FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\trk1
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General Information
Symbol
Dmel\trk1
Species
D. melanogaster
Name
FlyBase ID
FBal0017039
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
trkRA, trkRA41
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Nucleotide substitution: G?A.

Amino acid replacement: W211term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G10271550A

Reported nucleotide change:

G?A

Amino acid change:

W220term | trk-PA

Reported amino acid change:

W211term

Comment:

TGG to TGA; difference between reported and annotated amino acid number is due to authors using M10 as the start Met.

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 derived from homozygous females show deletion of posterior structures (abdominal segment 8 and Filzkorper).

Denticle belts posterior to the seventh abdominal segment and the Filzkorper are missing in trk1 mutants.

Defective in gonad assembly.

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

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.

Interacts with RpII140wimp maternal effect.

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 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.

Loss of supraoesophageal ganglion and dorsal shift in the position of the suboesophageal ganglion.

A single tor11D allele variably suppresses the phenotype caused by trk1 in embryos derived from females homozygous for trk1 and heterozygous for tor11D, depending on the temperature.

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).

In the anterior labral and acronal derivatives are missing. Significant reduction in size of supraoesophageal ganglion. In the posterior ectodermal and endodermal structures are affected.

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).

embryos from homozygous mothers lack anterior-most head structures and structures posterior to the seventh abdominal segment. At gastrulation cephalic furrow is shifted toward anterior and the germband extends all the way to the posterior end. During cellularization at the blastoderm stage a funnel of yolk free cytoplasm containing a small number of nuclei (between 10 and 30) forms at the posterior pole of the embryos extending from the egg periphery to the inner yolk mass. Analysis of germ-line clones indicates that the mutation is germ-line autonomous (Schupbach and Wieschaus, 1986).

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

trk1 is a suppressor of embryonic segment phenotype of tsltor.PF

Other
Additional Comments
Genetic Interactions
Statement
Reference

phlHsp83.PD partially restores abdominal segment 8 denticle belts in embryos derived from homozygous trk1 females.

phlΔN114.Hsp83 does not rescue abdominal segment 8 denticle belts in embryos derived from homozygous trk1 females.

The missing denticle belt and Filzkorper cuticle structures are partially restored in trk1 mutants by PtthScer\UAS.cMa overexpression driven by Scer\GAL4nos.UTR.T:Hsim\VP16.

Cuticles made by embryos from trk1+ ; tor11D/+ mothers embryos occasionally lack one abdominal segment.

The segmentation defects seen in embryos from cic1 homozygous are enhanced if the mothers are also trk1/+; tor11D/+.

Embryos from trk1 females carrying tsltor.PF show no rescue of the trk1 phenotype and do not show deletions of the middle segments ("splice" phenotype seen in wild-type embryos carrying tsltor.PF).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments

Homozygous embryos exhibit terminal patterning defects, these can be fully rescued by trk+t3004.

Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer
Comments
Comments

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

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (29)