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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.
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