Open Close
General Information
Symbol
Dmel\tor4
Species
D. melanogaster
Name
FlyBase ID
FBal0016912
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
torpm, torPM51
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G7707034A

Reported nucleotide change:

G?A

Amino acid change:

A485T | tor-PA; A480T | tor-PD

Reported amino acid change:

A485T

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

Ala at residue 485 (in the tyrosine kinase domain) replaced by Thr.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Pupariation is delayed in tor4 mutant larvae.

Embryos derived from tor4 females lack structures posterior to the 7th abdominal segment and the head regions are missing.

The stomatogastric nervous system, epiphysis, dorsopharyngeal organ and pharyngeal chordotonal organ are absent. Other sensory organs of the head develop normally. The brain hemispheres and optic lobes are fused medially.

Oesophagus, stomatogastric nervous system, labral nerve, epiphysis, dorsopharyngeal organ and pharyngeal monoscolopidial chordotonal organ are deleted.

Defective in gonad assembly when homozygous and in double mutant combination with dl.

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.

Terminal structures are missing, abdominal segment 7 is the posterior-most point, head skeleton is collapsed.

Posterior defect is significantly suppressed, in a dose-dependent manner, by Dsor1Su1.

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.

Dorsalized embryos: all cuticle cells along the dorsoventral axis behave like dorsal cells of the wild type embryo. zen expression pattern refines at stage 5, dpp pattern does not refine at all, twi and sna are expressed during late stages of embryogenesis. Differentiated embryos lack the labrum, head skeleton is reduced in size and all structures posterior to the seventh abdominal segment are deleted.

Embryos derived from homozygous tor4 females lack the median tooth of the labrum and the pharyngeal arms of the head skeleton are variably reduced. All structures posterior to abdominal segment 7 are absent.

Eggs derived from homozygous females cellularise normally but become abnormal at gastrulation; the cephalic furrow is shifted forward, the posterior midgut is missing and the germband forms to the posterior end of the embryo. The embryos lack anterior head structures and structures posterior to segment A7 (the labral segment and telson).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference

tor4 has phenotype, suppressible by Dsor1Su12

tor4 has phenotype, suppressible by Dsor1Su18

tor4 has phenotype, suppressible by Dsor1Su1

tor4 has phenotype, suppressible by Dsor1Su24

tor4 has phenotype, suppressible by Dsor1Su4

tor4 has phenotype, suppressible by Dsor1Su5

tor4 has phenotype, suppressible by Dsor1Su6

tor4 has phenotype, suppressible by Dsor1Su7

Additional Comments
Genetic Interactions
Statement
Reference

The posterior defect, but not the anterior defect, of embryos derived from tor4 females is variably suppressed by Dsor1Su1, Dsor1Su4, Dsor1Su5, Dsor1Su6, Dsor1Su7, Dsor1Su12, Dsor1Su18 and Dsor1Su24.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Schupbach, Wieschaus.

Comments
Comments

Transplantation of wild-type anterior cytoplasm into the anterior end of embryos derived from homozygous tor4 females can rescue the mutant anterior structures. Transplantation of wild-type posterior cytoplasm into the posterior end of embryos derived from homozygous tor4 females can rescue the mutant posterior structures. Rescuing activity decreases with age of both donor and host. Anterior wild-type cytoplasm cannot rescue posterior defects, and vice versa. Cytoplasm transplanted from tor4 mutant donors has no rescuing effect. Anterior cytoplasm from bcd6 mutant embryos and posterior cytoplasm from nosL7 mutant embryos can rescue both anterior and posterior defects when transplanted into the anterior or posterior end of tor4 mutant embryos.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (58)