A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\hepScer\UAS.cBa

General Information
SymbolDmel\hepScer\UAS.cBaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct a of BoutrosFlyBase IDFBal0092957
Feature typealleleAssociated geneDmel\hep
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
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
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Associated Sequence Data
DDBJ /
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DNA sequence
Protein sequence
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UniProtKB/Swiss-Prot
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Nature of the lesion
Statement
Reference
Construct: Expression of hep cDNA is governed by Scer\UAS regulatory sequences.
Carried in construct
Cytology
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adult thorax & macrochaeta, with Scer\GAL4pnr-MD237
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Statement
Reference
Expression of hep[Scer\UAS.cBa] under the control of Scer\GAL4[twi.PG] results in delayed or defective ventral furrow formation in a proportion of embryos.
Transient overexpression of hep[Scer\UAS.cBa] in adults under the control of Scer\GAL4[esg-NP5130] and Scer\GAL80[ts.αTub84B] induces increased proliferation of intestinal cells compared with controls. Transient overexpression of hep[Scer\UAS.cBa] in adults under the control of Scer\GAL4[esg-NP5130] and Scer\GAL80[ts.αTub84B] results in significant lifespan shortening compared with wild-type.
Expression of hep[Scer\UAS.cBa] under the control of Scer\GAL4[ptc-559.1] results in a dramatic increase in the number of intercalated cells and the formation of ectopic mixer cells at the segment boundaries during dorsal closure (in the abdominal segments of wild-type embryos at the end of dorsal closure, a mixer cell moves across the segment boundary from the anterior compartment to the posterior compartment and two cells from the ventral ectoderm intercalate into the leading edge, posterior to the mixer cell).
Ectopic expression of hep[Scer\UAS.cBa] driven by Scer\GAL4[69B] in embryos leads to cuticles with openings in the anterior part and puckering in the dorsal part. Ectopic expression of hep[Scer\UAS.cBa] driven by either Scer\GAL4[Abd-B-LDN] or Scer\GAL4[ptc-559.1] leads to male genital disc effects such as incomplete rotation and separation of the plate from the abdomen.
Animals expressing hep[Scer\UAS.cBa] under the control of Scer\GAL4[ppl.PP] show increased tolerance to paraquat compared to controls.
Expression of hepScer\UAS.cBa under the control of Scer\GAL4GMR.PF does not affect eye development.
Expression of hepScer\UAS.cBa under the control of Scer\GAL4GMR.PF has no effect on eye morphology.
Flies expressing hepScer\UAS.cBa, under the control of Scer\GAL4arm.PS, show a decreased sensitivity to paraquat compared to wild-type flies. This decreased sensitivity is also seen when hepScer\UAS.cBa is expressed under the control of the neuron-specific driver Scer\GAL4elav.Switch.PO, but only in the presence of RU486. However, expression of hepScer\UAS.cBa under the control of the muscle-specific driver Scer\GAL4Mhc.Switch.PO does not affect tolerance to paraquat. Overexpression of hepScer\UAS.cBa, driven by Scer\GAL4elav-C155, increases the lifespan of flies.
When expression is driven by Scer\GAL4hs.2sev, flies have rough eyes showing polarity phenotypes. Ommatidia are incorrectly rotated and sometimes exhibit the wrong chiral form.
Adults in which hepScer\UAS.cBa is expressed under the control of Scer\GAL4pnr-MD237 have a severely reduced scutellum, and there is a cleft in the tissue at the dorsal midline. The bristles are oriented in a different direction from normal, are loosely spaced and sometimes have kinks.
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Reference
hepScer\UAS.cBa/Scer\GAL4ato.3.6 is a suppressor of axon & dorsal cluster neuron phenotype of dsh1
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Reference
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Statement
Reference
The defects in ventral furrow formation seen in embryos expressing hep[Scer\UAS.cBa] under the control of Scer\GAL4[twi.PG] are completely suppressed in embryos derived from bsk[unspecified] female germline clones.
The axon overextension phenotype of Mkk4[e01485] neuroblast clones in mushroom bodies is suppressed by expression of hep[Scer\UAS.cBa] using Scer\GAL4[ey-OK107].
The increased tolerance of animals expressing hep[Scer\UAS.cBa] under the control of Scer\GAL4[ppl.PP] to paraquat is abolished by NLaz[NW5]/NLaz[NW5], with the double mutant flies showing the same sensitivity to paraquat as NLaz[NW5]/NLaz[NW5] single mutants.
Expression of hepScer\UAS.cBa, under the control of Scer\GAL4ato.3.6, in a dsh1 background results in a large increase of dorsal cluster neuron axons crossing the optic chiasm, indicating a complete dominance of the hep gain of function phenotype.
Coexpression of hepScer\UAS.cBa and Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.PI results in eye/antennal imaginal disc clones results in the invasion of the disc cells into the ventral nerve cord and regions of the brain.
The small, deformed eye phenotype of foxoScer\UAS.cPa; Scer\GAL4GMR.PF adults is enhanced by the presence of hepScer\UAS.cBa.
When hepScer\UAS.cBa is coexpressed with one copy of Traf1EP578, driven by Scer\GAL4GMR.PF, the number of ommatidia and the size of the compound eye are reduced to similar levels seen when two copies of Traf1EP578 are expressed. Coexpression of Traf2EP1516 with either hepScer\UAS.cBa, under the control of Scer\GAL4GMR.PF, does not affect the development of eyes.
The phenotype caused when hepScer\UAS.cBa is expressed under the control of Scer\GAL4pnr-MD237is enhanced by a single copy of pucE69; the scutellum is completely missing.
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Statement
Reference
The rough eye phenotype caused by expression of Hsap\MAPTV337M.Scer\UAS under the control of Scer\GAL4GMR.PF is enhanced by co-expression of hepScer\UAS.cBa; eye surface roughness is increased, eye size is decreased and necrotic black patches are formed in the eye.
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Rescues
Comments
Expression of hep[Scer\UAS.cBa] with Scer\GAL4[ey-OK107] rescues the axonal phenotypes seen in hep[r39] mushroom body clones.
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Bloomington
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hide Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym
hepScer\UAS.cBa
 
