Myosin X Interaction with KIF13B, a Crucial Pathway for Netrin-1-Induced Axonal Development

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Figure 5.
Figure 5.

DCC and PI3K activity-dependent axonal distribution of GFP-Myo X in response to Netrin-1 stimulation. A, Immunoprecipitation analysis of DCC association with Myo X in cultured cortical neurons that were treated with vehicle or Netrin-1 for 1 h. B, Quantifications of DCC binding with MyoX. Student's t test, p = 0.0122. C, Neurons transfected with GFP-Myo X or GFP-Myo X together with DCC miRNA were treated with vehicle or Netrin-1 and then stained with anti-Tau-1 antibody at DIV3. Scale bar, 10 μm. D, Quantification of axonal distribution of GFP-Myo X. One-way ANOVA, for Myo X group with vehicle stimulation and Myo X group with Netrin-1 stimulation, p < 0.0001; for Myo X and Myo X+DCC-KD groups, p < 0.0001. E, Quantification of dendritic distribution of GFP-Myo X. One-way ANOVA, for Myo X groups with vehicle and Myo X group with Netrin-1 stimulation, p = 0.0142, for Myo X and Myo X+DCC-KD groups, p = 0.0283. F, GFP-Myo X-expressing neurons were treated with vehicle and Netrin-1 with or without PI3 kinase inhibitor, wortmannin (10 nm) for 1 h and subjected to immunostaining with anti-Tau-1 antibody at DIV3. Scale bar, 10 μm. G, Quantification of axonal distribution of GFP-Myo X. One-way ANOVA, p < 0.0001 for both groups. H, Quantification of dendritic distribution of GFP-Myo X. One-way ANOVA, for vehicle and Nerin-1 groups, p = 0.0023; for Netrin-1 and Netrin-1+wortmannin groups, p = 0.0124. Data are presented as the mean ± SEM. The numbers of brain sections scored are from three different brains for each group and indicated on the graphs. ns, No significant difference; *p < 0.05; **p < 0.01; ***p < 0.001.

  1. The Journal of Neuroscience vol. 40 no. 48 9169-9185
  1. Free Access 
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