Skip to main content
. 2015 Dec 17;10(12):e0145169. doi: 10.1371/journal.pone.0145169

Fig 5. The kinase domain of Ror2 is required to rescue the NC migration defect in PTK7 morphant embryos.

Fig 5

Xenopus embryos were injected with different constructs in combination with 100 pg LacZ RNA as a lineage tracer and analyzed by whole-mount in situ hybridization using a twist antisense RNA probe. A Embryo injected with 10 ng control MO and 100 pg GFP RNA shows normal NC migration. B Embryo injected with 10 ng PTK7 MO and 100 pg GFP RNA shows inhibition of NC migration on the injected side, while NC migration is normal on the uninjected side. C Co-injection of 10 ng PTK7 MO together with 100 pg Ror2 RNA rescues the NC migration defect. D Embryo injected with 10 ng PTK7 MO and 100 pg of Ror2Δ469 RNA. The embryo shows a NC migration defect on the injected side. E Embryo injected with PTK7 MO and a kinase dead mutant of Ror2 (Ror2-3I) showing a NC migration defect on the injected side. F Graph summarizing the percentage of NC migration defects of a minimum of 5 independent experiments for each experimental condition. Asterisks indicates a p-value in a Student’s t-test < 0.001. Scale bar = 500 μm.