Fig. 3

Ldb2a knockdown promotes the specification of mesendoderm and mesoderm.

(A–B) In ldb2a morphants, ntl expression in the mesendoderm/mesoderm was expanded into the ectoderm. (C–D) The ectoderm was restricted (decreased gata2 expression). (E) Gastrula ventral or dorsal mesendoderm develops into haemangioblast/pronephric or myeloid populations respectively, during somitogenesis, while the mesoderm becomes somites and notochord. (F–I) During somitogenesis, expression of scl, pax2.1, hand2, and pu.1 in the lateral mesoderm was up-regulated in ldb2a morphants. Embryos were co-stained with uncx or myoD to define the stage. (J–M) Other mesendoderm and mesoderm derivatives were also increased including somite (myoD) and notochord (shh), although only in a proportion of most affected morphants. (N–O) At 24 hpf, ldb2a knockdown caused increased expression of an endothelial gene, flk1, in the vessels (lateral mesoderm-derived). (P) As a summary, the loss of ldb2a expression induces mesodermal and endodermal while restricting ectodermal fates, especially in the ventro-lateral and posterior regions, and this fate change is stable. (A–D): three independent experiments, with the total number of analysed embryos shown in each panel; (F–G): five independent experiments; (H–I): one experiment; (J–O): three independent experiments. The wildtype control refers to uninjected embryos that are stage matched.