FB2024_03 , released June 25, 2024
Allele: Dmel\tor1
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General Information
Symbol
Dmel\tor1
Species
D. melanogaster
Name
FlyBase ID
FBal0016909
Feature type
allele
Associated gene
Dmel\tor
Associated Insertion(s)
Carried in Construct
Also Known As
torWK, torWK34
Key Links
Genomic Maps

Allele class

loss of function allele

Mutagen
Nature of the Allele
Allele class

loss of function allele

(Sprenger et al., 1993, Sprenger and Nusslein-Volhard, 1992)
Mutagen
ethyl methanesulfonate
(Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Amino acid replacement: M522K.

(Sprenger et al., 1993, Sprenger and Nusslein-Volhard, 1992)

Met at residue 522 (in the tyrosine kinase domain) replaced by Lys.

(Sprenger and Nusslein-Volhard, 1992)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2R:7,706,865..7,706,865 [-]
Nucleotide change:

T7706865A

Reported nucleotide change:

T?A

Amino acid change:

M522K | tor-PA; M517K | tor-PD

Reported amino acid change:

M522K

(Sprenger and Nusslein-Volhard, 1992)
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

      Embryos from tor1/tor2 transheterozygous mothers do not display any obvious defect in primordial germ cell formation, as compared to controls.

      (Pae et al., 2017)

      Neural activity in tore00150/tor1 mutant class IV da neurons show a reduction in response to blue light (470 nm) illumination compared with controls. This is accompanied by a loss of larval light avoidance.

      (Yamanaka et al., 2013)

      Suppresses "splice" phenotype of torNRE, presumably because product is appropriately positioned to block diffusion of the tor ligand, even though it cannot transduce the terminal signal.

      (Casanova and Struhl, 1993)

      In tor1 trk1 embryos little or no tll expression is detected in the posterior of syncytial or cellular blastoderm embryos, at the anterior the early tll cap does not appear and an abnormal anterior tll stripe appears by the late syncytial blastoderm.

      (Pignoni et al., 1992)

      Does not interact with RpII140wimp maternal effect.

      (Parkhurst and Ish-Horowicz, 1991)

      Embryos derived from tor1, trk1 females lack A8 and filzkorper. Filzkorper are formed and segmentation is repressed in heat shocked embryos carrying tllhs.PS and derived from tor1, trk1 females.

      (Steingrimsson et al., 1991)

      Embryos carrying the hbΔ transcripts do not express kni and form no abdominal segments.

      (Wharton and Struhl, 1991)

      A hole is seen in the blastoderm layer below the pole cells in embryos. The ventral furrow is extended posteriorly. Segments A8 to the telson are deleted. Segments A5 to A7 are expanded. Some twisting of the germband is seen. Labral and acron-derived structures are deleted. There is cell death in the head and tail region. Cephalic furrow and anterior midgut invagination are shifted anteriorly.

      (Ambrosio et al., 1989)

      The anteriormost and posteriormost structures are lacking and the anterior pattern is shifted anteriorly. tor embryos display normal levels of bcd protein.

      (Driever and Nusslein-Volhard, 1988)

      Embryos derived from homozygous females lack the most anterior and posterior structures; the head skeleton is smaller than normal and the Filzkorper, anal plate and spiracles are missing.

      (Lehmann, 1988)

      Homozygous females produce embryos which have deletions of the most anterior head structures (labrum and chitinous mouth plates), and the most posterior abdominal structures (posterior midgut, telson and abdominal segment A8).

      (Schupbach and Wieschaus, 1986)

      recessive

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

      tor1 is a non-suppressor of phenotype of arm3

      (Cox et al., 2000)
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      tor1 is rescued by tor+t11.5

      (Cleghon et al., 1996)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (4)
      Notes on Origin
      Discoverer

      Wieschaus, Nusslein-Volhard.

      Comments
      Comments

      Germline mosaic analysis shows that tor is required in the germline.

      (Schupbach and Wieschaus, 1986)

      Transplantation of wild-type anterior cytoplasm into the anterior end of embryos derived from homozygous tor1 females can rescue the mutant anterior structures. Transplantation of wild-type posterior cytoplasm into the posterior end of embryos derived from homozygous tor1 females can rescue the mutant posterior structures. Cytoplasm transplanted from tor4 mutant donors has no rescuing effect.

      (Sugiyama and Okada, 1990)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (7)
      References (32)