|Feature type||allele||Associated gene||Dmel\tor|
|Also Known As||torXR1|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
|Mutagen||ethyl methanesulfonate, X ray|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
9.5 kb deletion.
9.5 kb deletion
|Phenotype Manifest In|
Embryos derived from homozygous females lack the abdominal segment 8 denticle belts.
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.
|Phenotype Manifest In|
|NOT suppressed by|
torrv66 has abdominal 8 ventral denticle belt | maternal effect phenotype, non-suppressible by phlHsp83.PD
|NOT Suppressor of|
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.
|Complementation & Rescue Data|
Mutant phenotype can be rescued by injection of a mammalian activated p21ras, p21v-ras.
|Stocks ( 0 )|
|Notes on Origin|
Used to eliminate tor expression from endogenous tor gene in studies on consequences of ectopic expression of tor.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
(Li et al., 2003, Martinho et al., 2004, Stevens et al., 2003, Li and Li, 2003, Casali and Casanova, 2001, Jimenez et al., 2000, Gayko et al., 1999, Li et al., 1998, Furriols et al., 1998, Li et al., 1997, Dahanukar and Wharton, 1996, Cleghon et al., 1996, Liaw et al., 1995, Hou et al., 1995, Casanova et al., 1994, Edgar et al., 1994, Reuter et al., 1993, Sprenger and Nusslein-Volhard, 1993, Klingler and Gergen, 1993, Liaw and Lengyel, 1993, Lu et al., 1993, Pignoni et al., 1992, Leptin et al., 1992, Sprenger and Nusslein-Volhard, 1992, Casanova, 1991, Wharton and Struhl, 1991, Stevens et al., 1990, Leptin and Grunewald, 1990, Sprenger et al., 1989, Driever et al., 1989, )
|Secondary FlyBase IDs|
|References ( 34 )|
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|Recent research papers ( 1 )|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|