FB2025_01 , released February 20, 2025
Allele: Dmel\torrv66
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General Information
Symbol
Dmel\torrv66
Species
D. melanogaster
Name
FlyBase ID
FBal0016988
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
torXR1
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

10.5kb deletion encompassing the tor gene.

9.5 kb deletion.

9.5kb deletion within the tor locus.

9.5 kb deletion

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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 from torrv66 homozygous mothers exhibit a fully penetrant posterior "terminal class mutant" phenotype by the end of embryogenesis, in which some posterior structures are missing (including abdominal segment 8, telson, and/or filzkorper), but do not exhibit any obvious defects in ventral cells during ventral furrow formation, as compared to controls.

torrv66 mutant homozygotes show a significant delay in reaching pupariation compared with heterozygous controls. The L2-L3 transition is delayed by ~7 hours. Adult flies are increased in size compared to controls.

Embryos derived from homozygous females lack the abdominal segment 8 denticle belts.

torrv66 partially suppresses the cuticle defects seen in embryos derived from tor12D/+ females.

Embryos derived from torrv66 homozygous mothers show defective gastrulation and completely lack the posterior midgut primordium. In contrast to wild-type pole cells that are internalized during gastrulation, pole cells from the vast majority of these embryos do not enter the embryo at gastrulation and are left outside. In wild-type embryos, pole cells become spherical as they start migrating at stage 4, then become elongated after cellularization and start to move out of the pole cell cluster. Pole cells in embryos derived from torrv66 mothers do become spherical at stage 4, suggesting that they start to migrate, but then remain this shape and stay in a tightly-packed cluster without further movement. Pole cells from cellularization stage torrv66 embryos hardly disperse and are slow in translocation movements when observed in Schneider culture medium, while pole cells from wild-type embryos are more active in both dispersion and translocation. torrv66 mutant soma can provide a normal environment for pole cell migration as transplanted wild-type pole cells can successfully migrate to the somatic gonad in torrv66 host embryos.

Embryos from homozygous females lack terminal structures.

All structures posterior to abdominal segment 7 fail to develop.

In embryos from homozygous mothers no PMG is formed though the AMG and visceral mesoderm form normally. The AMG migrates far into the posterior of the embryo, well beyond the point that the PMG would have migrated to, were it to be present, and makes its transition to an epithelium.

Embryos derived from homozygous females fail to form a posterior midgut.

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.

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

The ventral furrow extends over the whole length of the embryo in embryos derived from torrv66 homozygous females.

Embryos derived from homozygous females lack the labrum anteriorly, and the head is reduced in size. Posteriorly, A8 and the telson are deleted.

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

torrv66 has abnormal size phenotype, suppressible by tslΔ

Enhancer of
Statement
Reference
NOT Suppressor of
Statement
Reference

torrv66 is a non-suppressor of abnormal size phenotype of tslΔ

Phenotype Manifest In
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Suppressor of
NOT Suppressor of
Statement
Reference

torrv66 is a non-suppressor of phenotype of cic1

Other
Additional Comments
Genetic Interactions
Statement
Reference

The patterning and cuticle defects exhibited by late embryos from torrv66 homozygous mothers are enhanced by the zygotic hemizygosity for fogS4, as the embryos additionally miss head structures and exhibit a penetrant posterior-ventral cuticle hole phenotype, as compared to controls.

tslΔ torrv66 double mutants show a dramatically extended larval period compared to either mutant alone, with flies pupating 83 hours after controls. Double mutant adult flies are similar in size to tslΔ mutants alone.

The lack of the abdominal segment 8 denticle belts seen in embryos derived from homozygous torrv66 females is not rescued by either phlHsp83.PD or phlΔN114.Hsp83.

The phenotype of embryos derived from homozygous cic1 females is not altered if the females are also homozygous for torrv66.

Embryos derived from torrv66 females carrying tsltor.PF show no rescue of the torrv66 phenotype and do not show deletions of the middle segments ("splice" phenotype seen in wild-type embryos carrying tsltor.PF).

Animals doubly mutant for phlSu3 and torrv66 are completely non-viable and resemble torrv66 mutants.

Overexpression of 14-3-3ζhs.PL partly rescues the cuticle of embryos derived from torrv66 females.

Xenogenetic Interactions
Statement
Reference

Heat induced expression of Hsap\RAF1Δ305.hs in torrv66 embryos deletes the middle body segments. 5-20% embryos also show terminal structures.

Complementation and Rescue Data
Rescued by
Comments

Mutant phenotype can be rescued by injection of a mammalian activated p21ras, p21v-ras.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Klingler.

Revertant.

Comments
Comments

Used to eliminate tor expression from endogenous tor gene in studies on consequences of ectopic expression of tor.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (38)