|Name||Saccharomyces cerevisiae UAS construct a of Hacohen||FlyBase ID||FBal0086309|
|Feature type||allele||Associated gene||Dmel\sty|
|Mutagen||in vitro construct - regulatory fusion|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Carried in construct|
|Phenotype Manifest In|
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.
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.
|Phenotype Manifest In|
Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, styScer\UAS.cHa has eye phenotype, suppressible | partially by edlF20
styScer\UAS.cHa/Scer\GAL4Bx-MS1096 is a suppressor | partially of wing phenotype of Scer\GAL4Bx-MS1096, btl::EgfrScer\UAS.T:λ\cI-DD
styScer\UAS.cHa/Scer\GAL4Bx-MS1096 is a suppressor | partially of wing vein phenotype of Scer\GAL4Bx-MS1096, btl::EgfrScer\UAS.T:λ\cI-DD
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.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
Saccharomyces cerevisiae UAS construct a of Hacohen
|Secondary FlyBase IDs|
|References ( 10 )|