A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\fraScer\UAS.cKa

General Information
SymbolDmel\fraScer\UAS.cKaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct a of KolodziejFlyBase IDFBal0057431
Feature typealleleAssociated geneDmel\fra
Allele class
Mutagenin vitro construct - regulatory fusion
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Description
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FB2013_03
FB2013_02
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Construct: EcoRI-XbaI DNA fragment containing nucleotides 1-5038 from the shorter isoform of fra cDNA is cloned into pUAST.
Carried in construct
Cytology
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Expression of fra[Scer\UAS.cKa] in all R cells (using Scer\GAL4[GMR.long] as a driver) does not result in the redirection of R7 axons to the M3 layer, with many R8 axons remaining in the temporary layer.
Expression of fra[Scer\UAS.cKa] in a wild-type background n MN-LL1 neurons under the control of Scer\GAL4[eve.CQ2] leads to a greater proportion of dendritic branches innervating the intermediate neuropile. MN-DA3 expression of fra[Scer\UAS.cKa] leads to ectopic innervation of the intermediate neuropile in 50% of cases, converting the dendritic arbor to a MN-LL1-like morphology. Overexpression in MN-LL1 or MN-DA3 does not lead to ectopic midline targeting of dendrites.
Ventral nerve cord axon bundles of stage 16 embryos overexpressing fra[Scer\UAS.cKa] via Scer\GAL4[ftz.ng] do not display any incorrect midline crossing.
Expression of fraScer\UAS.cKa under the control of Scer\GAL4elav.PLu does not result in any axon guidance defects in embryos.
Expression of fraScer\UAS.cKa in the salivary gland, driven by Scer\GAL4prd.RG1, causes 75% of glands to aberrantly curve medially.
Embryos expressing fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng develop normally.
Scer\GAL41407 induced expression fails to cause defects in the CNS or PNS projections, viable adult flies are recovered.
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Overexpression of fra[Scer\UAS.cKa] under the control of Scer\GAL4[ppk.1.9] significantly suppresses the Trim9[46] midline crossing defects.
Co-expression of fra[Scer\UAS.cKa] with Rac1[V12.Scer\UAS] under the control of Scer\GAL4[ftz.ng] results in a strong synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1[V12.Scer\UAS]-overexpression alone. The frequency of crossovers across the midline in embryos expressing Rho1[V14.Scer\UAS] driven by Scer\GAL4[ftz.ng] is significantly increased by co-expression of fra[Scer\UAS.cKa]. Co-expression of sqh[T20A.S21A.Scer\UAS] under the control of Scer\GAL4[ftz.ng] suppresses the midline crossing phenotype in embryos expressing both Rho1[V14.Scer\UAS] and fra[Scer\UAS.cKa]. Ventral nerve cord axon bundles of stage 16 embryos overexpressing fra[Scer\UAS.cKa] via Scer\GAL4[ftz.ng] in a heterozygous Abl[4] genetic background display few incorrect midline crossings.
Expression of fra[Scer\UAS.cKa] in the early stages of axon pathfinding under the control of Scer\GAL4[prd.RG1] rescues axonal defects in even segments of fra[1]/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra[1]/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fra[Scer\UAS.cKa] in later stages of development, under the control of Scer\GAL4[elav.PLu] does not rescue the the defects in ventral nerve cord architecture seen in fra[1]/Df(2R)en-SFX31 mutants. Overexpression of fra[Scer\UAS.cKa] under the control of Scer\GAL4[prd.RG1] does not suppress the abnormal pathfinding phenotype observed in Df(2R)en-SFX31 mutants. Expression of fra[Scer\UAS.cKa] in the early stages of axon pathfinding under the control of Scer\GAL4[prd.RG1] rescues axonal defects in even segments of fra[1]/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra[1]/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fra[Scer\UAS.cKa] in later stages of development, under the control of Scer\GAL4[elav.PLu] does not rescue the the defects in ventral nerve cord architecture seen in fra[1]/Df(2R)en-SFX31 mutants.
Expression of fra[Scer\UAS.cKa] in elav[5] mutant EW and EG neurons (under the control of Scer\GAL4[eg-Mz360]) does not modify the proportion of contralateral projection defects in elav[5] mutant embryos. For example, EW axons fail to cross the midline in 755 of the neuromeres in such embryos.
Expression of fraScer\UAS.cKa under the control of Scer\GAL4elav.PLu does not enhance the sliE-158 longitudinal tract phenotype.
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Co-expression of fra[Scer\UAS.cKa] with Ggal\MLCK[ct.Scer\UAS] under the control of Scer\GAL4[ftz.ng] increases the frequency of axonal midline crossing abnormalities. Heterozygous Abl[4] almost completely suppresses the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCK[ct.Scer\UAS] with fra[Scer\UAS.cKa] under the control of Scer\GAL4[ftz.ng]. Homozygous Abl[4] enhances the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCK[ct.Scer\UAS] with fra[Scer\UAS.cKa] under the control of Scer\GAL4[ftz.ng]. The frequency of neuronal crossover projections induced by Scer\GAL4[ftz.ng]-driven expression of Abl::Hsap\ABL1::Hsap\BCR[P210.Scer\UAS] is significantly increased by co-expression of fra[Scer\UAS.cKa].
The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is enhanced by coexpression of fraScer\UAS.cKa.
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Expression of fra[Scer\UAS.cKa] in C4da neurons under the control of Scer\GAL4[ppk.PG] partially rescues the axonal defects seen in fra[3]/fra[4] mutants.
Expression of fra[Scer\UAS.cKa] under the control of Scer\GAL4[gcm.PU] rescues the defects in interface glial cell migration seen in fra[3]/fra[4] embryos. Expression of fra[Scer\UAS.cKa] under the control of Scer\GAL4[MZ1580] weakly rescues the defects in interface glial cell migration seen in fra[3]/fra[4] embryos. The defects in interface glial cell migration seen in fra[3]/fra[4] embryos are not rescued by expression of fra[Scer\UAS.cKa] under the control of any one of Scer\GAL4[repo], Scer\GAL4[pros.PMG], Scer\GAL4[elav.PU] or Scer\GAL4[Mz605].
Expression of fra[Scer\UAS.cKa] under the control of Scer\GAL4[eve.CQ2] rescues dendritic targeting to the midline in fra[3]/fra[4] mutant MN-VO4-6 and MN-VO4/5 neurons. Expression of fra[Scer\UAS.cKa] under the control of Scer\GAL4[eve.CQ2] selectively in MN-LL1 neurons in fra[3]/fra[4] mutant embryos efficiently rescues dendritic targeting to the intermediate neuropile. Moreover, this manipulation leads to a greater proportion of dendritic branches innervating the intermediate neuropile.
Expression of fraScer\UAS.cKa under the control of Scer\GAL415J2 does not rescue the dMP2 axonal phenotype of fra3/fra4 embryos. Expression of fraScer\UAS.cKa under the control of Scer\GAL4605 does rescue the dMP2 axonal phenotype of fra3/fra4 embryos.
Scer\GAL41407 induced expression in fra3/fra4 embryos rescues the commissure phenotype, commissures form normally in abdominal segments A1-A7. ISN motor axons also innervate their targets at near wild type levels. Scer\GAL4how-24B induced expression in fra3/fra4 embryos fails to rescue the ISN motor axon defects.
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Bloomington
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Reported As
Symbol Synonym
fraScer\UAS.cKa
 
