Fig. 7. Structural features of the sea urchin Ets1 and Alx1 proteins. (A,B) The P. lividus Ets1 protein contains a conserved MAPK phosphorylation consensus site and a putative ERK docking site in the Pointed domain. Partial sequence alignments between two sea urchin Ets1 protein sequences and the human Ets1, Ets2 and the Drosophila Pointed proteins showing the conservation of the PXTP motif (A) and ERK docking site (B). (C) The N-terminal region of the P. lividus Alx1 protein contains a putative MAPK phosphorylation consensus site (PSTP). Comparison of three different sea urchin Alx1 sequences showing conservation of this site. (D-K) Effects of mutations in the putative MAPK phosphorylation site of Ets1 on formation of PMCs and effects of activated Ras mRNA injections. (A) Control mesenchyme blastula stage. Overexpression of wild-type ets1 (E), ets1 T107D (F) or ets1 VP16 (H) converts a large number of cells into mesenchymal cells. Treatment with U0126 can block the effects of overexpressing ets1 (I) but not ets1 T107D (J). Mutating the putative MAPK phosphorylation site of the sea urchin Ets1 (etsT107A) abolishes its ability to promote epithelial-mesenchymal transition (G). (K) Overexpression of CA-Ras does not cause the same phenotype as overexpression of ets1 but causes a global epithelial remodeling. (vv) vegetal view.