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General Information
Symbol
Dmel\Ptp69D1
Species
D. melanogaster
Name
FlyBase ID
FBal0048914
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
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 DNA encoding most of the extracellular domain including the signal sequence.

Deletion removing N-terminal coding sequences, including the signal 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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

The adult sLNv neurons of Ptp69D1 heterozygotes do not show significant axon length differences compared to controls.

Very little ectopic midline crossing is seen in homozygous Ptp69D1 mutant stage 16 embryos.

Temperature shift experiments indicate that to survive after eclosion, Ptp69D1/Ptp69D10 animals must be shifted to the permissive temperature (18oC) from the restrictive temperature (25oC) as early pupae. The rate of eclosion drops from 100% at 18oC to 75% when Ptp69D1/Ptp69D10 animals are reared at 25oC for their first 24 hours and drops further to 40% if the animals are raised at 25oC until the early pupal stage. Ptp69D1/Df(3L)8ex34 embryos show motor axon defects; 26% of ISNb axons, 10% of ISN axons, 11% of SNa axons and 4% of SNc axons show defects. 6% of ISNb axons show a complete bypass phenotype and 9% show a partial bypass phenotype.

Ptp69D1/Df(3L)8ex25 hemizygotes show a very low frequency of ISNb and ISN phenotypes.

In mosaic animals, Ptp69D1 R1-R6 axons project through the lamina into the medulla, in contrast to wild type. Patterning, R cell fate determination and cellular morphogenesis are largely normal in homozygous clones in the eye. No transformations of R1-R6 into R7/8 neurons are seen as determined by rhabdomere morphology. R1-R6 axons from small mutant patches exhibit R7/8 like axon trajectories into the medulla. R1-R6 axons from larger mutant patches, result in massive hyperinnervation of the medulla, disrupting its structure.

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.

Ptp69D1/Df(3L)8ex25 heterozygotes show lethality at the pupal phase. Rare adults eclose but are feeble and die rapidly. Homozygotes show abnormalities in SNb (and, to a lesser extent, SNa) pathfinding in the embryo, resulting in bypass, detour and stall phenotypes. RP axons sometimes exhibit guidance errors within the CNS.

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

Ptp69D1/Ptp69D[+] is a non-enhancer of neuroanatomy defective | embryonic stage phenotype of cknK.Δ324-331

NOT Suppressor of
Statement
Reference

Ptp69D1/Ptp69D[+] is a non-suppressor of neuroanatomy defective | embryonic stage phenotype of cknK.Δ324-331

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

Ptp69D1 has RP neuron & axon phenotype, enhanceable by Ptp99A1

Suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Statement
Reference

Ptp69D1/Ptp69D[+], sli2 has axon | adult stage phenotype

Additional Comments
Genetic Interactions
Statement
Reference

The adult sLNv neurons of Ptp69D1, sli2 double heterozygotes exhibit significantly longer axon projections compared to controls.

Unlike in wild type, stage 16 Ptp10D1 Ptp69D1/Df(3L)8ex25 double mutant embryos exhibit a Fas2-positive commissural tract with several distinct bundles, oriented perpendicular to the longitudinal tracts. The inner longitudinal bundle is present, but the outer two bundles are missing or fused with the inner bundle. No complete breaks are seen in the Fas2-positive longitudinal tract. The anterior and posterior commissures are fused into a single commissural tract.

Ptp69D1/Df(3L)8ex25 enhances the ectopic midline crossing phenotype seen in sas15/Df(3R)ED5221 mutant stage 16 embryos.

Ptp69D1/Df(3L)8ex25 enhances the ectopic midline crossing phenotype seen in homozygous sas15 mutant stage 16 embryos. Segments of the outer longitudinal tract are missing. Multiple Fas2-positive axon bundles cross the midline in each segment, and these are perpendicular to the longitudinal tracts. The inner Fas2-positive bundle is intact, but one or both of the outer longitudinal bundles are missing. Complete breaks in the Fas2-positive longitudinal tract are seen. The anterior and posterior commissures are fused into a single commissural tract.

Expression of sasScer\UAS.cLa under the control of Scer\GAL4Fas2-Mz507 almost completely rescues the CNS defects seen in sas15/Df(3R)ED5221, Ptp69D1/Df(3L)8ex25 double mutant embryos.

Expression of sasScer\UAS.cLa under the control of Scer\GAL4Fas2-Mz507 almost completely rescues the CNS defects seen in sas15, Ptp69D1/Df(3L)8ex25 double mutant embryos.

A heterozygous or homozygous Ptp69D1 background fails to affect the penetrance of the ISNb bypass phenotype found in cknK.Δ324-331 heterozygotes or homozygotes.

Ptp4E1 Ptp69D1 double mutant embryos display only very mild central nervous system defects, in which the outer longitudinal bundle is slightly wavy.

