FB2024_03 , released June 25, 2024
Allele: Dmel\Ptp52F18.3
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General Information
Symbol
Dmel\Ptp52F18.3
Species
D. melanogaster
Name
FlyBase ID
FBal0128128
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

Amino acid replacement: S941P.

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

T16173022C

Amino acid change:

S940P | Ptp52F-PB

Reported amino acid change:

S941P

Comment:

Position of mutation on reference sequence inferred by FlyBase curator based on author statement (Figure 1 sequence).

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

Ptp52F18.3 heterozygotes and, more severely, Ptp52F18.3/Ptp52F8.10.3 transheterozygotes exhibit a significant decrease in the apoptosis levels in gastric caecum cells, and delays in both the histolysis of larval midgut and the removal of the gastric caeca during metamorphosis, as compared to controls.

Ptp52F18.3 mutants exhibit defects in motor neuron projection in late stage 16 embryos.

Homozygous mutants, and hemizygous mutants (over Df(2R)Jp4 or Df(2R)Jp8) show a range of phenotypes in the SNa branch of the segmental nerve. Additional branches are seen at random position, either the posterior of anterior branch is missing, or the SNa stalls near the bifurcation point. Ptp52F18.3/Df(2R)Jp8 mutant embryos also occasionally have completely missing SNa branches. In homozygous mutant embryos, growth cones of the pCC neuron that should grow onto lateral G branch 5 (LG5) stalls. AT later stages the longitudinal pathway is thin in 50% of segments, and the connection between the pCC and the pathway appears to be missing in some hemisegments. By stage 15, however, the medial 1D4 positive bundle (which contains the pCC axon) has a relatively normal appearance. Homozygous mutants, and hemizygous mutants (over Df(2R)Jp4 or Df(2R)Jp8) show a weak phenotype in the ISNb nerve branch. ISNb stalls in the VLM field, or shows a bypass phenotype at a low frequency. Homozygous mutants, and hemizygous mutants (over Df(2R)Jp4 or Df(2R)Jp8) show a range of phenotypes in the Intersegmental nerve (ISN). ISNs sometimes terminate at the first branchpoint, or more frequently terminate at the second branchpoint, and occasionally ISN appear to reach the terminal arbor position, but are thin or bifurcated.

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

Ptp52F18.3 has abnormal neuroanatomy phenotype, non-enhanceable by Ptp4E1

Suppressor of
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The presence of Ptp52F18.3 strongly suppresses the wing defects seen in male flies expressing fogScer\UAS.cRa under the control of Scer\GAL4Bx-MS1096.

Ptp4E1 Ptp52F18.3 double mutants have motor axon phenotypes indistinguishable from Ptp52F18.3 single mutants.

Ptp4E1 Ptp10D1 Ptp52F18.3 triple mutants have stronger motor axon phenotypes than Ptp52F18.3 single mutants. The triple mutants also exhibit an enhancement of the ISN truncation phenotype seen at the second branchpoint in Ptp10D1 Ptp52F18.3 double mutants.

Removal of Ptp52F function in fogScer\UAS.cRa overexpression mutants, through a Ptp52F18.3 mutant background, results in a strong suppression of the CNS phenotype. Only 3% of segments exhibit ectopic midline crossing, as compared to 44% for fogScer\UAS.cRa overexpression (under the control of Scer\GAL4elav-C155 and Scer\GAL4elav.PLu) in a wild-type background. For embryos with one copy of the driver (Scer\GAL4elav.PLu), the phenotype was suppressed from 27% to 5%. The longitudinal tracts appear normal in fogScer\UAS.cRa, Ptp52F18.3 embryos, resembling those seen in Ptp52F18.3 single mutants.

The addition of Ptp10D1 enhances the SNa and ISNb phenotypes seen in Ptp52F18.3 homozygotes alone. An ISNb stall phenotype is greatly enhanced in these embryos. The addition of Lar5.5 enhances the SNa phenotype seen in Ptp52F18.3 homozygotes alone. The addition of Ptp69D1/Df(3L)8ex25 enhances the SNa phenotype seen in Ptp52F18.3 homozygotes alone. The addition of Ptp99A1 doesn't enhance the strength of the SNa phenotype seen in Ptp52F18.3 homozygotes, but does decrease the penetrance of the ectopic branch phenotype. The addition of Ptp52F18.3 to Ptp69D1/Df(3L)8ex25 mutant embryos strongly enhances the ISNb phenotype seen. The addition of Ptp99A1 has no effect on the Ptp52F18.3 ISNb phenotype. The addition of Ptp10D1 strongly enhances the ISN phenotypers seen in Ptp52F18.3 mutants alone. The addition of Ptp52F18.3 to Ptp69D1/Df(3L)8ex25 mutant embryos strongly enhances the ISN phenotype seen. The central nervous system phenotype seen in Ptp52F18.3 embryos is suppressed by the addition of Lar5.5.

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 (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)