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

被引：26

作者：

Haupaix, Nicolas ^{[1
,2
]}

Stolfi, Alberto ^{[3
,4
]}

Sirour, Cathy ^{[1
,2
]}

Picco, Vincent ^{[1
,2
]}

Levine, Michael ^{[3
]}

Christiaen, Lionel ^{[4
]}

Yasuo, Hitoyoshi ^{[1
,2
]}

机构：

[1] Univ Paris 06, F-06230 Villefranche Sur Mer, France

[2] CNRS, Lab Biol & Dev Villefranche sur Mer, Observ Oceanol, F-06230 Villefranche Sur Mer, France

[3] Univ Calif Berkeley, Ctr Integrat Genom, Div Genet Genom & Dev, Dept Mol & Cell Biol, Berkeley, CA 94720 USA

[4] NYU, Dept Biol, Ctr Dev Genet, New York, NY 10003 USA

来源：

DEVELOPMENT | 2013年 / 140卷 / 21期

基金：

美国国家科学基金会; 美国国家卫生研究院;

关键词：

p120RasGAP; Ephrin; Ascidian; Ciona intestinalis; RECEPTOR TYROSINE KINASE; CIONA; FGF; GENE; DIFFERENTIATION; EXPRESSION; CHORDATE; RAS; ESTABLISHES; INHIBITION;

D O I：

10.1242/dev.098756

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：4347 / 4352

页数：6