|Feature type||allele||Associated gene||Dmel\ttk|
|Also Known As||ttklell, ttkle11|
|Map ( GBrowse )|
|Allele class||loss of function allele, amorphic allele - genetic evidence, hypomorphic allele - genetic evidence|
|Mutagen||Js, P-element activity|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
comment=Position of mutation on reference sequence inferred by FlyBase curator based on author statement. See Figure 4 of FBrf0155483. Mutation is a deletion of 1.7kb of 3' P-element and 0.8kb of flanking genomic DNA that encodes the zinc fingers in the ttk p69 protein according to FBrf0058514.
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
The nuclei in homozygous follicle cell clones are more densely packed as compared to the surrounding wild-type tissue.
Cells derived from mosaic clones of ttk[1e11] do not participate in dorsal appendage morphogenesis. Mutant cells clump together, block surrounding cells, and occasionally split the dorsal appendage. Cells derived from mosaic clones of ttk[1e11] at S10B show dramatic apical constriction of normally cuboidal cells. Basal surfaces of mutant cells are slightly shrunken and rounder than control cells, but far larger than their apical surfaces. Mutant nuclei are more closely packed at later stages of oogenesis, but this effect is not pronounced at early stages. Cells derived from mosaic clones of ttk[1e11] are taller than control cells.
ttk[1e11] mutant eye clones display severe degeneration of the corneal lens, with ommatidia and sensory bristles failing to properly develop. In 87% of ttk[1e11] 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 are observed in mutant clones.
Follicle cells in ttk1e11 clones show a decrease in the size of cell nuclei and quantification of the number of cells in these clones compared to the number in their sister clones shows that on average they are twice as large, which implies that ttk1e11 mutant cells have undergone an extra round of mitotic division.
In mosaic egg chambers in which border cells retain ttk[+] function, border cell migration is completed normally. However, homozygous border cells show a severe migration defect and remain at the anterior tip of the stage 10 egg chamber. Homozygous centripetal cells appear to be delayed in their inward migration.
Only 40% of eggs laid by ttk1/ttk1e11 mothers are wild-type,, the rest exhibit a dorsal appendage phenotype, 3% having only the nub of an appendage.
Glia undergo ectopic rounds of replication in mutant embryos. Stage 12 embryos have 17.8 +/- 2.23 glia associated with the longitudinal connectives (compared to 9.9 +/- 0.76 in wild-type 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. In homozygous clones in the developing pupal eye, some cone cells failed to develop. Photoreceptors appear normal even up to midpupal stage.
The number of lch5 neurons is approximately doubled in homozygous embryos.
Neurons and sheath cells of es and ch organs are duplicated at the expense of support cells. There is no modification of md neurons, they are present in the normal number and pattern.
Embryonic development arrests before dorsal closure. Transformation of ommatidial cells into nonommatidial cell types in mosaic flies.
ttk[+]/ttk1e11 is a suppressor | maternal effect | partially of lethal | partially phenotype of Scer\GAL4nos.PG, runScer\UAS.cLa
|Phenotype Manifest In|
ttk[+]/ttk1e11 is an enhancer of adult abdominal segment 3 & tormogen cell | supernumerary phenotype of phyl2/phyl4
ttk[+]/ttk1e11 is an enhancer of adult abdominal segment 3 & trichogen cell | supernumerary phenotype of phyl2/phyl4
ttk[+]/ttk1e11 is an enhancer of adult abdominal segment 4 & tormogen cell | supernumerary phenotype of phyl2/phyl4
ttk[+]/ttk1e11 is an enhancer of adult abdominal segment 4 & trichogen cell | supernumerary phenotype of phyl2/phyl4
|NOT Enhancer of|
ttk[+]/ttk1e11 is a suppressor of mesothoracic tergum & tormogen cell | supernumerary phenotype of phyl2/phyl4
|NOT Suppressor of|
The eye phenotype observed in ttk[1e11] clones is partially suppressed in a lz[mr2] mutant background. Ommatidial structures and sensory bristles are present, and the eye appears less scarred. No recruitment of R7 precursor cells is observed when ttk[1e11] mutant cells are generated in a lz[77a7] background.
The addition of ttk1e11/+ to h41/+ animals does not lead to a significant ectopic wing margin bristle phenotype.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
|Stocks ( 3 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 6 )|
|Secondary FlyBase IDs|
|References ( 34 )|
|Generate a list of|
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|Recent research papers ( 3 )|