A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\styScer\UAS.cHa

General Information
SymbolDmel\styScer\UAS.cHaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct a of HacohenFlyBase IDFBal0086309
Feature typealleleAssociated geneDmel\sty
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
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Associated Sequence Data
DDBJ /
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Protein sequence
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Nature of the lesion
Statement
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Construct: A 2.2kb sty cDNA fragment containing the entire coding region is expressed under the control of Scer\UAS regulatory sequences.
Carried in construct
Cytology
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Statement
Reference
Expression of sty[Scer\UAS.cHa] under the control of Scer\GAL4[sev.EP] results in a rough-eye phenotype.
Expression of styScer\UAS.cHa under the control of Scer\GAL4hs.2sev causes misrotation and disorganization of ommatidia, missing photoreceptors in 5% of ommatidia, and external roughening of the eye.
Expression of styScer\UAS.cHa under the control of Scer\GAL41151 leads to a decrease in the number of founder cells; there are ~7 dorsal founders and ~8 lateral founders per hemisegment in Scer\GAL41151>styScer\UAS.cHa pupae, compared to 17-22 and 20 of these founder types in control pupae. However, there is no comparable change in the number of fusion-competent myoblasts.
When expression is driven by Scer\GAL4GMR.PF eyes are small and rough.
Expression of styScer\UAS.cHa under the control of Scer\GAL4dpp.blk1 has no effect on furrow initiation in the eye disc.
When expression is driven by Scer\GAL4hs.2sev or Scer\GAL4elav-C155 the eyes of the resulting flies are small and disorganized. Majority of ommatidia lack one or more outer photoreceptor cells of the R3/R4/R1/R6 type. The R7 is missing in 11+-4% of Scer\GAL4hs.2sev-driven ommatidia and 18+-6% of Scer\GAL4elav-C155-driven ommatidia. R2/R5 and R8 are unaffected. When expression is driven by Scer\GAL4en-e16E, the number of chordotonal organs in the embryo is reduced. When expression is driven by Scer\GAL4BH1, wing veins fail to form, and the size of the wing blade is reduced. This phenotype is similar to that caused by loss of function Egfr or vn mutants. When expression is driven by Scer\GAL4CY2, resulting eggs had a ventralized egg shell and the resulting embryos were also ventralized. This phenotype is similar to that caused by Egfr loss of function mutants.
When expression is driven by Scer\GAL4mat.αTub67C.T:Hsim\VP16 the resulting phenotype resembles that caused by loss of function alleles in Egfr. When expression is driven by Scer\GAL4T155 the egg is ventralized and the dorsal appendages are fused and reduced. When expression is driven by Scer\GAL4dpp.blk1 the L3 vein of the adult wing is truncated. When expression is driven by Scer\GAL4Bx-MS1096 the L2, L3 and L4 veins of the adult wing are truncated. The size of the wing is somewhat reduced.
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Reference
Scer\GAL4sev.EP, styScer\UAS.cHa has eye phenotype, suppressible by Fas2EB112/Fas2[+]
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The rough-eye phenotype observed in flies expressing sty[Scer\UAS.cHa] under the control of Scer\GAL4[sev.EP] is suppressed in the presence of Fas2[EB112]/+.
When expression is driven by Scer\GAL4Bx-MS1096 in combination with btl::EgfrScer\UAS.T:λ\cI-DD, the wing size of the btl::EgfrScer\UAS.T:λ\cI-DD is largely normal and the wing veins, though still slightly thickened compared to wild type, are largely restored. When expression is driven by Scer\GAL4Bx-MS1096 in combination with htlScer\UAS.T:λ\cI-DD, the wing vein defects caused by htlScer\UAS.T:λ\cI-DD are largely suppressed. Lethality of phlScer\UAS.F179, Scer\GAL471B is rescued by styScer\UAS.cHa. Wings of phlScer\UAS.F179, styScer\UAS.cHa, Scer\GAL471B mutants are largely devoid of wing vein.
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hide Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym
styScer\UAS.cHa
 
styUAS.cHa
 
Name Synonym
Saccharomyces cerevisiae UAS construct a of Hacohen
Secondary FlyBase IDs
hide References ( 10 )
Research paper
Mao and Freeman, 2009, Development 136(3): 473--481
Fasciclin 2, the Drosophila orthologue of neural cell-adhesion molecule, inhibits EGF receptor signalling. [FBrf0206540]
Jarvis et al., 2006, Development 133(6): 1133--1142
Sprouty proteins are in vivo targets of Corkscrew/SHP-2 tyrosine phosphatases. [FBrf0190302]
Dutta et al., 2005, PLoS Biol. 3(10): e337
Drosophila Heartless acts with Heartbroken/Dof in muscle founder differentiation. [FBrf0191368]
Iwanami et al., 2005, Genes Cells 10(7): 743--752
Cell-type specific utilization of multiple negative feedback loops generates developmental constancy. [FBrf0187603]
Bai et al., 2001, Development 128(4): 591--601
The cell adhesion molecule Echinoid defines a new pathway that antagonizes the Drosophila EGF receptor signaling pathway. [FBrf0134572]
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]
Kumar and Moses, 2001, Cell 104(5): 687--697
EGF receptor and Notch signaling act upstream of Eyeless/Pax6 to control eye specification. [FBrf0134490]
Kramer et al., 1999, Development 126(11): 2515--2525
Sprouty: a common antagonist of FGF and EGF signaling pathways in Drosophila. [FBrf0108521]
Reich et al., 1999, Development 126(18): 4139--4147
Sprouty is a general inhibitor of receptor tyrosine kinase signaling. [FBrf0111472]
Hacohen et al., 1998, Cell 92(2): 253--263
sprouty encodes a novel antagonist of FGF signaling that patterns apical branching of the Drosophila airways. [FBrf0100567]