FB2024_03 , released June 25, 2024
Allele: Dmel\tinABD
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General Information
Symbol
Dmel\tinABD
Species
D. melanogaster
Name
FlyBase ID
FBal0197275
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
tin-ABD
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

Sequences encoding the tin D (dorsal mesoderm) enhancer have been inserted downstream of the tinAB genomic fragment.

Allele components
Component
Use(s)
Regulatory region(s)
Encoded product / tool
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

tinEC40/tinABD mutant embryos show cardioblast (CB) patterning defects.

The myofibrils of the dorsal vessel are arranged almost exclusively in an anterior-posterior orientation in tinABD ; tin346/tinEC40 larvae, in contrast to wild-type larvae where they are arranged spirally. In the posterior heart region of the dorsal vessel the pattern of myofibrils is highly irregular in the mutant larvae, forming abnormal cross-shaped or 'knotted' patterns. The aorta appears thinner than normal in the mutant larvae, whereas the heart frequently has a wider diameter than normal.

The heart tube is much thinner than normal in tinABD ; tin346/tinEC40 adults. The mutant myofibrils are arranged longitudinally and transverse spirally arranged myofibrils are almost completely absent.

tinABD ; tin346/tin346 and tinABD ; tinABD tin346/tinEC40 adults show a dramatic increase in heart failure rate after pacing of the heart by external electrical stimulus compared to the heart failure rate of control adults. The recovery rate after heart failure is dramatically decreased in the mutant adults.

tinABD ; tin346/tin346 and tinABD ; tinABD tin346/tinEC40 adults have a reduced lifespan compared to controls.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhanced by
Statement
Reference

tinABD, tinEC40 has heart primordium phenotype, non-enhanceable by edlk06602

NOT suppressed by
Statement
Reference

tinABD, tinEC40 has heart primordium phenotype, non-suppressible by edlk06602

Additional Comments
Genetic Interactions
Statement
Reference

The cardioblast patterning defects observed in tinEC40/tinABD mutant embryos are not modified by edlk06602.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescues
Comments

tin346 embryos that are expressing tinABD show nearly normal expression of general cardioblast markers. The morphology of the posterior 'heart' region of the dorsal vessel is abnormal in these embryos; the cardioblast rows are uneven, some cardioblasts appear intercalated, and the shape of the cardioblasts is less regular than in control embryos.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (7)