FGF signaling controls caudal hindbrain specification through Ras-ERK1/2 pathway

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Aragon F, Pujades C. FGF signaling controls caudal hindbrain specification through Ras-ERK1/2 pathway. BMC Dev. Biol. 2009 ; 9: 61. DOI 10.1186/1471-213X-9-61
http://hdl.handle.net/10230/16384
To cite or link this document: http://hdl.handle.net/10230/16384
dc.contributor.author Aragón Manresa, Ferran
dc.contributor.author Pujades Corbi, Cristina
dc.date.accessioned 2012-05-02T10:33:18Z
dc.date.available 2012-05-02T10:33:18Z
dc.date.issued 2009
dc.identifier.citation Aragon F, Pujades C. FGF signaling controls caudal hindbrain specification through Ras-ERK1/2 pathway. BMC Dev. Biol. 2009 ; 9: 61. DOI 10.1186/1471-213X-9-61
dc.identifier.issn 1471-213X
dc.identifier.uri http://hdl.handle.net/10230/16384
dc.description.abstract Background: During early steps of embryonic development the hindbrain undergoes a regionalization process along the anterior-posterior (AP) axis that leads to a metameric organization in a series of rhombomeres (r). Refinement of the AP identities within the hindbrain requires the establishment of local signaling centers, which emit signals that pattern territories in their vicinity. Previous results demonstrated that the transcription factor vHnf1 confers caudal identity to the hindbrain inducing Krox20 in r5 and MafB/Kreisler in r5 and r6, through FGF signaling [1]. Results: We show that in the chick hindbrain, Fgf3 is transcriptionally activated as early as 30 min after mvHnf1 electroporation, suggesting that it is a direct target of this transcription factor. We also analyzed the expression profiles of FGF activity readouts, such as MKP3 and Pea3, and showed that both are expressed within the hindbrain at early stages of embryonic development. In addition, MKP3 is induced upon overexpression of mFgf3 or mvHnf1 in the hindbrain, confirming vHnf1 is upstream FGF signaling. Finally, we addressed the question of which of the FGF-responding intracellular pathways were active and involved in the regulation of Krox20 and MafB in the hindbrain. While Ras-ERK1/2 activity is necessary for MKP3, Krox20 and MafB induction, PI3K-Akt is not involved in that process. Conclusion: Based on these observations we propose that vHnf1 acts directly through FGF3, and promotes caudal hindbrain identity by activating MafB and Krox20 via the Ras-ERK1/2 intracellular pathway.
dc.language.iso eng
dc.publisher BioMed Central
dc.relation.ispartof BMC Dev. Biol. 2009 ; 9: 61
dc.rights (c) 2009 Aragon and Pujades. Creative Commons Attribution License
dc.rights.uri http://creativecommons.org/licenses/by/2.0/
dc.subject.other Neurobiologia del desenvolupament
dc.subject.other Sistema nerviós central
dc.subject.other Factors de transcripció
dc.title FGF signaling controls caudal hindbrain specification through Ras-ERK1/2 pathway
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1186/1471-213X-9-61
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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