FB2024_03 , released June 25, 2024
Allele: Dmel\tkv5
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General Information
Symbol
Dmel\tkv5
Species
D. melanogaster
Name
FlyBase ID
FBal0016822
Feature type
allele
Associated gene
Dmel\tkv
Associated Insertion(s)
Carried in Construct
Also Known As
tkva33
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

loss of function allele

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Singer et al., 1997, Terracol and Lengyel, 1994)

loss of function allele

(Horsfield et al., 1998)
Mutagen
ethyl methanesulfonate
(Terracol and Lengyel, 1994)
Progenitor genotype
Cytology
Description

Amino acid replacement: W404term.

(Penton et al., 1994)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2L:5,220,412..5,220,412 [-]
Nucleotide change:

G5220412A

Amino acid change:

W458term | tkv-PA; W426term | tkv-PB; W470term | tkv-PC; W404term | tkv-PD

Reported amino acid change:

W404term

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.

(Penton et al., 1994)
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
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      77% of tkv5 null peripodial wing dsic cell clones induced at 48hr after egg laying do not survive to the late third instar. 78% of clones induced at 55hr AEL were eliminated. Surviving clones show abnormal cell size, clone size and morphology. Surviving clones are more common in presumptive hinge and notum regions than in wing blade. 67% of tkv5 mutant cell clones are eliminated from the eye peripodial epithelium.

      (Gibson et al., 2002)

      Clones in the eye reveal that lack of dpp signalling allows cells that are posterior to the morphogenetic furrow to continue cycling asynchronously as if they were anterior to the furrow. Furrow progression is delayed in mutant clones.

      (Horsfield et al., 1998)

      Clones induced in the developing eye at the anterior edge of the morphogenetic furrow show mislocalized nuclei, they fail to reach the apical surface where mitosis normally takes place. Nuclei are also misplaced when the clone is within the furrow and posterior to it. Cell fate specification is not, however, affected.

      (Penton et al., 1997)

      Clones induced in the wing during second larval instar are rarely recovered even in the late third instar wing pouch. Those that are observed consist of two to four cells. Clones can be recovered more readily in the notum and hinge regions.

      (Singer et al., 1997)

      Produces a higher number of clones and larger clones than put135. Clones induced in 2nd instar larvae that arose in ventral regions or were proximal to the distal tibia have no effect on bristle pattern. However clones close on the extreme dorsal surface of distal leg segments show a loss of dorsal structures, duplication of ventral structures and dorsal bifurcations. Duplicated structures frequently contain wild-type bristles. Clones in adult wings cause reduced wing size, ectopic vein formation, blisters and ectopic wing margin structures.

      (Penton and Hoffmann, 1996)

      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, portions of veins and crossveins are lost.

      (Terracol and Lengyel, 1994)

      homozygous lethal

      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressor of
      Statement
      Reference

      tkv5/tkv[+] is a suppressor of visible phenotype of Scer\GAL4A9, gbbUAS.cKa

      (Bangi and Wharton, 2006)

      tkv5/tkv[+] is a suppressor of visible phenotype of Scer\GAL4A9, dppUAS.cHa

      (Bangi and Wharton, 2006)
      Phenotype Manifest In
      Suppressor of
      Statement
      Reference

      tkv5/tkv[+] is a suppressor of wing vein phenotype of Scer\GAL4A9, gbbUAS.cKa

      (Bangi and Wharton, 2006)

      tkv5/tkv[+] is a suppressor of wing phenotype of Scer\GAL4A9, dppUAS.cHa

      (Bangi and Wharton, 2006)
      NOT Suppressor of
      Statement
      Reference

      tkv5 is a non-suppressor of wing vein phenotype of dpps1

      (Penton et al., 1994)

      tkv5 is a non-suppressor of wing vein phenotype of dpps5

      (Penton et al., 1994)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

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

      (Penton et al., 1994)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      tkv8/tkv5 is rescued by tkvUAS.YFP/Scer\GAL4arm.PS

      (Smith et al., 2012)

      tkv5 is rescued by tkvBrk25D1

      (Kim et al., 1996)
      Comments

      Mutant clones in the wing pouch do not survive beyond the two cell stage, whereas those outside the wing pouch grow well. The cell viability can be rescued by a tkv+ transgene (Q1A-8) that rescues cell viability.

      (Kim et al., 1996)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer

      Szidonya.

      Comments
      Comments

      Null allele.

      (Horsfield et al., 1998)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      References (15)