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Figure 2. CAX is required for cell migration in vivo. (a) Tissue distribution of frog CAX. In situ hybridization of CAX and the neural crest marker Twist in stage 26/27 Xenopus embryos. Arrowheads mark the neural crest streams. (b–d) Effect of CAX knockdown on neural crest migration in vivo. (b) In situ hybridization analyses of Twist and the additional neural crest marker Snail2 in exemplar stage 23/24 embryos injected with two antisense morpholinos (10 ng AMO1 or 20 ng AMO2). Dorsal views (left) and views along the anterior–posterior axis (right) for both the uninjected (control) and antisense morpholino–injected (*) sides of embryos (delineated by the dashed lines) are shown. Phenotypes were considered mild or severe. (c) Summary data quantifying the proportion of embryos displaying the indicated phenotype in response to increasing amounts of antisense morpholino. Results are from a single experiment where all six experimental manipulations were performed in parallel on the same batch of embryos (∼1,000 injections). (d) Summary data from seven knockdowns (using 10 ng AMO1 and Twist) quantifying the length of all three neural crest streams, normalized to that in the uninjected side of the same embryo. Results are from CAX-depleted morphant embryos coinjected with increasing amounts of mRNA (0.6 or 1.2 ng; color coded) for GFP-CAX (left) or from control embryos injected with mRNA alone (right). Bars, 500 µm. Error bars represent SEM. **, P < 0.01; ***, P < 0.001. |
