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Inhibiting Wnt signals in vivo directs anterior paraxial mesodermal cells into the cardiac fate. Shown here are whole-mount in situ hybridization analyses for ventricular myosin heavy chain (vMHC) expression in stage 12 chick embryos. At stage 7 the presumptive anterior paraxial mesoderm of each embryo was implanted with cell pellets expressing BMP-4 plus the Wnt antagonist Frzb-IgG (right), or BMP-4 plus control IgG (left). The anterior paraxial mesoderm is normally fated to give rise to the presumptive head mesenchyme. Whereas implantation of cells expressing only BMP-4 failed to affect subsequent vMHC expression (left), implantation of cells expressing BMP-4 plus Frzb-IgG resulted in increased vMHC staining in an enlarged heart (right). In addition, heart looping was reversed in over 50% of embryos containing the BMP-4 plus Frzb-IgG pellets (right). These results suggest that Wnt signals from the neural tube normally repress ectopic cardiogenesis in the anterior paraxial mesoderm. (For details, see Tzahor et al., p. 255; see related articles by Schneider et al., p. 304 and Marvin et al., p. 316.)