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General Information
D. melanogaster
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Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
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Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
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Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

ttkD2-50/Df(3R)awd-KRB mutant embryos exhibit severe somatic muscle defects, with loss of myoblast fusion and failure to form the normal organized muscle pattern, display abnormal gut morphology, failing to form the three midgut constrictions, and fail to form the dorsal vessel but number and morphology of visceral myoblasts are not significantly different, and the specification of heart precursors occurs normally, as compared to wild type.

ttkD2-50/ttkD2-50 mutant embryos display a significant increase in the number of muscle founder-like cells, and decrease in the number of fusion competent cells, as measured in segments A3-A6 at embryonic stage 12, compared with heterozygous controls, and there is no evidence of an aberrant cell cycle.

ttkD2-50 mutant embryos display defects in tracheal patterning. An absence or reduction of visceral branches is observed. By late embryogenesis, the tracheal pattern of ttkD2-50 mutants resembles that of stage 13 or 14 embryos.

Tracheal cells do not rearrange as normal in ttkD2-50 mutants, and reamin positioned in side-by-side pairs by late embryogenesis. Paired cells remain cuboidal, and do not intercalate. Autocellular junctions only occasionally form or zip up. Dorsal branches with no sign of autocellular junctions, and others with short stretches of autocellular junctions followed by long stretches of intercellular ones, are observed. Cell rearrangement is also disrupted in the lateral trunk.

ttkD2-50 mutants show impaired (in the dorsal branches and lateral trunk) or delayed (in the dorsal trunk) fusion events. The formation of filopodia is observed at the tips of the branches in mutants, but cells are defective in generating an intracellular lumen that penetrates the fusion cell during branch fusion.

By late embryogenesis, tracheal tubes of ttkD2-50 mutants are thicker and more convoluted compared to wild-type. The diameter of the largest part of the dorsal trunk is 25% wider in mutants than control embryos.

ttkD2-50 mutant embryos display defects in tracheal cuticle deposition. Taenidia (the regular ridges which decorate the luminal cuticle) are irregular in shape, size and pattern. The material filling the taenidia (procuticle) is disorganised, discontinuous, and frequently contains inclusions of electron-dense material. The larval epidermal cuticle is also affected in ttkD2-50 mutant animals.

Embryonic CNS axon phenotype of fused segmental commissures, no distinct anterior or posterior commissures can be detected. Longitudinal axon tracts appear thinner and are found closer to the midline. The segmental and intersegmental nerves contain more sensory axons due to cell fate transformations in the PNS. The exit glial cell cells are slightly enlarged but are still able to ensheath both the segmental and intersegmental axon bundles.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Phenotype Manifest In
Additional Comments
Genetic Interactions

The partial lethality due to runScer\UAS.cLa; Scer\GAL4nos.PG (3% viable) is partially suppressed by maternal heterozygosity for ttkD2-50 (rescues to 8% viable).

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

Expression of ttkp69.Scer\UAS under the control of Scer\GAL4twi.PB and Scer\GAL4how-24B partially rescues the muscle morphology defects of ttkD2-50 mutants.

Expression of ttkp69.Scer\UAS under the control of Scer\GAL4btl.PS in ttkD2-50 mutant animals rescues the tracheal intercalation defects. Terminal branch fusion defects of the lateral trunk are also rescued in these animals.

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    References (5)