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Fig. 6
Wnt promotes EMT initiation and cooperates with FGF to promote EMT termination in tailbud NMPs. (A-F) vimr1 and vimr2 expression was analyzed in 20-somite stage wild-type sibling (A,B), hemizygous HS:TCF?C (C,D) and homozygous HS:TCF?C (E,F) embryos. Wnt inhibition leads to the loss of vimr1 and vimr2. (G-J) Expression of vimr1 and vimr2 was also analyzed in HS:ca?-catenin embryos (I,J) and their wild-type siblings (G,H). Wnt overactivation leads to a loss of vimr1 and vimr2 expression and a shift towards the ventral anterior portion of the tailbud (black arrow in I,J). (K-T?) tbx16 and msgn1 expression was examined in control (K-L?,Q-R?), hemizygous HS:TCF?C (M-N?), homozygous HS:TCF?C (O-P?) and HS:ca?-catenin (S-T?) embryos. Wnt inhibition had little effect on tbx16 expression but led to decreased expression of msgn1. Wnt overactivation led to expansion of the tbx16 and msgn1 expression domains. (Ua-Xd) Epistasis experiments were performed to examine the control of vimr1 expression by the Wnt and FGF signaling pathways. HS:ca?-catenin embryos were heat shocked at the 12-somite stage and treated with SU5402 or vehicle only (DMSO). These embryos were subsequently fixed 3?h, 4?h, 5?h and 6?h after heat shock induction for in situ hybridization. DMSO-treated control embryos exhibited consistent expression of vimr1 during somitogenesis (Ua-d), whereas DMSO-treated HS:ca?-catenin embryos had decreased expression of the EMT marker in the tailbud (Va-d). Consistent with previous data (Fig. 3), FGF inhibitor-treated embryos had increased expression of vimr1 (Wa-d). HS:ca?-catenin embryos in the presence of SU5402 maintained strong expression of vimr1 (Xa-d). All tailbud images are lateral views, except where indicated otherwise.