Mesoderm induction by activin requires FGF-mediated intracellular signals
Author(s) -
Carole LaBonne,
Malcolm Whitman
Publication year - 1994
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.120.2.463
Subject(s) - activin type 2 receptors , fgf and mesoderm formation , acvr2b , mesoderm , biology , microbiology and biotechnology , fibroblast growth factor , activin receptor , signal transduction , embryonic induction , tgf beta signaling pathway , nodal signaling , xenopus , intermediate mesoderm , embryo , gastrulation , genetics , receptor , transforming growth factor , embryogenesis , embryonic stem cell , gene
We have examined the role of FGF signaling during activin-mediated mesoderm induction in Xenopus. Using dominant inhibitory mutants of FGF signal transducers to disrupt the FGF-signaling pathway at the plasma membrane or in the cytosol prevents animal cap blastomeres from expressing several mesodermal markers in response to exogenous activin. Dominant inhibitory mutants of the FGF receptor, c-ras or c-raf inhibit the ability of activin to induce molecular markers of both dorsal and ventral mesoderm including Xbra, Mix1 and Xnot. Some transcriptional responses to activin such as goosecoid and Xwnt8 are inhibited less effectively than others, however, suggesting that there may differing requirements for an FGF signal in the responses of mesoderm-specific genes to activin induction. Despite the requirement for this signaling pathway during activin induction, downstream components of this pathway are not activated in response to activin, suggesting that activin does not signal directly through this pathway.
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