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Fig. 6. Targeting XtSulf1/2 knockdown to neural tissue disrupts cranial neural crest migration and does not affect mesoderm differentiation. X. tropicalis embryos were injected into the two dorsal blastomeres in the animal hemisphere at the 8-cell stage with 30 ng of control morpholino (CMO) or with 10 ng of S1 AMO together with 20 ng of S2 AMO (S1/S2 AMO). At stage 16, CMO injected (A, B) and S1/S2 AMO injected (C, D) embryos show normal expression of slug (CMO = 78% normal, n = 23; S1/S2 AMO = 59% normal, n = 17) and MyoD (CMO = 90% normal, n = 20, S1/S2 AMO = 65% normal; n = 23). At stage 22, twist expression is disrupted in knockdown embryos (F, 66% disrupted twist expression, n = 15) and does not extend as far ventrally as seen in those injected with control morpholino (E). The expression of myoD and α-cardiac actin in CMO injected embryos at stage 22 are shown in G and I. There is normal expression of myoD (66%, n = 18) and α-cardiac actin (64%, n = 14) in S1/S2 knockdown embryos (H and J). (K) The expression of twist in embryos injected with control morpholino at stage 30. (L) Twist expression is disrupted in knockdown embryos (69%, n = 16). The expression of myoD and α-cardiac actin in CMO injected embryos at stage 30 are shown in M and O. There is normal somite expression of myoD (83%, n = 12) and α-cardiac actin (80%, n = 10) in stage 30 S1/S2 knockdown embryos (N and P). |