RT Journal Article SR Electronic T1 Studies on the Role of Fibroblast Growth Factor Signaling in Neurogenesis Using Conjugated/Aged Animal Caps and Dorsal Ectoderm-Grafted Embryos JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 6892 OP 6898 DO 10.1523/JNEUROSCI.17-18-06892.1997 VO 17 IS 18 A1 Ren-He Xu A1 Jaebong Kim A1 Masanori Taira A1 Dvora Sredni A1 Hsiang-fu Kung YR 1997 UL http://www.jneurosci.org/content/17/18/6892.abstract AB 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. Thesein vitro studies were confirmed in vivoin 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.