FlyBase Allele Report: Dmel\ttk[1]

General Information

Symbol

Dmel\ttk¹

Species

D. melanogaster

Name

FlyBase ID

FBal0017203

Feature type

allele

Associated gene

Dmel\ttk

Associated Insertion(s)

P{PZ}ttk¹

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

gain of function allele

Mutagen

PM hybrid dysgenesis

Nature of the Allele

Allele class

gain of function allele

(Okabe et al., 2001)

loss of function allele

(Okabe et al., 2001)

Mutagen

PM hybrid dysgenesis

(Serrano et al., 1995, Xiong and Montell, 1993)

Progenitor genotype

Associated Insertion(s)

P{PZ}ttk¹

Cytology

Description

ttk cDNA of the TTK69 isoform lacks the distal 80% of the 3' UTR sequence, owing to a readthrough into P-element sequences.

(Okabe et al., 2001)

P-element insertion into last intron.

(Giesen et al., 1997)

P-element insertion 0.45kb from the 3' end of the coding region of the 4.5kb cDNA within an intron.

(Xiong and Montell, 1993)

Allele components

Component

Use(s)

Inserted element

P{PZ}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

3R:31,729,632..31,732,395 [+]

(Okabe et al., 2001, Giesen et al., 1997, Lai et al., 1996, Serrano et al., 1995, Xiong and Montell, 1993)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal visual behavior | recessive

(Xiong and Montell, 1993)

viable

(Ciglar et al., 2014, Lai et al., 1996)

visible

(Lai et al., 1996)

visible | semidominant

(Okabe et al., 2001)

Phenotype Manifest In

Detailed Description

Statement

Reference

ttk¹/ttk¹ flies are viable and develop with no aberrant muscle development.

(Ciglar et al., 2014)

ttk¹ mutant eyes have supernumerary R7 cells in some ommatidia, though the eyes are overtly the same as wild type by SEM. The number and appearance of cone cells in each ommatidium of ttk¹ pupal eye discs are normal.

(Shi and Noll, 2009)

Eggs laid by ttk^twp/ttk¹ or homozygous ttk¹ mothers exhibit a weak dorsal appendage phenotype, with 12% show some defect. Only 40% of eggs laid by ttk¹/ttk^1e11 mothers are wild-type,, the rest exhibit a dorsal appendage phenotype, 3% having only the nub of an appendage.

(French et al., 2003)

Shows a semidominant double bristle phenotype - similar to that caused by overexpression of the TTK69 isoform.

(Okabe et al., 2001)

CNS development is normal.

(Giesen et al., 1997)

Rough eye phenotype due to supernumerary R7 cells. Mutant phenotype can be enhanced by ttk⁰⁰²¹⁹.

(Lai et al., 1996)

The compound eye of ttk^bose1/ttk¹ flies is similar to wild-type.

(Yamamoto et al., 1996)

Many ommatidia contain supernumerary R7 cells and decreased numbers of R1-R6 cells.

(Xiong and Montell, 1993)

embryonic lethal no effect on ftz gene expression.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

aop^yan-XE18, ttk¹ has visible phenotype

(Lai et al., 1997)

Phenotype Manifest In

Enhancer of

Statement

Reference

ttk¹ is an enhancer of phenotype of phyl^hs.sev

(Tang et al., 1997)

NOT Enhancer of

Statement

Reference

ttk[+]/ttk¹ is a non-enhancer of wing margin bristle | ectopic phenotype of hry⁴¹

(Badenhorst et al., 2002)

Suppressor of

Statement

Reference

ttk[+]/ttk¹ is a suppressor | partially of ommatidium phenotype of Sos^JC2, sev⁶

(Dong et al., 1999)

ttk[+]/ttk¹ is a suppressor | partially of photoreceptor cell R7 phenotype of Sos^JC2, sev⁶

(Dong et al., 1999)

ttk[+]/ttk¹ is a suppressor | partially of ommatidium phenotype of Sos^JC2/Sos[+], sev⁶

