FB2024_03 , released June 25, 2024
Allele: Dmel\tor11D
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General Information
Symbol
Dmel\tor11D
Species
D. melanogaster
Name
FlyBase ID
FBal0016919
Feature type
allele
Associated gene
Dmel\tor
Associated Insertion(s)
Carried in Construct
Also Known As
torRL3, torsplc, torsoRL3
Key Links
Genomic Maps

Allele class

loss of function allele

antimorphic allele - genetic evidence

hypermorphic allele - genetic evidence

gain of function allele

Mutagen
Nature of the Allele
Allele class

antimorphic allele - genetic evidence

(Tearle and Nusslein-Volhard, 1987)

gain of function allele

(Li et al., 2003, Yip et al., 1997, Perkins et al., 1996, Doyle and Bishop, 1993, Savant-Bhonsale and Montell, 1993, Sprenger and Nusslein-Volhard, 1992, Kraut and Levine, 1991, Strecker et al., 1991, Warrior and Levine, 1990, Ambrosio et al., 1989)

hypermorphic allele - genetic evidence

(Strecker et al., 1991, Casanova and Struhl, 1989)

loss of function allele

(Sprenger et al., 1993)
Mutagen
ethyl methanesulfonate
(Schupbach and Wieschaus, 1989, Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Single amino acid change in extracellular domain at amino acid 242: a leucine is substituted for a histidine.

(Casanova and Struhl, 1993)

Amino acid replacement: H242L.

(Sprenger et al., 1993, Sprenger and Nusslein-Volhard, 1992)

His at residue 242 (in the extracellular domain) replaced by Leu.

(Sprenger and Nusslein-Volhard, 1992)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2R:7,707,886..7,707,886 [-]
Nucleotide change:

A7707886T

Reported nucleotide change:

A?T

Amino acid change:

H242L | tor-PA; H242L | tor-PD

Reported amino acid change:

H242L

(Casanova and Struhl, 1993, Sprenger and Nusslein-Volhard, 1992)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      At 29[o]C, embryos derived from heterozygous females can hatch, but 7.4% of the larvae show deletion, fusion of broken abdominal denticle bands.

      (Ding et al., 2010)

      At 25[o]C, heterozygous tor11D animals pupariate 9.2 hours before controls and form smaller adult males.

      (Rewitz et al., 2009)

      Embryos produced by homozygous females at 22oC lack a segmented trunk region and fail to hatch.

      (Brunner et al., 1994)

      Expansion of terminal portions of the embryo at the expense of the middle body segments (see also Casanova, Genes Dev 3:2025 ): so-called "splice" phenotype.

      (Casanova and Struhl, 1993)

      Defects in the abdominal region but not at the termini. At 22oC embryos display between 5 and 8 abdominal denticle belts, have a normal head, telson structures and filzkorper. At 27oC most abdominal segments are deleted and embryos differentiate only terminal structures including spiracles, filzkorper, anal plates and anal tufts, but disorganised head skeletons.

      (Doyle and Bishop, 1993)

      Embryos are defective in the central segmented region. Dominant phenotype is enhanced by Dsor1Su1 and suppressed by a reduction in the gene dosage of Dsor1+.

      (Tsuda et al., 1993)

      Lack of csw activity suppresses the tor11D dominant spliced phenotype.

      (Perkins et al., 1992)

      At 25oC embryos have a complete loss of thoracic and abdominal structures, at 18oC a few embryos have normal segmentation and survive. tor11D suppresses early gap and segmentation gene expression.

      (Ambrosio et al., 1989)

      Embryos derived from homozygous females have a splice phenotype of greatly expanded terminal domains and few if any intervening body segments at 25-29oC. Embryos from heterozygous or hemizygous females often show a weak splice phenotype such as partial deletion of segments in the middle of the abdomen at 25-29oC. Embryos derived from females doubly homozygous for tor11D and either trk1 or tsl1 have a typical splice phenotype at 25oC. A single tor11D allele variably suppresses the phenotypes caused by trk1, tsl1, fs(1)N12 or fs(1)M31906 in embryos derived from females homozygous for ones of these alleles and heterozygous for tor11D depending on the temperature.

      (Casanova and Struhl, 1989)

      Eggs derived from homozygous females cellularise normally but become abnormal at gastrulation. At 23-25oC, no ventral furrow is formed, and instead at the time when the anlage of the posterior midgut is moving dorsally, the ventral cells from 2-50% egg length become very thin. The posterior midgut anlage initially assumes a normal shape, but it advances only to approximately 30% egg length and never closes off properly. The cephalic furrow and anterior midgut are not visible. Only one of the two "dorsal head clusters" in the anterior head region is formed. At 18oC, the embryos develop an almost normal cuticle pattern with the exception of small deletions and segmental fusions centered over the fourth abdominal segment. At 22oC, an intermediate phenotype is produced, where larger deletions of posterior head structures, thoracic segments and abdominal segments occur, leaving only irregular patches of intervening segments between the head and posterior abdominal segments. At 29oC an extreme mutant phenotype is seen, in which only head and telson structures form, whereas cuticle derived from the thorax and anterior abdomen are missing.

