A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\AblScer\UAS.cFa

General Information
SymbolDmel\AblScer\UAS.cFaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct a of FogertyFlyBase IDFBal0095895
Feature typealleleAssociated geneDmel\Abl
Allele class
Mutagenin vitro construct - regulatory fusion
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Description
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FB2013_03
FB2013_02
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Allele class
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Mutations Mapped to the Genome
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Associated Sequence Data
DDBJ /
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Protein sequence
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Construct: Abl is expressed under the control of Scer\UAS regulatory sequences.
Carried in construct
Cytology
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ventral adult lateral neuron & axon, with Scer\GAL4P2.4.Pdf
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Statement
Reference
Expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[GMR.PF] does not affect eye development at 25[o]C, but when the temperature is increased to 29.5[o]C, increasing the expression level of Abl[Scer\UAS.cFa], retinal development is disrupted. The retina in these mutants increases in size (as evidenced by the outward bulging of the retina). Expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[1407] results in ISNb axons occasionally failing to innervate their target muscles and instead following ISN, leading to a 'bypass' phenotype.
Expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[GMR.PU] results in a rough eye phenotype.
Overexpression of AblScer\UAS.cFa, under the control of Scer\GAL4P2.4.Pdf, induces a small increase in axonal outgrowth of the sLNv.
Embryos expressing AblScer\UAS.cFa under the control of Scer\GAL4elav.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).
AblScer\UAS.cFa animals exhibit a ISNb bypass phenotype.
Flies expressing AblScer\UAS.cFa under the control of Scer\GAL4GMR.PF have a mild rough eye phenotype. Expression of AblScer\UAS.cFa under the control of Scer\GAL4elav-C155 results in a low level of guidance errors in the ISNb.
Expression of AblScer\UAS.cFa under the control of Scer\GAL4hs.PB results in multilayering of the follicle epithelium. Expression of AblScer\UAS.cFa under the control of Scer\GAL4T155 has little effect on follicle cells.
When AblScer\UAS.cFa is expressed under the control if Scer\GAL4elav.PLu or Scer\GAL4sca-537.4, the bundles of longitudinal connectives of the medial pathway ectopically crosses the midline, in a dose dependant manner.
Embryos expressing AblScer\UAS.cFa under the control of Scer\GAL431 have no visible defects in the central nervous system. Flies expressing AblScer\UAS.cFa under the control of Scer\GAL4hs.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.
ISNb axons often show a bypass phenotype in embryos expressing AblScer\UAS.cFa under the control of Scer\GAL41407 or Scer\GAL4elav.PLu.
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Reference
AblScer\UAS.cFa, Scer\GAL4P2.4.Pdf has ventral adult lateral neuron & axon phenotype, non-suppressible by bskDN.Scer\UAS
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Statement
Reference
AblScer\UAS.cFa, Scer\GAL4GMR.PF is a suppressor of retina | heat sensitive phenotype of Scer\GAL4GMR.PF, mspsd03376
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Statement
Reference
Co-expression of msps[d03376] under the control of Scer\GAL4[1407] suppressed the ISNb bypass phenotype seen upon expression of Abl[Scer\UAS.cFa]. Co-expression of msps[P] with Abl[Scer\UAS.cFa] under the control of Scer\GAL4[GMR.PF] partially suppresses the Abl[Scer\UAS.cFa] retinal size increase. Co-expression of msps[d03376] and Abl[Scer\UAS.cFa] under the control of Scer\GAL4[GMR.PF] neutralizes the opposing effects on retinal size, resulting in an eye that is nearly normal in size, albeit still abnormal in lens pattern. Co-expression of Abl[Scer\UAS.cFa] enhances the chb[Scer\UAS.T:Avic\GFP] mutant eye phenotype when both transgenes are expressed under the control of Scer\GAL4[GMR.PF].
