In Ptp69D¹/+, msi¹/+ adults, thoracic mechanosensory neurons exhibit decreased connectivity: reduced contralateral branch synaptic arborizations; and synapse numbers.

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 sas^Scer\UAS.cLa under the control of Scer\GAL4^Fas2-Mz507 almost completely rescues the CNS defects seen in sas¹⁵/Df(3R)ED5221, Ptp69D¹/Df(3L)8ex25 double mutant embryos.

Expression of sas^Scer\UAS.cLa under the control of Scer\GAL4^Fas2-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 ckn^K.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.

bif^R47/+; 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)Ptp99A^R3.

The addition of Ptp52F^18.3 or Ptp52F^8.10.3 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.

Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 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)Ptp99A^R3 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 Lar^5.5/Lar^13.2 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 Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 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 Lar^5.5/Lar^13.2 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 Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 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 Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 quadruple mutant embryos.

The longitudinal axon bundles are irregular and often fuse to each other in Ptp10D¹⁰¹; Ptp69D¹/Ptp69D^8ex25, Ptp10D¹ ; Ptp69D¹/Ptp69D^8ex25 or Df(1)Δ59; Ptp69D¹/Ptp69D^8ex25 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/Ptp69D^8ex25 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/Ptp69D^8ex25 embryos. The midline glia appear normal in Ptp10D¹; Ptp69D¹/Ptp69D^8ex25 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 Ptp10D^EP1332; Ptp69D¹/Ptp69D^8ex25 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 Ptp10D^EP1332 under the control of Scer\GAL4^elav-C155. Ptp10D¹; Lar^13.2/Lar^5.5; Ptp69D¹ Ptp99A^R3/Ptp69D^8ex25 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 Ptp69D^8ex25 triple mutant embryos (in 37% of segments), and in some cases they are as thick as in wild-type embryos. Ptp10D¹; robo¹/robo¹; Ptp69D¹/Ptp69D^8ex25 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/Ptp69D^8ex25 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.