(Dong et al., 1999)

ttk[+]/ttk¹ is a suppressor | partially of photoreceptor cell R7 phenotype of Sos^JC2/Sos[+], sev⁶

(Dong et al., 1999)

NOT Suppressor of

Statement

Reference

ttk[+]/ttk¹ is a non-suppressor of wing margin bristle | ectopic phenotype of hry⁴¹

(Badenhorst et al., 2002)

Other

Statement

Reference

sv^spa-pol, ttk¹ has eye phenotype

(Shi and Noll, 2009)

sv^spa-pol, ttk¹ has ommatidium phenotype

(Shi and Noll, 2009)

sv^spa-pol, ttk¹ has interommatidial bristle phenotype

(Shi and Noll, 2009)

sv^spa-pol, ttk¹ has eye photoreceptor cell phenotype

(Shi and Noll, 2009)

sv^spa-pol, ttk¹ has cone cell | pupal stage phenotype

(Shi and Noll, 2009)

aop^yan-XE18, ttk¹ has photoreceptor cell R7 phenotype

(Lai et al., 1997)

Additional Comments

Genetic Interactions

Statement

Reference

sv^spa-pol ttk¹ double mutant eyes show a much stronger rough eye phenotype than either single mutant: the surface of the eye is nearly flat with irregularly spaced bristles. Only a few malformed ommatidia, many of which have open holes at their apices, are visible. Photoreceptors in the remaining ommatidia have strongly deformed rhabdomeres. sv^spa-pol ttk¹ pupal eye discs have no cone cells.

(Shi and Noll, 2009)

The addition of or ttk¹/+ to h⁴¹/+ animals does not lead to a significant ectopic wing margin bristle phenotype.

(Badenhorst et al., 2002)

The partial lethality due to run^Scer\UAS.cLa; Scer\GAL4^nos.PG (3% viable) is partially suppressed by maternal heterozygosity for ttk¹ (rescues to 19% viable).

(Wheeler et al., 2002)

In sev⁶ hemizygotes that are also heterozygous for Sos^JC2, 14.7% of ommatidia contain R7 cells. This phenotype is dominantly suppressed by ttk¹.

(Dong et al., 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Complements

ttk^twp

(French et al., 2003)

ttk^1e11

(Lai and Li, 1999)

Partially complements

ttk^1e11

(French et al., 2003)

Fails to complement

ttk¹⁵⁰

(Horn et al., 2003)

ttk^rM730

(Lai and Li, 1999)

Comments

94% of the ommatidia in ttk¹/ttk^1e11 flies were wild-type, as opposed to 50-60% in ttk¹ homozygotes. There are 65% of normal ommatidia in ttk¹/ttk^rM730 flies and most mutant ommatidia contain ectopic photoreceptors.

(Lai and Li, 1999)

Images (0)

Mutant

Wild-type

Stocks (2)

4163

107606

Notes on Origin

Discoverer

Comments

ttk¹ is a loss of function allele for the TTK88 isoform and a gain of function allele for the TTK69 isoform.

(Okabe et al., 2001)

Despite extensive outcrossing of the ttk¹ stock, the identity of which was confirmed by analysis of its DNA, it no longer shows a large fraction, but less than 1%, of ommatidia with supernumerary R7 cells. A possible explanation might be that in the original stock a mutation closely coupled with ttk¹, but later lost, was responsible for the large fraction (~40%) of ommatidia with supernumerary R7 cells and reduced number (~20%) of outer photoreceptor cells (see FBrf0058514 and FBrf0087523).

(Shi and Noll, 2009)

Disrupts the mRNA encoding ttk protein p88. Mutant phenotype can be restored to wild type by Js P-element mobilisation.

(Xiong and Montell, 1993)

Mutation affects the p88 ttk protein.

(Giesen et al., 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

ttk¹

(Ciglar et al., 2014, Shi and Noll, 2009, Araujo et al., 2007, Vander Zwan et al., 2003)

Name Synonyms

Secondary FlyBase IDs

References (23)

Report Sections

Open Close