The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab) is decreased by expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[elav.PU] to 29%.
The rough eye phenotype caused by expression of Hem[Scer\UAS.T:Myr-Src64B] under the control of Scer\GAL4[GMR.PU] is enhanced by co-expression of Abl[Scer\UAS.cFa]. The rough eye phenotype caused by expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[GMR.PU] is enhanced by co-expression of Ptp61F[dsRNA.Scer\UAS.WIZ] and is suppressed co-expression of Ptp61F[m.Scer\UAS].
Expression of bskDN.Scer\UAS, has no effect on Scer\GAL4P2.4.Pdf>AblScer\UAS.cFa-induced axonal arborization of the sLNv.
Co-expression of chbEP3403 and AblScer\UAS.cFa under the control of Scer\GAL4elav.PLu in embryos results in an increased frequency of axons ectopically crossing the midline compared to embryos expressing either chbEP3403 or AblScer\UAS.cFa singly under the control of Scer\GAL4elav.PLu. Co-expression of chbEP3403 enhances the expressivity of the ISNb axons phenotype caused by expression of AblScer\UAS.cFa under the control of Scer\GAL4elav.PLu, although the effect is subtle. The ISNb bypass phenotype caused by expression of AblScer\UAS.cFa under the control of Scer\GAL4elav.PLu is reduced by chb4/chb4.
Co-expression of roboScer\UAS.cKa, roboΔCC2.Scer\UAS or roboΔCC3.Scer\UAS enhances the rough eye phenotype caused by expression of AblScer\UAS.cFa under the control of Scer\GAL4GMR.PF. Co-expression of leaScer\UAS.cSa enhances the rough eye phenotype caused by expression of AblScer\UAS.cFa under the control of Scer\GAL4GMR.PF. Co-expression of robo3Scer\UAS.cSa enhances the rough eye phenotype caused by expression of AblScer\UAS.cFa under the control of Scer\GAL4GMR.PF. Co-expression of AblScer\UAS.cFa and roboScer\UAS.cKa under the control of Scer\GAL4elav-C155 dramatically increases the frequency of the ISNb bypass phenotype seen when each is expressed alone under the control of Scer\GAL4elav-C155. Co-expression of AblScer\UAS.cFa and roboΔCC3.Scer\UAS under the control of Scer\GAL4elav-C155 dramatically increases the frequency of the ISNb bypass phenotype seen when each is expressed alone under the control of Scer\GAL4elav-C155.
Expression of AblScer\UAS.cFa under the control of Scer\GAL4T155 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.
The ISNb bypass phenotype of embryos expressing AblScer\UAS.cFa under the control of Scer\GAL4elav.PLu is partially suppressed by LarScer\UAS.cKa.
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Comments
The increased bouton number per muscle area that is seen at the larval neuromuscular junction of Abl[4]/Df(3L)st-j7 animals is rescued by expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[elav-C155] but is not rescued by expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[how-24B].
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Bloomington
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Reported As
Symbol Synonym
AblScer\UAS.cFa
 
AblUAS.cFa
 
Name Synonym
Saccharomyces cerevisiae UAS construct a of Fogerty
Secondary FlyBase IDs
hide References ( 14 )
Research paper
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]
Lowery et al., 2010, Genetics 185(4): 1311--1325
Parallel Genetic and Proteomic Screens Identify Msps as a CLASP-Abl Pathway Interactor in Drosophila. [FBrf0211499]
Song et al., 2010, Development 137(21): 3719--3727
Disabled is a bona fide component of the Abl signaling network. [FBrf0212092]
Ku et al., 2009, Mol. Cell. Biol. 29(13): 3623--3632
Organization of F-actin via concerted regulation of Kette by PTP61F and dAbl. [FBrf0215460]
Lin et al., 2009, Development 136(18): 3099--3107
Abi plays an opposing role to Abl in Drosophila axonogenesis and synaptogenesis. [FBrf0208583]
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, Nat. 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]