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.
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.