FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\tutlex383
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General Information
Symbol
Dmel\tutlex383
Species
D. melanogaster
Name
FlyBase ID
FBal0241902
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Imprecise excision of P{lacW}tutlk14703 results in a 11,430bp deficiency within the tutl gene, disrupting all tutl transcripts.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

Approximately 10% of tutlex383 embryonic segments have gaps in the longitudinal connectives and commissures. A minor enhancement of this phenotype is observed in embryos that are trans-heterozygous tutlex383/Df(2L)ed-dp.

Sixty-percent of tutlex383 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 tutlex383 and tutl01085 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 tutlex383 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 tutlex383 and tutl01085 have a similar embryonic motor axon projection defects to tutlex383 homozygotes, but with lower frequency.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

tutl[+]/tutlex383 is an enhancer of abnormal neuroanatomy phenotype of fraGA957

NOT Enhancer of
Statement
Reference

tutl[+]/tutlex383 is a non-enhancer of abnormal neuroanatomy phenotype of robo[+]/robo15, sli1

tutl[+]/tutlex383 is a non-enhancer of abnormal neuroanatomy phenotype of robo15, sli[+]/sli1

Phenotype Manifest In
Enhancer of
Statement
Reference

tutl[+]/tutlex383 is an enhancer of symmetrical commissure phenotype of fraGA957

NOT Enhancer of
Statement
Reference

tutl[+]/tutlex383 is a non-enhancer of commissure phenotype of robo[+]/robo15, sli1

tutl[+]/tutlex383 is a non-enhancer of commissure phenotype of robo15, sli[+]/sli1

Additional Comments
Genetic Interactions
Statement
Reference

A tutlex383 heterozygous background dramatically enhances the fraGA957 mutant phenotype. fraGA957, tutlex383 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 tutlex383 heterozygous background dramatically enhances the Df(1)NP5 mutant phenotype. Df(1)NP5 ; tutlex383 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 sli1/+, robo5/+, tutlex383/+ do not appear different from double sli1/+, robo5/+ mutants, indicating that tutl does not function as an inhibitor of the sli pathway.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments

Post-mitotic neuronal expression of tutlHL01565.Scer\UAS, tutlGH15753.Scer\UAS, tutlAT02763.Scer\UAS, tutlLD28224.Scer\UAS or tutlGH08133.Scer\UAS under the control of either Scer\GAL4sim.PS or Scer\GAL4elav-C155 fully rescues the midline crossing defects found in tutlex383 and tutlex383/Df(2L)ed-dp mutants. Expression under the control of Scer\GAL4repo does not rescue the phenotype, indicating that expression near the midline is important for rescue.

Post-mitotic neuronal expression of tutlAT02763.Scer\UAS under the control of Scer\GAL4elav-C155 is sufficient to rescue adult lethality found in tutlex383 mutants.

Expression of either tutlGH15753.Scer\UAS or tutlAT02763.Scer\UAS via Scer\GAL4elav-C155 can reduce the motor axon projection defects found in tutlex383 homozygotes.

Expression of either tutlGH15753.Scer\UAS or tutlAT02763.Scer\UAS driven by the pan-neuronal driver Scer\GAL4elav-C155 rescues most aspects of tutlk14703/tutlex383 mutant eye defects.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (2)