Figure 4.

Polycystin-2 and Xnr3 Synergize to Induce the LRO Precursor Tissue of the Superficial Mesoderm

(A–F) Increased xnr3 (A–C) and reduced foxj1 expression (D–F) in stage 10.5 pkd2 morphants (B and E) as compared with control specimens (A and D). Dotted lines in A and B indicate plane of histological sections shown in A′, and B′, respectively. Note that foxj1 expression was rescued upon co-injection of a full-length pkd2 mRNA (F).

(G–I) Reduced foxj1 expression in early gastrula stages (st. 10.5) following Tg treatment (G, DMSO control embryo; H, Tg treated specimen; I, quantification of results).

(J–S) xnr3 and pkd2 synergize SM foxj1 induction. Loss of xnr3 resulted in attenuated foxj1 expression (K and O) compared with control uninjected specimens (J and O), which was highly efficiently rescued by co-injection of full-length xnr3 mRNA (L and O). Both dorsal (M) and ventral (N) overexpression of xnr3 mRNA caused an increase of endogenous or induction of ectopic foxj1, respectively (M–O). Injections of reduced MO doses of Xnr3-MO (O, R; 2 × 0.6pmol) or Pkd2-MO (O, Q; 2 × 0.75pmol) caused mild reductions of foxj1 expression. Co-injection of low doses of MOs resulted in strong inhibitory effects (O and S).

(T) Schematic depiction of known (black) and proposed (green) interactions required for SM specification. For details refer to main text. Increase of expression highlighted with white arrowheads and decrease with black arrowheads. Numbers in parentheses indicate the number of embryos analyzed for each condition.

See also Figures S4 and S5.