In Ptp10D1; Ptp69D1/Df(3L)8ex25 double mutant embryos, two longitudinal bundles are observed that sometimes fuse into one, and the ventral nerve cord is narrowed, suggesting that the outer bundle is missing. The mutant nerve cords also display occasional ectopic midline crossing defects by single axons in the posterior commissure. Ptp10D1; Ptp69D1/Df(3L)8ex25 double mutants have ISNb branches that fail to reach muscle 12 (stall phenotype), however, these branches maintain a growth-cone like appearance.

Ptp4E1 Ptp10D1; Ptp69D1/Df(3L)8ex25 triple mutant embryos show midline crossing defects in the ventral nerve cord. There are always two, and sometimes three, longitudinal bundles in the triple mutant. The triple mutants have a stronger ISNb phenotype than any of the component double mutants. This is a "clump" phenotype in which 90% of ISNbs terminate in a darkly staining blob at the dorsal border of muscle 6. In cases where the ISNb passes this point, it is often misrouted, or bypasses the muscle field by growing along the ISN. The axons often ectopically project interiorly to muscle 12 from the ISN. In Ptp4E1 Ptp10D1; Ptp69D1/Df(3L)8ex25 triple mutants, the ratio of very thin SNa nerves is increased, compared to Ptp10D1; Ptp69D1/Df(3L)8ex25 double mutants.

bifR47/+; Ptp69D1/+ double mutants show clumps and breaks in the lamina, while neither single heterozygote shows this phenotype.

The ISNb bypass phenotype seen in Ptp69D1/Df(3L)8ex34 embryos is suppressed by one copy of Ptp99A1 or Df(3R)Ptp99AR3.

The addition of Ptp52F18.3 or Ptp52F8.10.3 to Ptp69D1/Df(3L)8ex25 mutant embryos strongly enhances the ISNb and ISN phenotypes seen.

In Ptp10D1 Ptp69D1 double mutant late stage 16 and early stage 17 embryos longitudinal axons abnormally cross the midline.

Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos show severe motor axon defects. The two inner bundles of the ventral nerve cord are very similar to that of wild-type, but the outer bundle, which develops later, is often discontinuous in late stage 16 triple mutant embryos. In addition, about one third of the ISNb nerves fail to leave the intersegmental nerve at the exit junction and continue to grow out along the common intersegmental nerve pathway in these triple mutant embryos. In most of these bypass hemisegments, only one intersegmental nerve branch is visible, and it is usually thicker than normal.

Ptp10D1 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos produce a phenotype in which the three longitudinal ventral nerve cord bundles are partially fused and many axons cross the midline.

The Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 triple mutant embryonic phenotype involves ectopic midline crossing and longitudinal bundle fusion by the ventral nerve cord. The axons that abnormally cross the midline in the triple mutant embryos often grow diagonally to the other side without respecting the normal borders of the anterior and posterior commissures. In many cases, all of the connective axons appear to be rerouted across the midline, producing complete connective breaks.

Most of the ventral nerve cord axons abnormally cross the midline and the longitudinal bundles are almost absent in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 quadruple mutant embryos. The longitudinal tracts are depleted of axons and the commissures are completely fused and much thicker than normal. No axons are ever observed to enter the ventrolateral muscle field in the quadruple mutant embryos.

In Ptp10D1 Ptp69D1 double mutant embryos, the normal SNa bifurcation is not observed in some hemisegments. The mutant SNa nerves either stall at the bifurcation point or, more commonly, have only one branch (either anterior or posterior) extending beyond this point.

Approximately half of the SNa nerves fail to bifurcate in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 triple mutant embryos.

Approximately half of the intersegmental nerves terminate at the first lateral branch point position and most of the remainder stop at the second lateral branch point in Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos.

Only about 15% of the intersegmental nerves terminate at the first lateral branch point position and most of the remainder stop at the second lateral branch point in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 quadruple mutant embryos.

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. The Fas2-positive axon bundles of the longitudinal connectives are fused or interrupted in some segments in Ptp10DEP1332; Ptp69D1/Ptp69D8ex25 double mutant embryos and the outer bundle never forms. Only the outer bundle is strongly affected in these embryos. Misrouting of axon bundles across the midline is seen in a few segments of each embryo. The phenotype is rescued by expression of Ptp10DEP1332 under the control of Scer\GAL4elav-C155. 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.

Severity of Ptp69D1 mutant phenotypes is enhanced by Ptp99A1. This enhanced phenotype is completely rescued by one copy of Ptp69D+t10.5. The severity of the RP axon phenotype is enhanced by Ptp99A1.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Associated with: a lethal mutation in mirr. Ptp69D1 was generated by local transposition of the P{lacW}mirrcre2 insertion into the Ptp69D locus, followed by imprecise excision. mirrcre2 fails to complement the lethality of Ptp69D1, suggesting that a lethal mutation in mirr is retained in the Ptp69D1 stock.

Comments
Comments

Rank order for penetrance of SNb mutant phenotypes is Ptp69D1 > Ptp69D2 > Ptp69D1/Ptp69D3 > Ptp69D3.

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

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (21)