fraUAS.cKa
 
Name Synonym
Saccharomyces cerevisiae UAS construct a of Kolodziej
Secondary FlyBase IDs
hide References ( 15 )
Research paper
Timofeev et al., 2012, Neuron 75(1): 80--93
Localized netrins act as positional cues to control layer-specific targeting of photoreceptor axons in Drosophila. [FBrf0218874]
Morikawa et al., 2011, Proc. Natl. Acad. Sci. U.S.A. 108(48): 19389--19394
Different levels of the Tripartite motif protein, Anomalies in sensory axon patterning (Asap), regulate distinct axonal projections of Drosophila sensory neurons. [FBrf0216734]
Song et al., 2011, J. Genet. Genomics 38(1): 1--11
TRIM-9 functions in the UNC-6/UNC-40 pathway to regulate ventral guidance. [FBrf0213082]
von Hilchen et al., 2010, Development 137(8): 1251--1262
Netrins guide migration of distinct glial cells in the Drosophila embryo. [FBrf0210391]
Mauss et al., 2009, PLoS Biol. 7(9): e1000200
Midline signalling systems direct the formation of a neural map by dendritic targeting in the Drosophila motor system. [FBrf0208790]
Dorsten et al., 2007, Dev. Biol. 308(1): 120--132
Frazzled regulation of myosin II activity in the Drosophila embryonic CNS. [FBrf0200818]
Joly et al., 2007, Dev. Biol. 301(2): 542--554
Engrailed controls the organization of the ventral nerve cord through frazzled regulation. [FBrf0194180]
Simionato et al., 2007, Dev. Biol. 301(1): 166--177
The Drosophila RNA-binding protein ELAV is required for commissural axon midline crossing via control of commissureless mRNA expression in neurons. [FBrf0193348]
Bhat, 2005, Genetics 170(1): 149--159
Slit-roundabout signaling neutralizes Netrin-Frazzled-mediated attractant cue to specify the lateral positioning of longitudinal axon pathways. [FBrf0187630]
Kolesnikov and Beckendorf, 2005, Dev. Biol. 284(1): 102--111
NETRIN and SLIT guide salivary gland migration. [FBrf0187388]
Kim et al., 2002, Dev. Biol. 249(2): 367--381
Constitutively active myosin light chain kinase alters axon guidance decisions in Drosophila embryos. [FBrf0151882]
Keleman and Dickson, 2001, Neuron 32(4): 605--617
Short- and long-range repulsion by the Drosophila Unc5 Netrin receptor. [FBrf0141688]
Kolodziej et al., 1996, Cell 87(2): 197--204
frazzled encodes a Drosophila member of the DCC immunoglobulin subfamily and is required for CNS and motor axon guidance. [FBrf0090650]
Supplementary material
Hu, 2005, Proc. Natl. Acad. Sci. USA 102(12):
[title not yet available] [FBrf0191477]
Letter
Hiramoto et al., 2000, Nature 406(6798): 886--889
The Drosophila Netrin receptor Frazzled guides axons by controlling Netrin distribution. [FBrf0129858]