FB2024_03 , released June 25, 2024
Allele: Dmel\Ptp69D18
Open Close
General Information
Symbol
Dmel\Ptp69D18
Species
D. melanogaster
Name
FlyBase ID
FBal0152280
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Nucleotide substitution: G?A. Amino acid replacement: G757E.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G12738384A

Reported nucleotide change:

G?A

Amino acid change:

G758E | Ptp69D-PA; G758E | Ptp69D-PB

Reported amino acid change:

G757E

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

At 25oC, the survival rates of homozygotes are: adult survival - 0%, eclosion - 0%, pupation 23%. At 18oC, the survival rates of homozygotes are: adult survival - 82%, eclosion - 85%, pupation 107%. Temperature shift experiments indicate that to survive after eclosion, Ptp69D18/Df(3L)8ex34 animals must be at the mid pupal stage prior to the shift to the restrictive temperature (25oC). The rate of eclosion drops from more than 80% at 18oC to less than 20% when Ptp69D18/Df(3L)8ex34 animals are shifted to the nonpermissive temperature prior to the onset of pupation. Temperature shift experiments also reveal a requirement for Ptp69D function during late embryonic development. Ptp69D18 embryos show motor axon defects; 15% of ISNb axons, 9% of ISN axons, 17% of SNa axons and 8% of SNc axons show defects.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (3)