|Feature type||allele||Associated gene||Dmel\th|
|Also Known As||th5, Diap15|
|Map ( GBrowse )|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
comment=G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation. (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: W273@. This mutation is within the second BIR domain.
Amino acid replacement: W273@. W273 falls near the middle of the second BIR domain.
|Phenotype Manifest In|
14% of th5/th21-2s egg chambers have border follicle cell migration defects, 25% have extra follicle cells and 3% have more than 15 nurse cells. 3% of th5/th21-2s egg chambers show polarity defects. Homozygous follicle cells clones result in border follicle cell migration defects.
th5 homozygotes progress normally through gastrulation but arrest at the beginning of germ band extension, and within 90 min thereafter, adopt a characteristic morphology reflecting catastrophic events associated with widespread and synchronous apoptosis and arrest at stage 7.
Heterozygotes are phenotypically wild type.
Embryos show increased cell death as assessed by TUNEL staining. The onset of this apoptosis appears several hours after development arrests.
Epidermis of embryos does not form a cuticle. Homozygotes and hemizygotes undergo normal cellularization and initial gastrulation. During germ band extension all morphogenetic movements cease, cells adopt a rounded morphology (suggesting disruption if intercellular adhesion) and the yolk cell fragments and moves to the surface of the embryo. Cephalic furrow regresses. Surface of cells contain blebs and vesicular fragments characteristic of dying cells. Embryos show a significant increase in TUNEL-positive cells, but no significant change in acridine orange staining. Double mutants with Df(3L)H99 show a phenotype indistinguishable from that of th5 mutants alone.
Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1, Scer\GAL4GMR.PU, th5/th[+] has visible phenotype, suppressible | partially by Hsp60DdsRNA.Sym.Scer\UAS/Hsp60Da.Sym.Scer\UAS, Scer\GAL4GMR.PU
th5 has increased cell death phenotype, suppressible by BuffyScer\UAS.cQa/Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
|NOT suppressed by|
th5/th[+] is an enhancer of visible phenotype of Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1, Scer\GAL4GMR.PU
th5 is an enhancer of lethal phenotype of NcScer\UAS.T:Avic\GFP-EGFP, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
|Phenotype Manifest In|
Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1, Scer\GAL4GMR.PU, th5/th[+] has ommatidium phenotype, suppressible | partially by Hsp60DdsRNA.Sym.Scer\UAS/Hsp60Da.Sym.Scer\UAS, Scer\GAL4GMR.PU
|NOT suppressed by|
th5/th[+] is an enhancer of ommatidium phenotype of Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1, Scer\GAL4GMR.PU
th5/th[+] is an enhancer of ommatidium phenotype of Scer\GAL4GMR.PU, Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1
A th mutant background enhances the moderately rough eye phenotype observed upon expression of mbl[C.Scer\UAS] under the control of Scer\GAL4[hs.2sev].
80% of chic01320/chick13321 ; th5/+ egg chambers have border follicle cell migration defects. 77% of chic01320/chic221 ; th5/+ egg chambers have border follicle cell migration defects.
The addition of WGMR.PG to th5 heterozygotes leads to an enhancement of cell killing. The subsequent addition of ArkCD4/ArkCD4 suppresses that enhancement. The developmental arrest phenotype is also suppressed, embryos developing through stage 10. In about 5% of cases although no cell death is seen, arrest at stage 7 is still seen.
Homozygous th5 embryos that express BacA\p35Scer\UAS.cHa under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 undergo normal morphogenesis until stage 11, after which massive cell death resumes.
The Hsp60D[dsRNA.Sym.Scer\UAS]-mediated suppression of the eye degeneration phenotype caused by Hsap\MJD[tr.Q78.Scer\UAS.T:Ivir\HA1] overexpression via Scer\GAL4[GMR.PU] is not much affected by heterozygosity for th. The enhancement of the eye degeneration resulting from the overexpression of Zzzz\CAG[127Q.Scer\UAS.T:Ivir\HA1] via Scer\GAL4[GMR.PU] in a th/+ background is not suppressed when Hsp60D[dsRNA.Sym.Scer\UAS] is co-expressed. Heterozygosity for th enhances the eye degeneration resulting from the overexpression of Hsap\MJD[tr.Q78.Scer\UAS.T:Ivir\HA1] via Scer\GAL4[GMR.PU]. Heterozygosity for th enhances the eye degeneration resulting from the overexpression of Zzzz\CAG[127Q.Scer\UAS.T:Ivir\HA1] via Scer\GAL4[GMR.PU].
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 17 )|