Knockdown of Amyloid Precursor Protein in Zebrafish Causes Defects in Motor Axon Outgrowth
Figure 6
Truncated APP fragments cannot rescue the APPb morphant phenotype.
(A) Schematic representation of the full length Amyloid Precursor Protein (APP) and the truncated mutations used in this study. (B) Full length APP is required for normal embryonic development. As depicted by the graph, embryos co-injected with APPb-MO and APPb-cΔ99R or APPb-c99 or hAPP-cΔ18R or hAPP-cΔ83R or hAPP-cΔ99R or AICD mRNA did not rescue the APPb morphant embryos. By contrast, excluding hAPP-cΔ18R, these truncated APP fragments increased the number of abnormal embryos in the APPb morphants. (C) The morphological effects on embryonic development of over-expression of the truncated mutants of APP mRNA (350 pg). The APPb-c99, hAPP-cΔ83R, hAPP-cΔ99R and AICD have limited domain negative effects on embryo development compared with full length APPb and hAPP. (D) Human APP-cΔ18R partially rescued the defective phenotypes of axons Vp and VII observed in APPb morphants compared to full length hAPP. (E) Human APP-cΔ18R partially rescued the defective phenotypes of spinal cord axons observed in APPb morphants compared to full length hAPP.