vivo, we developed a method based on the overexpression of the soluble antagonist by transient transfection of WOP cells with a Frzb1 expression vector and injection of transfected cells into the placenta of pregnant females

There is increasing evidence for a positive role of Wnt signaling molecules in the activation of myogenesis in amniote embryos (Münsterberg et al., 1995; Stern et al., 1995; Capdevila et al., 1998; Tajbakhsh et al., 1998), but the mechanism of this process remains elusive. At least another molecule, Sonic hedgehog, is also required to initiate myogenesis in the presomitic mesoderm (Borycki et al., 1998). Moreover, Noggin, a target of Wnt signaling, seems to contribute to the process mainly by neutralizing the inhibitory actions of BMPs (Hirsinger et al., 1997; Marcelle et al., 1997; Pourquie et al., 1996). It has been proposed that Shh and Wnts may initiate myogenesis by activating the myogenic regulatory factor Myf5 in newly formed somites (Münsterberg et al., 1995); in the mouse, activation of Myf5 in the dorsomedial lip of the dermomyotome leads to epaxial myogenesis. Studies with explant cultures have shown that other signals from the surface ectoderm, which can be replaced by Wnt7a, appear to preferentially activate MyoD in the hypaxial (ventral) domain of somites (Cossu et al., 1996; Tajbakhsh et al., 1998). Interestingly, Shh, which is expressed medially, is indispensable for epaxial but not for hypaxial myogenesis (Borycki et al., 1999). Therefore, Wnts together with Shh may contribute to the activation of myogenesis through the activation of Myf5 or MyoD (Tajbakhsh et al., 1998), although, an additional role for Wnts in the maintenance/expansion of the myogenic cell population is also possible. Recently, putative receptors of Wnts have been identified (Bhanot et al., 1996), both as classic transmembrane proteins, termed Frizzled, and as soluble, presumably secreted 4247 Development 126, 4247-4255 (1999) Printed in Great Britain © The Company of Biologists Limited 1999 DEV2457