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Allele Dmel\tutlex383
| General Information | |||
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| Symbol | Dmel\tutlex383 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0241902 | |
| Feature type | allele | Associated gene | Dmel\tutl |
| Allele class | |||
| Mutagen | P-element activity | ||
Recent Updates
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
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Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References | |||
| Associated Sequence Data | |||
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Imprecise excision of P{lacW}tutl[k14703] results in a 11,430bp deficiency within the tutl gene, disrupting all tutl transcripts. | ||
| Cytology | |||
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Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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Detailed Description
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Statement Reference Approximately 10% of tutl[ex383] embryonic segments have gaps in the longitudinal connectives and commissures. A minor enhancement of this phenotype is observed in embryos that are trans-heterozygous tutl[ex383]/Df(2L)ed-dp.
Sixty-percent of tutl[ex383] homozygous embryos exhibit axon defasciculation with some axons projecting to the midline. Fas2-positive axon tracts maintain their relative distance from the midline, but axons emanating from all three fascicles bundle together as they cross the midline.
Embryos trans-heterozygous for tutl[ex383] and tutl[01085] have defects in commissures, longitudinal connective, and Fas2-positive axon tracts that maintain their relative distance from the midline, but that have axons emanating from all three fascicles bundle together as they cross the midline.
In tutl[ex383] embryos, the ISNb motor axons succesfully reach the vicinity of their respective targets. However, the majority of them fail to send one or more of the final axon branches to contact their muscle targets. Half of the hemisegments also lack ISNd nerves.
Embryos trans-heterozygous for tutl[ex383] and tutl[01085] have a similar embryonic motor axon projection defects to tutl[ex383] homozygotes, but with lower frequency. | |||
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External Data
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Interactions
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Phenotypic Class
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| Enhancer of | |||
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| NOT Enhancer of | |||
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Phenotype Manifest In
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| NOT Enhancer of | |||
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Additional Comments
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Genetic Interactions
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Statement Reference A tutl[ex383] heterozygous background dramatically enhances the fra[GA957] mutant phenotype. fra[GA957], tutl[ex383] double mutants typically have only one thin and fragmented commissure along the entire length of the embryo, indicating an extreme reduction in commissure formation and fragmented longitudinal connectives.
A tutl[ex383] heterozygous background dramatically enhances the Df(1)NP5 mutant phenotype. Df(1)NP5 ; tutl[ex383] double mutants typically have only one thin and fragmented commissure along the entire length of the embryo, indicating an extreme reduction in commissure formation and fragmented longitudinal connectives.
Triple trans-heterozygous sli[1]/+, robo[5]/+, tutl[ex383]/+ do not appear different from double sli[1]/+, robo[5]/+ mutants, indicating that tutl does not function as an inhibitor of the sli pathway. | |||
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Xenogenetic Interactions
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Statement Reference | |||
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Complementation & Rescue Data
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| Rescued by | |||
| Not rescued by | |||
| Comments | Post-mitotic neuronal expression of tutl[HL01565.Scer\UAS], tutl[GH15753.Scer\UAS], tutl[AT02763.Scer\UAS], tutl[LD28224.Scer\UAS] or tutl[GH08133.Scer\UAS] under the control of either Scer\GAL4[sim.PS] or Scer\GAL4[elav-C155] fully rescues the midline crossing defects found in tutl[ex383] and tutl[ex383]/Df(2L)ed-dp mutants. Expression under the control of Scer\GAL4[repo] does not rescue the phenotype, indicating that expression near the midline is important for rescue.
Post-mitotic neuronal expression of tutl[AT02763.Scer\UAS] under the control of Scer\GAL4[elav-C155] is sufficient to rescue adult lethality found in tutl[ex383] mutants.
Expression of either tutl[GH15753.Scer\UAS] or tutl[AT02763.Scer\UAS] via Scer\GAL4[elav-C155] can reduce the motor axon projection defects found in tutl[ex383] homozygotes.
Expression of either tutl[GH15753.Scer\UAS] or tutl[AT02763.Scer\UAS] driven by the pan-neuronal driver Scer\GAL4[elav-C155] rescues most aspects of tutl[k14703]/tutl[ex383] mutant eye defects. | ||
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Stocks
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Notes on Origin
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| Discoverer | |||
 External Crossreferences & Linkouts
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Synonyms & Secondary IDs
( 1 ) | |||
| Reported As | |||
| Symbol Synonym | tutlex383 | ||
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References
( 1 ) | |||
| Research paper |
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