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General Information
Symbol
Dmel\Ptp10D1
Species
D. melanogaster
Name
FlyBase ID
FBal0104058
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

Imprecise excision of the P{EP} element, resulting in a deletion (extending from the insertion site) that removes Ptp10D exon 1.

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 ( 1 )
 

Ptp10D1 together with Ptp4E1 in double heterozygous state (but not as single heterozygotes) exacerbate retinal degeneration in a fly model of Parkinson's disease ectopically expressing Hsap\SNCAScer\UAS.cJa.

Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

No ectopic midline crossing is seen in homozygous Ptp10D1 mutant stage 16 embryos.

Ptp10D1/Df(1)Δ59 mutants show clumps and breaks in the lamina.

Mutant larvae have truncated ISNs that fail to innervate dorsal muscles. Collateral branches extend from the ISN in the right hemisegment, forming ectopic synapses onto dorsal muscles in both hemisegments.

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

Ptp10D1 is a suppressor of viable phenotype of Ptp4E1

NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Statement
Reference

Ptp10D[+], Ptp4E1, Ptp10D1, Ptp4E[+] is an enhancer of retina | adult stage | progressive phenotype of Hsap\SNCAUAS.cJa, Scer\GAL4ninaE.PT

Ptp10D[+], Ptp4E1, Ptp10D1, Ptp4E[+] is an enhancer of ommatidium | adult stage | progressive phenotype of Hsap\SNCAUAS.cJa, Scer\GAL4ninaE.PT

Ptp4E1/Ptp10D1 is an enhancer of motor neuron phenotype of Ptp52F18.3

NOT Enhancer of
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Ptp4E1 Ptp10D1 double mutants exhibit bubble-like cysts with an enlarged diameter in unicellular (lateral trunk, ganglionic branch) and intracellular (lateral ganglionic branch) tracheal branches, but not in multicellular branches (dorsal trunk) or intracellular fusion branches. This phenotype is significantly reduced by Scer\GAL4btl.PS-mediated expression of expB.Scer\UAS.T:Ivir\HA1.

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.

Ptp10D1 enhances the ectopic midline crossing phenotype that is seen in sas15/Df(3R)ED5221 mutant stage 16 embryos. 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.

Ptp10D1 enhances the ectopic midline crossing phenotype seen in homozygous sas15 mutant stage 16 embryos.

A Ptp10D1 mutant background enhances the ectopic midline crossing phenotype seen in stage 16 embryos expressing sasScer\UAS.cLa under the control of Scer\GAL4sim.PU. No effect is seen when sasScer\UAS.cLa is expressed under the control of Scer\GAL4elav.PU.

A Ptp10D1 mutant background enhances the ectopic midline crossing phenotype seen in stage 16 embryos expressing sasScer\UAS.cLa in glia under the control of Scer\GAL4repo.PU. The inner Fas2-positive axon bundle crosses the midline, but the outer bundles usually do not. The pattern of glial nuclei is quite disorganised; the double row of nuclei along each longitudinal tract is replaced by aggregations of varying width, and there is no segmentally repeated pattern of nuclei near the midline.

Ptp10D1 Ptp4E1 double mutants die as hatched larvae with collapsed tracheae. The tracheae have large bubble-like cysts on select branches and dorsal tracheal trunk are serpentine (indicating an increased length). The overall branching pattern of the tracheal network is normal.

The junctions between the transverse connective and lateral trunk branches are enlarged in stage 14 Ptp10D1 Ptp4E1 double mutant embryos. The anterior branches of the lateral trunk (which have not yet fused across segmental borders) have large cysts and the ganglionic branches have small cysts, By stage 15, cysts are seen at all transverse connective/lateral branch junctions and along the lateral trunk and ganglionic branches in the double mutant embryos. The visceral branch also develops large cysts at this stage.

Ultrastructural analysis of sections through lateral trunk branches shows that the cysts seen in Ptp10D1 Ptp4E1 double mutant embryos have variable diameters, averaging around 4.6μm. Cysts and normal lumens are never seen in the same section, suggesting that cysts in unicellular tubes are expanded forms of lumen sealed with adherens junctions.

Cysts are seen in the ganglionic branches and the diameter of the ganglionic branches is larger than normal in Ptp10D1 Ptp4EKG02328 double mutant embryos.

Expression of Egfr2.A887T.Scer\UAS under the control of Scer\GAL4btl.PS enhances the tracheal defects seen in Ptp10D1 Ptp4E1 double mutant embryos; the increase in diameter of the transverse connective/lateral trunk junction is further enhanced, and cysts appear on all dorsal branches.

Ptp4E1, Ptp10D1/Y double mutant animals can hatch out into first instar larvae, but die immediately after hatching.

Ptp4E1 Ptp10D1 double mutants show mild central nervous system defects. The longitudinal axons appear wavy and the outermost longitudinal axon tract is discontinuous and often invades the middle (intermediate) longitudinal axon tract.

