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Régulation de la voie MEK/ERK par la signalisation éphrine lors du développement neural chez l'ascidie Ciona intestinalis

Abstract : During my thesis study, I was involved in functional studies to demonstrate that p120-RasGAP, a GTPase-activating-protein (GAP), is a cytoplasmic mediator of the ephrin-mediated ERK attenuation. To confirm this notion, I conducted a co-immunoprecipitation experiment and demonstrated that p120-RasGAP associates with an ephrin receptor, Eph3, when the latter is activated by an ephrin ligand in ascidian embryos. These results strongly indicate that FGF and ephrin signals converge at the level of Ras and control its activity antagonistically. Following this finding, I looked for other cell fate specification events controlled by the antagonism between ephrin and FGF signals. In ascidian embryos, FGF signals are known to induce neural fates in ectodermal cells which otherwise adopt epidermal fates. Ascidian neural induction takes place at the 32-cell stage, resulting in specification of specific four cells as ERK1/2-active neural precursors among 16 ectodermal cells. I was able to demonstrate that ephrin/Eph/RasGAP signals counterbalance FGF neural inducing signals to generate the ON-OFF response of ERK activation among the ectodermal cells. Finally, in collaboration with a PhD student in Dr. Mike Levine’s lab (UC Berkeley), the antagonism between ephrin and FGF signals plays a role in regionalisation of the neural plate along the anterior-posterior axis.
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Submitted on : Tuesday, September 2, 2014 - 1:08:05 AM
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  • HAL Id : tel-01059798, version 1


Nicolas Haupaix. Régulation de la voie MEK/ERK par la signalisation éphrine lors du développement neural chez l'ascidie Ciona intestinalis. Sciences agricoles. Université Nice Sophia Antipolis, 2014. Français. ⟨NNT : 2014NICE4003⟩. ⟨tel-01059798⟩



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