Lee et al., 2004) Abl^Scer\UAS.cFa, Scer\GAL4^elav-C155 has anterior fascicle phenotype, enhanceable by robo^Scer\UAS.cKa (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has ommatidium phenotype, enhanceable by lea^Scer\UAS.cSa (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has ommatidium phenotype, enhanceable by robo3^Scer\UAS.cSa (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has ommatidium phenotype, enhanceable by robo^{ΔCC2.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has ommatidium phenotype, enhanceable by robo^{ΔCC3.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa, Scer\GAL4^GMR.PF has ommatidium phenotype, enhanceable by robo^Scer\UAS.cKa (Wills et al., 2002)
Suppressed by
Statement Reference Abl^Scer\UAS.cFa, Lar^Scer\UAS.cKa has anterior fascicle phenotype, suppressible \| partially by Scer\GAL4^elav.PLu (Wills et al., 1999) Abl^Scer\UAS.cFa, Scer\GAL4^elav.PLu has anterior fascicle phenotype, suppressible \| partially by chb⁴/chb⁴ (Lee et al., 2004) Abl^Scer\UAS.cFa, Scer\GAL4^unspecified has anterior fascicle phenotype, suppressible by N^Scer\UAS.cBa (Crowner et al., 2003)
NOT suppressed by
Statement Reference Abl^Scer\UAS.cFa, Scer\GAL4^P2.4.Pdf has ventral adult lateral neuron & axon phenotype, non-suppressible by bsk^DN.Scer\UAS (Leyssen et al., 2005)
Enhancer of
Statement Reference Abl^Scer\UAS.cFa is an enhancer of anterior fascicle phenotype of Scer\GAL4^elav-C155, robo^{ΔCC3.Scer\UAS} (Wills et al., 2002) Abl^Scer\UAS.cFa is an enhancer of embryonic neuron phenotype of Scer\GAL4^elav.PLu, chb^EP3403 (Lee et al., 2004) Abl^Scer\UAS.cFa is an enhancer of anterior fascicle phenotype of Scer\GAL4^elav-C155, robo^Scer\UAS.cKa (Wills et al., 2002) Scer\GAL4^unspecified/Abl^Scer\UAS.cFa is an enhancer of anterior fascicle \| conditional - heat sensitive phenotype of N^l1N-ts1 (Crowner et al., 2003)
Additional Comments
Genetic Interactions
Statement Reference The ISNb bypass phenotype of embryos expressing Abl^Scer\UAS.cFa under the control of Scer\GAL4^elav.PLu is partially suppressed by Lar^Scer\UAS.cKa. (Wills et al., 1999) Expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^T155 in capt¹⁰ mosaic egg chambers alters both the level and distribution of actin filaments in the capt¹⁰ mutant cells. In a few egg chambers, the epithelial morphology is profoundly disrupted. (Baum and Perrimon, 2001) Co-expression of robo^Scer\UAS.cKa, robo^{ΔCC2.Scer\UAS} or robo^{ΔCC3.Scer\UAS} enhances the rough eye phenotype caused by expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^GMR.PF. Co-expression of lea^Scer\UAS.cSa enhances the rough eye phenotype caused by expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^GMR.PF. Co-expression of robo3^Scer\UAS.cSa enhances the rough eye phenotype caused by expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^GMR.PF. Co-expression of Abl^Scer\UAS.cFa and robo^Scer\UAS.cKa under the control of Scer\GAL4^elav-C155 dramatically increases the frequency of the ISNb bypass phenotype seen when each is expressed alone under the control of Scer\GAL4^elav-C155. Co-expression of Abl^Scer\UAS.cFa and robo^{ΔCC3.Scer\UAS} under the control of Scer\GAL4^elav-C155 dramatically increases the frequency of the ISNb bypass phenotype seen when each is expressed alone under the control of Scer\GAL4^elav-C155. (Wills et al., 2002) Co-expression of chb^EP3403 and Abl^Scer\UAS.cFa under the control of Scer\GAL4^elav.PLu in embryos results in an increased frequency of axons ectopically crossing the midline compared to embryos expressing either chb^EP3403 or Abl^Scer\UAS.cFa singly under the control of Scer\GAL4^elav.PLu. Co-expression of chb^EP3403 enhances the expressivity of the ISNb axons phenotype caused by expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^elav.PLu, although the effect is subtle. The ISNb bypass phenotype caused by expression of Abl^Scer\UAS.cFa under the control of Scer\GAL4^elav.PLu is reduced by chb⁴/chb⁴. (Lee et al., 2004) Expression of bsk^DN.Scer\UAS, has no effect on Scer\GAL4^P2.4.Pdf>Abl^Scer\UAS.cFa-induced axonal arborization of the sLNv. (Leyssen et al., 2005)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescues	Abl^Scer\UAS.cFa/Scer\GAL4¹⁴⁰⁷ rescues Abl^unspecified (Wills et al., 2002) Scer\GAL4^elav-C155/Abl^Scer\UAS.cFa rescues Abl¹ (Wills et al., 2002)
Partially rescues	Scer\GAL4³¹/Abl^Scer\UAS.cFa partially rescues Abl¹/Df(3L)st-j7 (Fogerty et al., 1999)
Comments
Stocks ( 2 )
Bloomington	8596 w^; wg^Sp-1/CyO; P{UAS-Abl.F}3 8567 w^; P{UAS-Abl.F}2/CyO; TM2/TM6B, Tb¹
Notes on Origin
Discoverer

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	Abl^Scer\UAS.cFa Abl^UAS.cFa
Name Synonym	Saccharomyces cerevisiae UAS construct a of Fogerty (Fogerty et al., 1999)
Secondary FlyBase IDs

References ( 9 )
Research paper	Leyssen et al., 2005, EMBO J. 24(16): 2944--2955 Amyloid precursor protein promotes post-developmental neurite arborization in the Drosophila brain. [FBrf0187512] Lee et al., 2004, Neuron 42(6): 913--926 The microtubule plus end tracking protein Orbit/MAST/CLASP acts downstream of the tyrosine kinase Abl in mediating axon guidance. [FBrf0179303] Crowner et al., 2003, Curr. Biol. 13(11): 967--972 Notch Steers Drosophila ISNb Motor Axons by Regulating the Abl Signaling Pathway. [FBrf0159717] Wills et al., 2002, Neuron 36(4): 611--622 A Drosophila homolog of cyclase-associated proteins collaborates with the abl tyrosine kinase to control midline axon pathfinding. [FBrf0152273] Baum and Perrimon, 2001, Nature Cell Biol. 3(10): 883--890 Spatial control of the actin cytoskeleton in Drosophila epithelial cells. [FBrf0139770] Maurel-Zaffran et al., 2001, Neuron 32(2): 225--235 Cell-autonomous and -nonautonomous functions of LAR in R7 photoreceptor axon targeting. [FBrf0139775] Bashaw et al., 2000, Cell 101(7): 703--715 Repulsive axon guidance: abelson and enabled play opposing roles downstream of the roundabout receptor. [FBrf0128391] Fogerty et al., 1999, Oncogene 18(1): 219--232 Dominant effects of the bcr-abl oncogene on Drosophila morphogenesis. [FBrf0106495] Wills et al., 1999, Neuron 22(2): 301--312 The tyrosine kinase Abl and its substrate enabled collaborate with the receptor phosphatase Dlar to control motor axon guidance. [FBrf0108074]

Allele Dmel\AblScer\UAS.cFa

Allele Dmel\Abl^Scer\UAS.cFa