|Feature type||allele||Associated gene||Dmel\tor|
|Also Known As||torWK, torWK34|
|Map ( GBrowse )|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: M522K.
Met at residue 522 (in the tyrosine kinase domain) replaced by Lys.
|Phenotype Manifest In|
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.
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.
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.
Embryos carrying the hbΔ transcripts do not express kni and form no abdominal segments.
A hole is seen in the blastoderm layer below the pole cells in embryos. The ventral furrow is extended posteriorly. Segments A8 to the telson are deleted. Segments A5 to A7 are expanded. Some twisting of the germband is seen. Labral and acron-derived structures are deleted. There is cell death in the head and tail region. Cephalic furrow and anterior midgut invagination are shifted anteriorly.
The anteriormost and posteriormost structures are lacking and the anterior pattern is shifted anteriorly. tor embryos display normal levels of bcd protein.
Embryos derived from homozygous females lack the most anterior and posterior structures; the head skeleton is smaller than normal and the Filzkorper, anal plate and spiracles are missing.
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).
|Phenotype Manifest In|
|NOT Suppressor of|
|Complementation & Rescue Data|
|Stocks ( 4 )|
|Notes on Origin|
Transplantation of wild-type anterior cytoplasm into the anterior end of embryos derived from homozygous tor1 females can rescue the mutant anterior structures. Transplantation of wild-type posterior cytoplasm into the posterior end of embryos derived from homozygous tor1 females can rescue the mutant posterior structures. Cytoplasm transplanted from tor4 mutant donors has no rescuing effect.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
(Hartmann et al., 2001, Gao et al., 1996, Cleghon et al., 1996, Sprenger and Nusslein-Volhard, 1993, Sprenger et al., 1993, Pignoni et al., 1992, Sprenger and Nusslein-Volhard, 1992, Struhl et al., 1992, Steingrimsson et al., 1991, Wharton and Struhl, 1991, Sugiyama and Okada, 1990, Hooper et al., 1989, Lehmann, 1988, Driever and Nusslein-Volhard, 1988, Tearle and Nusslein-Volhard, 1987, Schupbach and Wieschaus, 1986, )
|Secondary FlyBase IDs|
|References ( 27 )|
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|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|