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General Information
Symbol
Dmel\ttkrM730
Species
D. melanogaster
Name
FlyBase ID
FBal0051010
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P-element insertion 1.2kb upstream of the first exon.

P-element insertion within enhancer elements of ttk.

Insertion components
P{PZ}ttkrM730
Product class / Tool use(s)
Encoded product / tool
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

ttkrM730 mutant eye clones display severe degeneration of the corneal lens, with ommatidia and sensory bristles failing to properly develop.

In 90% of ttkrM730 mutant third instar eye disc clones, 2-3 presumptive R7 photoreceptor cells are observed seven rows posterior to the morphogenetic furrow, compared to just one R7 cell in control tissue. A reduced number of cone cells is observed in mutant clones.

The number of neurons associated with the pentascolopidial sensory organ is approximately double that of wild type in mutant embryos.

Homozygous clones in the adult eye cause degeneration of the corneal lens and a failure of photoreceptor development. Rhabdomeres of photoreceptors are not observed in clones, but residual cellular structures in the mutant ommatidia are still recognizable. Genetically mosaic ommatidia are not seen near the boundary of the clone. Ectopic neurons are not seen between or below the developing ommatidia in homozygous clones in third instar larvae. Larval eye development seems close to normal in the absence of ttk, although the ommatidial clusters in clones were somewhat disorganised. Cone cell development appears normal.

Large mitotic clones in the eye were rarely observed, small clones often causes scars.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

HDAC11-3, ttkrM730 has visible phenotype, enhanceable by Mi-24/Mi-2[+]

HDAC13-10, ttkrM730 has visible phenotype, enhanceable by Mi-24/Mi-2[+]

HDAC15-5, ttkrM730 has visible phenotype, enhanceable by Mi-24/Mi-2[+]

Suppressed by
Statement
Reference
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

ttkrM730 has eye | somatic clone phenotype, suppressible | partially by lzmr2

h41/h[+], ttkrM730 has wing margin bristle | ectopic phenotype, suppressible by sc[+]/sc1

h41/h[+], ttkrM730 has wing margin bristle | ectopic phenotype, suppressible by scase-1/sc[+]

Enhancer of
Statement
Reference

ttk[+]/ttkrM730 is an enhancer of wing margin bristle | ectopic phenotype of acHw-49c

ttk[+]/ttkrM730 is an enhancer of wing margin bristle | ectopic phenotype of acHw-1

ttk[+]/ttkrM730 is an enhancer of phenotype of aopA141

ttkrM730 is an enhancer of eye phenotype of Ras85DV12

Other
Additional Comments
Genetic Interactions
Statement
Reference

The eye phenotype observed in ttkrM730 clones is partially suppressed in a lzmr2 mutant background. Ommatidial structures and sensory bristles are present, and the eye appears less scarred.

The addition of ttkrM730/+ to acHw-49c/+ animals leads to an 1.35 enhancement of the ectopic wing margin bristle phenotype. The addition of ttkrM730/+ to acHw-1/+ animals leads to an 1.4 enhancement of the ectopic wing margin bristle phenotype. The addition of ttkrM730/+ to emcE12/+ or emcip15/+ animals leads to a weak ectopic wing margin bristle phenotype. The addition of ttkrM730/+ to h41/+ animals leads to a ectopic wing margin bristle phenotype. The addition of scase-1/Y to h41/+, ttkrM730/+ animals leads to a complete suppression of the ectopic margin bristle phenotype. The addition ofsc1/Y to h41/+, ttkrM730/+ animals leads to an almost complete suppression of the ectopic margin bristle phenotype. The addition of Df(3R)awd-KRB to h41/+, ttkrM730/+ animals leads to a suppression of the ectopic margin bristle phenotype. CtBP87De-10 combined with ttkrM730 exhibit an ectopic margin bristle phenotype.

The partial lethality due to runScer\UAS.cLa; Scer\GAL4nos.PG (3% viable) is not suppressed by maternal heterozygosity for ttkrM730.

The number of neurons associated with the pentascolopidial sensory organ in ttkrM730 mutant embryos is significantly increased if they are also mutant for Mi-24. ttkrM730 Rpd31-3 double mutants have ectopic sensory bristles on the wing veins. ttkrM730 Rpd35-5 double mutants have ectopic sensory bristles on the wing veins. ttkrM730 Rpd33-10 double mutants have ectopic sensory bristles on the wing veins.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments

65% of the ommatidia in ttk1/ttkrM730 flies were wild-type, compared to 50-60% in ttk1 homozygotes. There are 65% of normal ommatidia in ttk1/ttkrM730 flies and most mutant ommatidia contain ectopic photoreceptors.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (10)