Ras-mediated FGF signaling is required for the formation of posterior but not anterior neural tissue in Xenopus laevis.
Fibroblast growth factor (FGF) has been proposed to be involved in the specification and patterning of the developing vertebrate nervous system. There is conflicting evidence, however, concerning the requirement for FGF signaling in these processes. To provide insight into the signaling mechanisms that are important for neural induction and anterior-posterior neural patterning, we have employed the dominant negative Ras mutant, N17Ras, in addition to a truncated FGF receptor (XFD). Both N17Ras and XFD, when expressed in Xenopus laevis animal cap ectoderm, inhibit the ability of FGF to generate neural pattern. They also block induction of posterior neural tissue by XBF2 and XMeis3. However, neither XFD nor N17Ras inhibits noggin, neurogenin, or XBF2 induction of anterior neural markers. MAP kinase activation has been proposed to be necessary for neural induction, yet N17Ras inhibits the phosphorylation of MAP kinase that usually follows explantation of explants. In whole embryos, Ras-mediated FGF signaling is critical for the formation of posterior neural tissues but is dispensable for neural induction.
Ribisi
S
S
Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California, 94720, USA.
Mariani
F V
FV
Aamar
E
E
Lamb
T M
TM
Frank
D
D
Harland
R M
RM
D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins; D019521:Body Patterning; D002352:Carrier Proteins; D019070:Cell Lineage; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004475:Ectoderm / Q000378:metabolism / Q000637:transplantation; D004627:Embryonic Induction; D016332:Fetal Tissue Transplantation; D005346:Fibroblast Growth Factors / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005775:Gastrula / Q000166:cytology / Q000378:metabolism; D005799:Genes, Dominant / Q000235:genetics; D024002:HMGB Proteins; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009420:Nervous System / Q000166:cytology / Q000196:embryology* / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D011506:Proteins / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017468:Receptors, Fibroblast Growth Factor / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D055748:SOXB1 Transcription Factors; D015398:Signal Transduction; D014157:Transcription Factors; D029867:Xenopus Proteins; D014982:Xenopus laevis / Q000196:embryology* / Q000378:metabolism; D018631:ras Proteins / Q000235:genetics / Q000378:metabolism*; D000099176:Noggin Protein
D051792:Basic Helix-Loop-Helix Proteins; D002352:Carrier Proteins; D004268:DNA-Binding Proteins; D005346:Fibroblast Growth Factors; D024002:HMGB Proteins; D018398:Homeodomain Proteins; D020928:Mitogen-Activated Protein Kinases; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D011506:Proteins; D012333:RNA, Messenger; D017468:Receptors, Fibroblast Growth Factor; D055748:SOXB1 Transcription Factors; D014157:Transcription Factors; D029867:Xenopus Proteins; D018631:ras Proteins; D000099176:Noggin Protein; C491174:Meis3 protein, Xenopus; C101907:neurogenin, Xenopus; C527781:sox2 protein, Xenopus