XB-IMG-144959
Xenbase Image ID: 144959
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FIGURE 3. WIF-1 inhibits Wnt signaling and affects somite formation in Xenopus embryos. a–f, WIF-1 dorsalizes Xenopus embryos. hWIF-1 RNA (500 pg per blastomere) was injected into dorsal blastomeres (a, c, e) or ventral blastomeres (b, f) at the 4-cell stage. Dorsal injections led to anteriorization and hyperdorsalization of the embryos, as revealed by the formation of an enlarged head at the tadpole stage (a), an expanded cement gland (cg) field at the neurula stage (c), and an enlarged notochord visible in sections (e; control embryo in d). Ventral injections led to the formation of a partial secondary axis in 20% of the embryos (b) containing muscle (mus) and neural tissue (nt) (f). g–i, WIF-1 synergizes with chordin to generate a complete secondary axis (Table 1). g, Co-injection of chordin and Xenopus sFRP-3/Frzb RNAs gave rise to embryos with a complete but cyclopic secondary axis. h, By contrast, co-injection of chordin and hWIF-1 gave rise to embryos with a complete secondary axis; two separated eyes are evident. i, Co-injection of chordin and WD RNA does not promote two-eyed ectopic heads. j–p, WIF-1 affects the process of somite formation. 4-cell embryos were injected on one side with 100 pg pCS2+/hWIF-1 DNA and beta-galactosidase RNA. beta-Galactosidase activity is seen as brown dots and embryos were probed for XMyoD (j–n). The posterior domain of XMyoD expression in presomitic mesoderm was suppressed by hWIF-1 injection at the late neurula stage (j, dorsal view; k, posterior view). Segmentation is impaired by hWIF-1 injection, as revealed by XMyoD expression in mature somites of a stage-20 embryo (l) and a stage-26 embryo (m, n), and by a Hoechst-stained horizontal section of a stage-26 embryo (o, p). Note the disorganization of somites with occasional fusions (arrows in o). The process of somite rotation (rot) is delayed and myotome nuclei do not align properly (p). Image published in: Hsieh JC et al. (1999) Copyright © 1999. Image reproduced with permission of the Publisher, Macmillan Publishers Ltd. Larger Image Printer Friendly View |