hepUAS.cBa
 
Name Synonym
Saccharomyces cerevisiae UAS construct a of Boutros
Secondary FlyBase IDs
hide References ( 19 )
Research paper
Mathew et al., 2011, Mol. Cell. Biol. 31(24): 4978--4993
Role for traf4 in polarizing adherens junctions as a prerequisite for efficient cell shape changes. [FBrf0216703]
Biteau et al., 2010, PLoS Genet. 6(10): e1001159
Lifespan extension by preserving proliferative homeostasis in Drosophila. [FBrf0212112]
Gettings et al., 2010, PLoS Biol. 8(6): e1000390
JNK Signalling Controls Remodelling of the Segment Boundary through Cell Reprogramming during Drosophila Morphogenesis. [FBrf0211014]
Rallis et al., 2010, Dev. Biol. 339(1): 65--77
Signal strength and signal duration define two distinct aspects of JNK-regulated axon stability. [FBrf0209975]
Rousset et al., 2010, Development 137(13): 2177--2186
The Drosophila serine protease homologue Scarface regulates JNK signalling in a negative-feedback loop during epithelial morphogenesis. [FBrf0211045]
Hull-Thompson et al., 2009, PLoS Genet. 5(4): e1000460
Control of metabolic homeostasis by stress signaling is mediated by the lipocalin NLaz. [FBrf0207766]
Srahna et al., 2006, PLoS Biol. 4(11): e348
A signaling network for patterning of neuronal connectivity in the Drosophila brain. [FBrf0192599]
Uhlirova and Bohmann, 2006, EMBO J. 25(22): 5294--5304
JNK- and Fos-regulated Mmp1 expression cooperates with Ras to induce invasive tumors in Drosophila. [FBrf0194142]
Wang et al., 2005, Cell 121(1): 115--125
JNK extends life span and limits growth by antagonizing cellular and organism-wide responses to insulin signaling. [FBrf0187242]
Cha et al., 2003, Mol. Cell. Biol. 23(22): 7982--7991
Discrete functions of TRAF1 and TRAF2 in Drosophila melanogaster mediated by c-Jun N-terminal kinase and NF-kappaB-dependent signaling pathways. [FBrf0167884]
Lee et al., 2003, Development 130(17): 4001--4010
blistery encodes Drosophila tensin protein and interacts with integrin and the JNK signaling pathway during wing development. [FBrf0160724]
Shulman and Feany, 2003, Genetics 165(3): 1233--1242
Genetic modifiers of tauopathy in Drosophila. [FBrf0167629]
Wang et al., 2003, Dev. Cell 5(5): 811--816
JNK signaling confers tolerance to oxidative stress and extends lifespan in Drosophila. [FBrf0167481]
Kumar and Moses, 2001, Cell 104(5): 687--697
EGF receptor and Notch signaling act upstream of Eyeless/Pax6 to control eye specification. [FBrf0134490]
Kumar and Moses, 2001, Development 128(14): 2689--2697
The EGF receptor and notch signaling pathways control the initiation of the morphogenetic furrow during Drosophila eye development. [FBrf0138358]
McEwen et al., 2000, Development 127(16): 3607--3617
The canonical Wg and JNK signaling cascades collaborate to promote both dorsal closure and ventral patterning. [FBrf0128573]
Weber et al., 2000, Development 127(16): 3619--3629
Jun mediates Frizzled-induced R3/R4 cell fate distinction and planar polarity determination in the Drosophila eye. [FBrf0128678]
Zeitlinger and Bohmann, 1999, Development 126(17): 3947--3956
Thorax closure in Drosophila: involvement of fos and the JNK pathway. [FBrf0111528]
Boutros et al., 1998, Cell 94(1): 109--118
Dishevelled activates JNK and discriminates between JNK pathways in planar polarity and wingless signaling. [FBrf0103240]