FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Ptpmeg1
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General Information
Symbol
Dmel\Ptpmeg1
Species
D. melanogaster
Name
FlyBase ID
FBal0193794
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

A 4bp insertion, GTAC, has been introduced into the Ptpmeg gene. This produces a frameshift, which leads to truncation within the PDZ domain.

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

Homozygous Ptpmeg1 causes accelerated migration of border cells during oogenesis.

Ptpmeg1 adults often become trapped alive in their food.

Ptpmeg1 mutants show mushroom lobe defects. The alpha lobes are reduced, appearing thin, short or with a thin tip. In a small proportion of mutants, the alpha lobes are missing altogether. Tthe beta lobes often aberrantly touch the midline or are completely fused with the contralateral beta lobe. These defects are recessive and cell body and dendritic regions of mushroom body neurons appear normal.

An increase in mushroom body defects occurs as development progresses in Ptpmeg1 mutants; from 0% to ~55% in dorsal lobes and from ~10% to ~80% in medial lobes between 48 hours post-pupal formation (PPF) and the adult stage. A similar increase in defects can be observed in Ptpmeg1/Df(3L)ED201 mutants. At 24 hours PPF no significant level of defects can be observed but ~15-20% of dorsal lobes exhibit defects at 36 hours and 48 hours PPF and nearly 50% of mutants show defects by the first day of adulthood. In addition to the reduction in the distal region of dorsal lobes, dots of axonal material can frequently be observed near these regions, suggesting that axons retract in the dorsal lobes of Ptpmeg1/Df(3L)ED201 mutants.

Ptpmeg1 mutant clones containing either 1-10 or 10-50 mutant α/β cells do not show mushroom body axon defects. However, clones containing substantial amounts of Ptpmeg1 brain tissue outside of the mushroom bodies do show mushroom body axon defects.

In Ptpmeg1 mutants, ellipsoid body axons reach the midline but their extension toward ventral regions halts prematurely, leaving an omega-shaped ellipsoid body that is open along its ventral aspect. These ellipsoid body axon defects persist into adulthood and can also be observed in Ptpmeg1/Df(3L)ED201 mutants.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference

Ptpmeg1 has mushroom body phenotype, suppressible by sccP

Ptpmeg1 has ellipsoid body phenotype, suppressible by sccP

Additional Comments
Genetic Interactions
Statement
Reference

sccP is able to suppress the mushroom body and ellipsoid body phenotypes of Ptpmeg1 mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of PtpmegScer\UAS.cWa under the control of Scer\GAL4elav.PLu fully rescues the alpha lobe defects and partially rescues the beta lobe defects of Ptpmeg1 homozygotes. Scer\GAL4elav.PLu>PtpmegScer\UAS.cWa expression partially rescues the alpha lobe defects of Ptpmeg1/Df(3L)ED201 mutants.

Expression of PtpmegScer\UAS.cWa under the control of Scer\GAL4elav.PLu rescues the ellipsoid body defects of Ptpmeg1 mutants but expression of this transgene within the ellipsoid body itself, under the control of Scer\GAL4EB1, fails to rescue these defects.

Expression of PtpmegΔFERM.Scer\UAS under the control of Scer\GAL4elav.PLu results in a strong rescue of the ellipsoid body defects of Ptpmeg1 mutants, a rescue of the beta lobe overextension phenotype but no rescue of the alpha lobe reduction.

Expression of PtpmegG494A.F494A.Scer\UAS under the control of Scer\GAL4elav.PLu results in an effective rescue of the ellipsoid body defects of Ptpmeg1 mutants, while the ability of the transgene to rescue mushroom body defects is reduced compared to expression of a wild-type transgene.

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Stocks (1)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
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Name Synonyms
Secondary FlyBase IDs
    References (3)