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General Information
Symbol
Dmel\Ptp69D8ex25
Species
D. melanogaster
Name
FlyBase ID
FBal0048917
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Deletion of most or all of the DNA encoding the cytoplasmic domain.

Deletion break falls between the fibronectin type III repeats and the PTP enzymatic domain, possibly breaking in the transmembrane domain, and removes the carboxy-terminal portion of the protein including the cytoplasmic domain.

Caused by aberration
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Lar mutants exhibit truncation phenotypes of the ISN. Combining Ptp69D or Ptp99A mutants increases the penetrance and severity of the ISN defects, the ISN pathway is truncated at specific branchpoint positions. Triple mutants lacking Lar, Ptp69D or Ptp99A exhibit much stronger ISN phenotypes than any single or double mutant. Lar, Ptp69D or Ptp99A triple mutants also exhibit fusion bypass phenotype of the SNb axons. Fusion bypass is seldom observed in any genotype in which Ptp69D is wild type. Removal of Ptp99A or Lar produces a 10- to 20- fold increase in the frequency of fusion bypass and an increase in complete stall phenotypes.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Suppressor of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The longitudinal axon bundles are irregular and often fuse to each other in Ptp10D101; Ptp69D1/Ptp69D8ex25, Ptp10D1 ; Ptp69D1/Ptp69D8ex25 or Df(1)Δ59; Ptp69D1/Ptp69D8ex25 double mutant embryos. The outer Fas2-positive bundle is usually missing or reduced to short, discontinuous Fas2-positive regions, and breaks in the inner two bundles are also seen. Three or more Fas2-positive axon bundles that cross the midline are seen within the commissural tracts of each segment (this is not seen in wild-type embryos). Ptp10D1; Ptp69D1/Ptp69D8ex25 embryos have broader commissures than wild-type embryos, and the intercommissural space at the midline of the embryo is compressed along the antero-posterior axis. Reduction in the longitudinal tracts is seen especially in the intersegmental regions between the neuromeres. Diagonal crossing of the midline is sometimes seen, with the axon bundle traversing the intersegmental region between neuromeres where no axons normally grow, and longitudinal bundles often stop abruptly, causing breaks in the longitudinal tracts. The longitudinal pioneer growth cones follow normal pathways in Ptp10D1 ; Ptp69D1/Ptp69D8ex25 embryos. The midline glia appear normal in Ptp10D1; Ptp69D1/Ptp69D8ex25 double mutant embryos. The MP1 and MP2 lineages are indistinguishable from wild type and the median neuroblast lineage develops normally. Fas2-positive axons are seen crossing the midline in 95.5% of segments in Ptp10D1/Ptp10D101; Ptp69D4/Ptp69D8ex25 double mutant embryos (this is never seen in wild-type embryos). Ptp10D1; Lar13.2/Lar5.5; Ptp69D1 Ptp99AR3/Ptp69D8ex25 Ptp99A1 quadruple mutants have severely disrupted longitudinal tracts and most axons cross the midline. The bundles that cross the midline do not respect the normal boundaries of the commissures and the anterior and posterior commissures appear fused. Homozygous comm5 embryos lack commissural axons. Commissures are formed in Ptp10D1; comm5 Ptp69D1/comm5 Ptp69D8ex25 triple mutant embryos (in 37% of segments), and in some cases they are as thick as in wild-type embryos. Ptp10D1; robo1/robo1; Ptp69D1/Ptp69D8ex25 triple mutant embryos have a severe phenotype in which most Fas2-positive axons converge on the midline. Some circles around the midline are still seen, but many axons fasciculate into a single thick bundle that extends along the midline. Vestiges of the lateral longitudinal pathways are seen in some segments. The Ptp10D1; Ptp69D1/Ptp69D8ex25 double mutant phenotype is significantly enhanced by one copy of sli2; more Fas2-positive axons cross the midline, the longitudinal tracts move closer together and more extensive commissural fusion is seen.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Df(3L)8ex25/Ptp69D1 transheterozygotes are deleted for the entire Ptp69D gene.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Ptp69D8ex25
Name Synonyms
Secondary FlyBase IDs
    References (5)