p120RasGAP mediates ephrin/Eph-dependent attenuation of FGF/ERK signals during cell fate specification in ascidian embryos

Nicolas Haupaix, Alberto Stolfi, Cathy Sirour, Vincent Picco, Michael Levine, Lionel Christiaen, Hitoyoshi Yasuo

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

ERK1/2 MAP kinase exhibits a highly dynamic activation pattern in developing embryos, which largely depends on fibroblast growth factor (FGF) signals. In ascidian embryos, FGF-dependent activation of ERK1/2 occurs differentially between sister cells during marginal zone and neural lineage patterning. Selective attenuation of FGF signals by localised ephrin/Eph signals accounts for this differential ERK activation, which controls the binary fate choice of each sibling cell pair. Here, we show that p120 Ras GTPase-activating protein (p120RasGAP) is a crucial mediator of these ephrin/Eph signals. First, inhibition of p120RasGAP has a similar effect to inhibition of ephrin/Eph function during marginal zone and neural patterning. Second, p120RasGAP acts epistatically to ephrin/Eph signals. Third, p120RasGAP physically associates with Eph3 in an ephrin-dependent manner. This study provides the first in vivo evidence that the functional association between Eph and RasGAP controls the spatial extent of FGF-activated ERK.

Original languageEnglish (US)
Pages (from-to)4347-4352
Number of pages6
JournalDevelopment (Cambridge)
Volume140
Issue number21
DOIs
StatePublished - Nov 1 2013

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Developmental Biology

Keywords

  • Ascidian
  • Ciona intestinalis
  • Ephrin
  • p120RasGAP

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