A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\torrv66

General Information
SymbolDmel\torrv66SpeciesD. melanogaster
NameFlyBase IDFBal0016988
Feature typealleleAssociated geneDmel\tor
Also Known AstorXR1
Allele classloss of function allele, amorphic allele - genetic evidence
Mutagenethyl methanesulfonateX ray
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
10.5kb deletion encompassing the tor gene.
9.5 kb deletion.
9.5kb deletion within the tor locus.
9.5 kb deletion
 
Cytology
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Statement
Reference
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.
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Statement
Reference
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Statement
Reference
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Statement
Reference
torrv66 is a suppressor of embryonic segment phenotype of tsltor.PF
hideNOT Suppressor of
Statement
Reference
torrv66 is a non-suppressor of phenotype of cic1
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Statement
Reference
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Statement
Reference
The lack of the abdominal segment 8 denticle belts seen in embryos derived from homozygous tor[rv66] females is not rescued by either phl[Hsp83.PD] or phl[ΔN114.Hsp83].
Filzkorper are not seen in embryos laid by torrv66 females when trkC-108.T:ea RNA is injected into the posterior pole.
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.
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Statement
Reference
Heat induced expression of Hsap\RAF1Δ305.hs in torrv66 embryos deletes the middle body segments. 5-20% embryos also show terminal structures.
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Rescued by
Comments
Mutant phenotype can be rescued by injection of a mammalian activated p21ras, p21v-ras.
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Discoverer
Klingler.
Revertant.
 
hide Comments
Used to eliminate tor expression from endogenous tor gene in studies on consequences of ectopic expression of tor.
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hide Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym
torrv66
 
Name Synonym
Secondary FlyBase IDs
hide References ( 34 )
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hide Recent research papers ( 1 )
Grillo et al., 2012, Sci. Rep. 2: 762
Conserved and divergent elements in Torso RTK activation in Drosophila development. [FBrf0219757]
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All reviews listed in FlyBase were published before 2011