      (Schupbach and Wieschaus, 1989)

      temperature-sensitive semidominant

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

      tor11D has ventral denticle belt | maternal effect | heat sensitive phenotype, enhanceable by phl[+]/RafHsp83.PD

      (Ding et al., 2010)

      tor11D has ventral denticle belt | maternal effect | heat sensitive phenotype, enhanceable by phl[+]/RafΔN114.Hsp83

      (Ding et al., 2010)

      tor11D, trk[+]/trk1 has embryonic segment | maternal effect phenotype, enhanceable | maternal effect by cic1/cic[+]

      (de las Heras and Casanova, 2006)

      tor11D, trk[+]/trk1 has embryonic/first instar larval cuticle | maternal effect phenotype, enhanceable | maternal effect by cic1/cic[+]

      (de las Heras and Casanova, 2006)
      Suppressed by
      Statement
      Reference

      cic1/cic[+], tor11D, trk1 has embryonic segment | maternal effect phenotype, suppressible | maternal effect | partially by Stat92E[+]/Stat92E06346

      (de las Heras and Casanova, 2006)

      cic1/cic[+], tor11D, trk[+]/trk1 has embryonic/first instar larval cuticle | maternal effect phenotype, suppressible | maternal effect | partially by Stat92E[+]/Stat92E06346

      (de las Heras and Casanova, 2006)

      tor11D has phenotype, suppressible by Stat92E06346/Stat92E06346

      (Li et al., 2002)

      tor11D has phenotype, suppressible by rl1/rl10

      (Brunner et al., 1994)

      tor11D has phenotype, suppressible by Su(tor)1-1631

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)1-1134

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)1-119

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)1-1285

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)1-1352

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-1131

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-151

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-1801

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-187-11

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-187-31

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-1911

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by bowl17

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by bowl60

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by bowl85

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-2371

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-2781

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-2801

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-3211

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-3411

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-3991

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-31

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-3361

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-4081

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-481

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-4417

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-468

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-561

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-871

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)2-931

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-1681

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-138

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-142

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-2931

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-3071

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-3331

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-3371

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-3441

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-81

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)3-911

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by drke0A

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Ras85DSutor-341

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Ras85DSutor-404

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by SosSutor-157

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by SosSutor-405

      (Doyle and Bishop, 1993)

      tor11D has phenotype, suppressible by Su(tor)1-1061

      (Doyle and Bishop, 1993)
      Enhancer of
      Statement
      Reference

      trk[+], tor[+], trk1, tor11D is an enhancer of embryonic/first instar larval cuticle phenotype of cic1

      (de las Heras and Casanova, 2006)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Presence of tor11D/+ suppresses the delay in pupariation seen in Ilp8αTub84B.T:Zzzz\FLAG male flies.

      (Vallejo et al., 2015)

      The denticle belt phenotype seen in larvae derived from derived from tor11D/+ females at 29[o]C is enhanced by phlHsp83.PD (penetrance is increased to 31.8%) and, to a lesser degree, by phlΔN114.Hsp83 (penetrance is increased to 17.1%).

      (Ding et al., 2010)

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

      Cuticles made by embryos from cic1/+; trk1/+; tor11D/+ mothers exhibit major deletion of embryonic segments.

      The severe segment deletion phenotype visible in the cuticles made by embryos from cic1/+; trk1/+; tor11D/+ mothers is partially suppressed when those mothers are also Stat92E06346/+.

      (de las Heras and Casanova, 2006)

      The tor11D phenotype is enhanced by rlSu14, rlSu23 and Dsor1Su1; considerable numbers of embryos laid by females heterozygous for tor11D and rlSu14, rlSu23 or Dsor1Su1 fail to hatch at 28oC.

      (Lim et al., 1999)

      rl1/rl10 suppresses the mutant phenotype of embryos derived from tor11D mothers.

      (Brunner et al., 1994)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer

      Schupbach.

      Comments
      Comments

      See also Klinger, Nature 335:275 ; Strecker, Science 243:1062 ; Casanova, Genes Dev 3:2025 ). The tor11D allele is constitutively active, and shows evidence of temperature- and dose-dependent ectopic activity.

      (Casanova and Struhl, 1993)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (10)
      References (35)