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General Information
Symbol
Dmel\tkv4
Species
D. melanogaster
Name
FlyBase ID
FBal0016821
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
tkva12
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G5220196A

Amino acid change:

W530term | tkv-PA; W498term | tkv-PB; W542term | tkv-PC; W476term | tkv-PD

Reported amino acid change:

W476term

Comment:

G to A nucleotide change at the second or third position of the wild type Trp codon leads to a nonsense mutation (exact site of mutation unspecified). The mutation was annotated at the second base of the codon.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: W476term.

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 ( 1 )
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

Eight days after induction of intestinal stem cell (ISC) clones, the number of cells in tkv4 mutant clones is significantly higher than in wild-type clones. After injury by feeding bleomycin, mutant clones have more cells than both wild-type clones and mutant clones before injury.

In tkv4 heterozygous mutants, the L2 wing vein position is slightly farther from the anterior-posterior boundary than in wild-type flies, consistent with the position of the anterior pMad peak in tkv4 heterozygotes.

tkv4 clones generated in larval histoblast cells display reduced contact to the nest edge, and typical histoblast invasive behaviour is not observed. Mutant histoblasts proliferate at normal rates and do not delaminate or die.

Homozygous clones in the eye disc are rarely recovered. Cells in homozygous clones that are recovered and which straddle the morphogenetic furrow can constrict apically and shorten along their apicobasal axis and form an apparently normal morphogenetic furrow (although it is occasionally delayed compared to neighbouring wild-type cells).

Wing disc clones of tkv4 have poor viability.

Clones of tkv4 homozygous cells in the pupal retina have defects in the apical profiles and packing of secondary pigment cells relative to tertiary pigment cells. Single, isolated tkv4 homozygous secondary pigment cells in the pupal retina have a restricted apical profile compared to neighbouring wild-type inter-ommatidial cells which expand apically to fill the unoccupied space.

Homozygous clones in the wing disc extrude from the wing epithelium.

tkv4 clones generated in the wing pouch area of the wing disc undergo apoptosis.

Mutant embryos have breaks of variable width and position in the visceral mesoderm. Defects in salivary gland migration are seen.

Homozygous clones do not survive in the wing pouch of the wing disc but can survive in the notum region of the wing disc.

Homozygous germ line clones (either germ line stem cells or spermatocytes) are generated in the testis, but they do not persist to the same extent as wild-type control clones.

Homozygous clones generally fail to develop in the distal and medial wing blade. Round vesicles of invaginated tissue, which may be formed by homozygous clones, are sometimes present in flies in which clones have been induced. Homozygous clones are readily found in the costa and alula region.

Homozygous clones do not survive in the wing pouch.

Clones in the imaginal disc anterior to the morphogenetic furrow have no detectable phenotype. Clones posterior to the furrow are also normal demonstrating the furrow can progress normally through and beyond a mutant clone. Within clones traversing the furrow neuronal differentiation is retarded, slowing of the furrow is more marked in the middle of the clone suggesting partial rescue by surrounding wild type tissue. Clones at the posterior or lateral margins of the eye discs act as absolute barriers to neuronal differentiation. Clones on the posterior margin can cause autonomous overproliferation.

Mutant clones induced up to the beginning of third instar development are dramatically under-represented in the wing. Clones generated 60 hrs AEL and 72 hrs AEL are observed exclusively in the most peripheral regions of the blade, the costa and the alula and neighboring region. These clones cause no mutant phenotype. No clones are induced in the wing blade proper. When induced 84 hrs AEL (early third instar), mutant wing clones are still dramatically under-represented, though regularly seen in the alula and costa. Clones also appear between L5 and the posterior margin and occasionally between L4 and the posterior margin. Clones induced 60 hrs AEL are never observed in the wing blade of the L3 wing disc, though they are present in all other regions. Clones induced 84hrs AEL are observed in the entire wing disc, and are of wild type size. These clones cannot undergo proper differentiation. Wing clones induced in mid-to-late third instar larvae are small due to their late induction time but cause visible mutant phenotypes: gaps, splits, vein indentations and additional vein material abutting normal veins. Wing veins are lost when the clone lies on the dominant, protruding, side of the vein. Cells at the edge on the clone are sometimes able to form vein material, reminiscent of the phenotypes of the "loss of vein" class of genes.

Mosaic studies show that embryos with a paternally supplied tkv+ are partially ventralized, similar to dpphr56 embryos. Embryos lacking both maternal and zygotic tkv differentiate rings of ventral denticle belts around the entire dorsoventral axis. No dorsal hairs are evident and dorsolateral as well as lateral pattern elements are missing. Remnants of telson and abdominal segments 7 and 8 are internalized, and reduced to a narrowed tube. These embryos are indistinguishable from dppH61 embryos.

