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Figure 4 | Neural Development

Figure 4

From: Redundancy and compensation in axon guidance: genetic analysis of the Drosophila Ptp10D/Ptp4E receptor tyrosine phosphatase subfamily

Figure 4

CNS axon guidance defects in double and triple mutants. Stage 17 embryos were stained with (a,b,f) 1D4 and (c-e,g,h) anti-Myc as in Figure 3. (a) The Ptp4E, Ptp69D CNS shows very mild defects with 1D4 in which the outer longitudinal bundle is slightly wavy. (e) The SemaIIb-τmyc axons are almost indistinguishable from wild-type, although there is some slight fraying of the longitudinal segments of the pathways. (b) The Ptp10D; Ptp69D CNS has a strong ectopic midline crossing defect in which 1D4 axons grow across the posterior commissure (arrow); a thinner bundle is observed in the anterior commissure (arrowhead). Only one or two longitudinal bundles are visible, and the width of the CNS axon ladder indicates that the outer bundle is missing. (c) SemaIIb-τmyc axons in Ptp10D; Ptp69D. A thin axon bundle crosses the CNS in the posterior commissure (arrowhead). (d) An extreme Ptp10D, Ptp69D phenotype, with axons that project out of the CNS (arrows), and stalled growth cones along the longitudinal tract (asterisk). (f) 1D4 staining in Ptp4E Ptp10D; Ptp69D triple mutants show thick bundles that cross the midline in each segment (asterisk). There are two or three distinct longitudinal bundles (arrowhead). (g,h) Thick bundles of SemaIIb-τmyc axons in the triple mutant cross the midline in the posterior commissure (g, arrowhead; h, top arrowhead). A stalled axonal projection in this commissure is seen in (g, asterisk). Other abnormally crossing axons are indicated with arrowheads in (h). Anterior is up in all panels. Scale bars are 10 microns.

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