Phosphorylation of the growth arrest-specific protein Gas2 is coupled to actin rearrangements during Go-->G1 transition in NIH 3T3 cells.
Phosphorylation of the growth arrest-specific protein Gas2 is coupled to actin rearrangements during Go-->G1 transition in NIH 3T3 cells.
复制标题
在NIH 3T3细胞中，在GO中 - > G1过渡期间，生长阻塞特异性蛋白质GAS2的磷酸化与肌动蛋白重排耦合。
DOI：
10.1083/jcb.124.5.743
复制
发表时间：
1994-03
影响因子：
7.8
通讯作者：
Schneider, C
中科院分区：
文献类型：
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作者：
Brancolini, C;Schneider, C
生长停滞特异性 (Gas2) 蛋白已被证明是微丝系统的一个组成部分，在生长停滞的小鼠和人类成纤维细胞中高度表达，并在静止细胞的血清刺激后过度磷酸化。 (Brancolini, C.、S. Bottega 和 C. Schneider. 1992. J. Cell Biol. 117:1251-1261)。在这项研究中，我们证明了在 Go-->G1 转变过程中，向血清饥饿的 NIH 3T3 细胞中添加 20% FCS 所诱导的 Gas2 磷酸化动力学，暂时与肌动蛋白细胞骨架的重组耦合。为了更好地剖析 Gas2 磷酸化和微丝结构修饰之间的关系，我们使用了膜褶皱（PDGF 和 PMA）和应力纤维形成（L-α-溶血磷脂酸 LPA）的特定刺激（Ridley, A. J., and A. Hall. 1992. Cell. 70:389-399）。与 20% FCS 类似，所有这些都能够下调 Gas2 生物合成。 PDGF 和 PMA 会诱导 Gas2 过度磷酸化，并在时间上与 Gas2 所在处的膜波纹的出现相结合。另一方面，LPA 作为应力纤维形成的特定刺激物，无法诱导可检测到的 Gas2 过度磷酸化。因此，Gas2 过度磷酸化与膜波纹的形成特别相关，这可能意味着 Gas2 在此过程中的作用。
Growth arrest-specific (Gas2) protein has been shown to be a component of the microfilament system, that is highly expressed in growth arrested mouse and human fibroblasts and is hyperphosphorylated upon serum stimulation of quiescent cells. (Brancolini, C., S. Bottega, and C. Schneider. 1992. J. Cell Biol. 117:1251-1261). In this study we demonstrate that the kinetics of Gas2 phosphorylation, during Go-->G1 transition, as induced by addition of 20% FCS to serum starved NIH 3T3 cells, is temporally coupled to the reorganization of actin cytoskeleton. To better dissect the relationship between Gas2 phosphorylation and the modification of the microfilament architecture we used specific stimuli for both membrane ruffling (PDGF and PMA) and stress fiber formation (L-alpha-lysophosphatidic acid LPA) (Ridley, A. J., and A. Hall. 1992. Cell. 70:389-399). All of them, similarly to 20% FCS, are able to downregulate Gas2 biosynthesis. PDGF and PMA induce Gas2 hyperphosphorylation that is temporally coupled with the appearance of membrane ruffling where Gas2 localizes. On the other hand LPA, a specific stimulus for stress fiber formation, fails to induce a detectable Gas2 hyperphosphorylation. Thus, Gas2 hyperphosphorylation is specifically correlated with the formation of membrane ruffling possibly implying a role of Gas2 in this process.