Fig. 7. Effects of Xror2 and its mutant constructs on morphogenetic movements of animal caps stimulated with activin. Two-cell stage embryos were injected with mRNAs of globin (A,F), Xror2 (B,G), Xror2-3I (C), Xror2-TM (D,I), Xror2-KR (E) or a mixture of Xror2 and Xror2-TM (H) in the animal pole region of both blastomeres. Doses of injected mRNA (ng/embryo) are indicated in parentheses. Note that doses of mRNA used in F-I are lower than in A-E. Animal caps (stages 8-8.5) were treated with (right panels in A-E; F-I) or without (left panels in A-E) activin A as indicated and cultured until sibling stage 18. A-E and F-I are separate experiments. Activin treatment initiated elongation of control animal caps (A,F). Xror2 (B), Xror2-3I (C) and Xror2-TM (D) suppressed elongation of animal caps by activin. In Xror2-TM-expressing animal caps, a neural groove-like structure with pigmented cells (black arrowheads) was observed in activin-treated ones. Elongation of Xror2-KR-expressing animal caps treated with activin was slightly reduced (E), compared with globin-expressing animal caps. Xror2 or Xror2-TM with lower doses show moderate inhibition of activin-induced elongation of animal caps (G,I). Co-expression of Xror2 and Xror2-TM shows cumulative effects on the inhibition of activin-induced elongation, indicating that wild-type and Xror2-TM do not compete with each other (H).