Df(1)ovo4 Ptp10D1 double mutants show mild central nervous system defects. The longitudinal axons appear wavy and the outermost longitudinal axon tract is discontinuous and often invades the middle (intermediate) longitudinal axon tract. A mild fraying of the longitudinal bundles is observed.

Ptp4E1 Ptp10D1 double mutant larvae have severe tracheal defects.

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.

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.

bifR47/+; Ptp10D1/+ double mutants show clumps and breaks in the lamina, while neither single heterozygote shows this phenotype.

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

Ptp69DΔIg.Scer\UAS driven by Scer\GAL4elav-C155 rescues the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

Ptp69Dwedge.Scer\UAS driven by Scer\GAL4elav-C155 rescues the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

Ptp69DDA1.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4elav-C155 rescues the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

Ptp69DΔPTP2.Scer\UAS driven by Scer\GAL4elav-C155 rescues the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

Ptp69DΔFNIII.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4elav-C155 fails to rescue the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

Ptp69DDA1DA2.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4elav-C155 fails to rescue the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

In Ptp10D1 Lar5.5/Lar13.2 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos 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.

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.

In Ptp10D1 Lar5.5/Lar13.2 double mutant embryos, the normal SNa bifurcation is not observed in some hemisegments. This phenotype is only observed at low frequency.

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

Approximately half of the SNa nerves fail to bifurcate in Ptp10D1 Lar5.5/Lar13.2 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos.

Approximately half of the SNa nerves either do not reach the bifurcation point at all or are very thin and wandering in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 quadruple 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.

Approximately half of the intersegmental nerves terminate at the second lateral branch position in Ptp10D1 Lar5.5/Lar13.2 double mutant embryos. The remainder of the intersegmental nerves either terminate between the second lateral branch and the terminal arbor or make an abnormally small terminal arbor in these double mutant embryos.

The longitudinal axon bundles are irregular and often fuse to each other in Ptp10D1; 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).

No central nervous system abnormalities (by Fas2 staining) are seen

in Ptp10D1; Lar5.5/Lar13.2 double mutant 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.

Ptp69Dunspecified in double mutant combination with either Ptp10D1

or Ptp10D1/Ptp10D101 results in alterations in many central

nervous system axonal pathways in the embryo. The contralaterally

projecting interneuronal axons of the NB 2-5 lineage cross the midline

and turn anteriorly in a normal manner, but then double back across

the midline after about two segments and grow posteriorly in the ipsilateral

longitudinal tract. The axons of the ipsilateral intersegmental neurons

grow anteriorly for a short distance and stop. The ISNd motorneuron

extends an axon toward the midline that stalls and never enters the

ISN root. In the NB 4-2 lineage, the RP2 axons stall before reaching

their target, and the CoR axons do not branch onto all of their target

muscles. The projection of local interneurons across the midline in

the anterior commissure appears wild type, except that the axons always

defasciculate into two bundles after crossing the midline. Ectopic

interneuronal projections form on the ipsilateral side, and project

across segmental boundaries in the anterior direction (these axons

never form in wild type). In the NB 3-1 lineage, the RP neurons (RP1,

RP3, RP4 and RP5) extend axons normally across the commissure and into

the ISNb nerve, although they do not form normal synapses. The interneuronal

projections are radically altered; they still cross the midline, but

do not form defined anterior and posterior projections in the contralateral

connective. Instead, they grow anteriorly in a circular path around

the neuropil, contacting the midline at the end of their trajectory.

No alterations in the numbers or positions of cell bodies of the progeny

of NBs 3-1, 4-2 or 2-5 are seen in these embryos.

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

The age-progressive retinal degeneration characteristic for flies expressing Hsap\SNCAScer\UAS.cJa under the control of Scer\GAL4ninaE.PT is significantly enhanced by combination with Ptp10D1 and Ptp4E1 in double heterozygous state, combination with single copy of each allele alone does not exacerbate the retinal phenotype.

Ptp69DEC.Scer\UAS.T:Mmus\Ptprm driven by Scer\GAL4elav-C155 fails to rescue the Ptp10D1 Ptp69D1 double mutant ventral nerve cord phenotype.

Complementation and Rescue Data
Comments

Expression of Ptp4EScer\UAS.T:Avic\GFP under the control of Scer\GAL4btl.PS completely rescues the tracheal defects of Ptp4E1 Ptp10D1 double mutant embryos.

Scer\GAL4btl.PS-driven Ptp4EScer\UAS.T:Avic\GFP-expression is capable of rescuing the lethality and tracheal phenotypes associated with the Ptp4E1-Ptp10D1 double mutant genotypes. Similarly to ubiquitous overexpression of Ptp4EScer\UAS.T:Avic\GFP driven by Scer\GAL4αTub84B.PL, pan-neural overexpression of Ptp4EScer\UAS.T:Avic\GFP driven by Scer\GAL4elav.PLu does not rescue the lethality in a Ptp4E1-Ptp10D1 background.

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References (12)