Distinct functions for ERK1 and ERK2 in cell migration processes during zebrafish gastrulation.

S.F.G. Krens, S. He, G.E.M. Lamers, A.H. Meijer, J. Bakkers, T. Schmidt, H.P. Spaink, B.E. Snaar-Jagalska

Research output: Contribution to journal/periodicalArticleScientificpeer-review

Abstract

The MAPKs are key regulatory signaling molecules in many cellular processes. Here we define differential functions for ERK1 and ERK2 MAPKs in zebrafish embryogenesis. Morpholino knockdown of ERK1 and ERK2 resulted in cell migration defects during gastrulation, which could be rescued by co-injection of the corresponding mRNA. Strikingly, Erk2 mRNA cross-rescued ERK1 knockdown, but erk1 mRNA was unable to compensate for ERK2 knockdown. Cell-tracing experiments revealed a convergence defect for ERK1 morphants without a severe posterior-extension defect, whereas ERK2 morphants showed a more severe reduction in anterior-posterior extension. These defects were primary changes in gastrulation cell movements and not caused by altered cell fate specification. Saturating knockdown conditions showed that the absence of FGF-mediated dual-phosphorylated ERK2 from the blastula margin blocked initiation of epiboly, actin and tubulin cytoskeleton reorganization processes and further arrested embryogenesis, whereas ERK1 knockdown had only a mild effect on epiboly progression. Together, our data define distinct roles for ERK1 and ERK2 in developmental cell migration processes during zebrafish embryogenesis.
Original languageEnglish
Pages (from-to)370-383
JournalDevelopmental Biology
Volume319
Issue number2
DOIs
Publication statusPublished - 2008

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