Homozygotes display dorsally open cuticle, severe defective head and contracted epidermis giving the cuticle a rounded appearance. Lethal when heterozygous with tkv6. Female transheterozygotes with tkv1 are viable and display a wing phenotype, wing veins are very thick and short along the proximal distal axis, transheterozygotes with Df(2L)tkv3 display extremely thickened wing veins. Adult Df(2L)tkv3/tkv4 females lay eggs, some of the embryos from these females crossed to wild type males die showing a weakly ventralised phenotype.

Viable with strong tkv phenotype over Tp(2;3)tkv (Szidonya and Reuter, 1988). homozygous lethal

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhancer of
Statement
Reference

tkv4/tkv[+] is a non-enhancer of wing phenotype of MoeC858

NOT Suppressor of
Statement
Reference

tkv4/tkv[+] is a non-suppressor of wing phenotype of MoeC858

tkv4 is a non-suppressor of eye phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa

tkv4 is a non-suppressor of wing vein phenotype of dpps1

tkv4 is a non-suppressor of wing vein phenotype of dpps5

Other
Additional Comments
Genetic Interactions
Statement
Reference

Loss of the anterior crossvein is seen in 40% of tkv4 Df(2R)en-SFX31 double heterozygous flies.

Expression of cbtScer\UAS.cRa under the control of Scer\GAL4Act.PU in tkv4 clones rescues the low cell viability seen in single mutant tkv4 clones.

24 hours after induction of tkv4, Df(2L)flp147E double mutant clones in the second instar larval stage, mutant wing disc cells show apical constriction and shortening along their apical-basal axis compared with neighbouring control cells. At 26-60 hours after clone induction, mutant cells are further shortened, and are part of a deep epithelial invagination. Mutant cells have normal apical-basal polarity. At 60 hours after clone induction, some mutant cells are confined to the basal portion of the epithelium, and these extruded mutant clones have an internal lumen. Other clones show extrusion and no internal lumen.

tkv4, Df(2L)flp147E double mutant clones generated in the prospective wing hinge region of the wing disc display epithelial invaginations.

Cells in smo3 tkv4 double homozygous clones straddling the morphogenetic furrow fail to constrict apically and do not shorten along their apicobasal axis, failing to form a morphogenetic furrow.

Expression of Cad86CScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PP in smo3 tkv4 double homozygous clones in the region of the morphogenetic furrow can result in the formation of an epithelial invagination in some cases. Cells at the centre of this invagination are shorter along their apicobasal axis compared to smo3 tkv4 double homozygous clones or to wild-type cells within the morphogenetic furrow.

The wing defects seen in Moec858 homozygotes are unnaffected by tkv4/+.

As tkv4 clones in the wing pouch do not survive due to apoptosis, and bskflp147E single mutant clones show no segregation defects in the wing, tkv4 bskflp147E clones can be used to study whether tkv4 affects segregation of cells at the A/P boundary. The majority of bskflp147E tkv4 clones of A origin in contact with the A/P boundary of the wing disc are misplaced into the P territory, causing a displacement of the A/P compartment boundary toward P. However, clones of P origin remain in the P compartment.

The frequency of recovery of tkv4 bskflp147E double mutant clones (induced during the first larval instar) in the wing disc pouch of late-third instar larvae is only 24% compared to sibling wild-type clones, probably due to the formation of cyst-like structures followed by extrusion from the basal side of the epithelium. The double mutant clones are shorter along their apical-basal axis than normal, have lost contact to the apical epithelial surface and form cyst-like structures with the apical cell membranes facing the centre of the clone instead of the disc lumen. F-actin is enriched at the centre of the double mutant clones, whereas a dense apical network of microtubules, which is present in wild-type cells, is markedly reduced. Basal microtubules appear normal. Some tkv4 bskflp147E double mutant clones are seen in adult wings, as extruded cyst-like structures located between the dorsal and ventral wing surfaces. These mutant cells display hairs, characteristic structures of the adult epithelium, indicating that the extruded cells have undergone differentiation.

tkv4 heterozygosity does not reduce animal size when dallysec.Scer\UAS.T:Hsap\MYC is driven by Scer\GAL429BD.

Embryos doubly mutant for rib1 and tkv4 form only the transverse connectives and visceral branches.

tkv4, tkv5, tkv7, tkv427 and Df(2L)tkv2 fail to complement dpp short vein alleles for the wing vein defect.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (4)
Notes on Origin
Discoverer

Szidonya.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (56)