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Mesoderm induction by activin requires FGF-mediated intracellular signals
Abstract
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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Citations
Cited by
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Bikfalvi, A., Klein, S., Pintucci, G., & Rifkin, D. B. (1997) · Endocrine Reviews · doi:10.1210/edrv.18.1.0292 · Cited by 959
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Harland, R., & Gerhart, J. (1997) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.13.1.611 · Cited by 839
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Self-citationMesoderm formation in response to Brachyury requires FGF signalling
Schulte-Merker, S., & Smith, J. C. (1995) · Current Biology · doi:10.1016/s0960-9822(95)00017-0 · Cited by 276
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Faure, S., Lee, M. A., Keller, T., Dijke, P. T., & Whitman, M. (2000) · Development · doi:10.1242/dev.127.13.2917 · Cited by 257
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Metadata
- Authors
- LaBonne, C., & Whitman, M.
- Venue
- Development
- Publisher
- The Company of Biologists
- Published
- 1994-02-01
- Volume
- 120
- Issue
- 2
- Pages
- 463-472
- ISSN
- 0950-1991 (ISSN-L)
- 1477-9129
- OpenAlex
- W2347083990
- Cited by
- 228
- References
- 0
- FWCI
- 10.17
- Type
- journal article
- Language
- en
- Open access
- closed
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