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Volume 17, Number 18, Issue of September 15, 1997 pp. 6892-6898
Copyright ©1997 Society for NeuroscienceStudies on the Role of Fibroblast Growth Factor Signaling in Neurogenesis Using Conjugated/Aged Animal Caps and Dorsal Ectoderm-Grafted Embryos
Received Jan. 28, 1997; revised June 9, 1997; accepted July 1, 1997.
Ren-He Xu1, Jaebong Kim2, Masanori Taira3, Dvora Sredni4, and Hsiang-fu Kung2 1 Intramural Research Support Program,
Science Applications International Corporation-Frederick, and 2 Laboratory of Biochemical Physiology, Division of Basic Sciences, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201, 3 Laboratory of Molecular Embryology, Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113, Japan, and 4 Interdisciplinary Department, Bar Ilan University, Ramat Gan, Israel 52900 Basic fibroblast growth factor (bFGF) has been shown to induce neural fate in dissociated animal cap (AC) cells or in AC explants cultured in low calcium and magnesium concentrations. However, long-term disclosure of the cap may cause diffusion of the secreted molecule bone morphogenetic protein 4 (BMP-4), a neural inhibitor present in the AC. This may contribute to the subsequent neurogenesis induced by bFGF. Here we used conjugated and aged blastula AC to avoid diffusion of endogenous molecules from the AC. Unlike noggin, bFGF failed to induce neural tissue in this system. However, it enhanced neuralization elicited by a dominant negative BMP receptor (DN-BR) that inhibits the BMP-4 signaling. Posterior neural markers were turned on by bFGF in AC expressing DN-BR or chordin. Blocking the endogenous FGF signal with a dominant negative FGF receptor (XFD) mainly inhibited development of posterior neural tissue in neuralized ACs. These in vitro studies were confirmed in vivo in embryos grafted with XFD-expressing ACs in the place of neuroectoderm. Expression of some regional neural markers was inhibited, although markers for muscle and posterior notochord were still detectable in the grafted embryos, suggesting that XFD specifically affected neurogenesis but not the dorsal mesoderm. The use of these in vitro and in vivo model systems provides new evidence that FGF, although unable to initiate neurogenesis on its own, is required for neural induction as well as for posteriorization.
Key words: FGF; BMP; neurogenesis; anteroposterior patterning; Xenopus; embryo
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