|Feature type||allele||Associated gene||Hsap\TBP|
|Mutagen||in vitro construct - site directed mutagenesis|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Carries an expanded poly-Q tract in the second CAG repeat block with 80 glutamines.
|Carried in construct|
|Phenotype Manifest In|
Expression of Hsap\TBP[80Q.Scer\UAS] in the eye under the control of Scer\GAL4[GMR.PU] results in the collapse of the eye structure, a loss of pigmentation and severely disorganised photoreceptors. Ommatidial fusion is also observed. The eye defects worsen as flies age. While flies expressing Hsap\TBP[80Q.Scer\UAS] under the control of Scer\GAL4[elav.PU] at young ages perform similarly to aged-matched wild-type flies, they exhibit a late-onset locomotor impairment. Flies expressing Hsap\TBP[80Q.Scer\UAS] under the control of Scer\GAL4[elav.PU] exhibit shortened lifespan compared with wild-type controls.
|Phenotype Manifest In|
Hsap\TBP80Q.Scer\UAS, Scer\GAL4GMR.PU has eye phenotype, enhanceable by Su(H)VDRC.cUa, Scer\GAL4GMR.PU
Hsap\TBP80Q.Scer\UAS, Scer\GAL4GMR.PU has eye phenotype, suppressible | partially by Su(H)Scer\UAS.T:Hsap\MYC, Scer\GAL4GMR.PU
Expression of Su(H)[VDRC.cUa] under the control of Scer\GAL4[GMR.PU] enhances the eye abnormalities caused by the overexpression of Hsap\TBP[80Q.Scer\UAS]. Overexpression of Su(H)[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[GMR.PU] partially suppresses the eye abnormalities caused by the overexpression of Hsap\TBP[80Q.Scer\UAS] with an improvement in both the shape and organisation of ommatidia. Ommatidial fusion is no longer observed and pigment loss is less severe.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 1 )|