Morphogenic effects of ezrin require a phosphorylation-induced transition from oligomers to monomers at the plasma membrane.
Morphogenic effects of ezrin require a phosphorylation-induced transition from oligomers to monomers at the plasma membrane.
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ezrin的形态学作用需要磷酸化引起的从质膜上的低聚物向单体的过渡。
DOI：
10.1083/jcb.150.1.193
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发表时间：
2000-07-10
期刊：
影响因子：
--
通讯作者：
Arpin M
中科院分区：
文献类型：
--
作者：
Gautreau A;Louvard D;Arpin M
ERM（ezrin、radixin、moesin）蛋白质充当质膜和肌动蛋白细胞骨架之间的接头。它们的NH 2-和COOH-末端结构域之间的相互作用发生在封闭单体的分子内和头-尾寡聚体的分子间。在体外，ERM蛋白COOH末端结构域中保守的苏氨酸残基（ezrin中的T567）的磷酸化会破坏这种相互作用。在这里，我们已经分析了这种磷酸化事件在体内的作用，通过衍生稳定的克隆生产野生型，T567 A和T567 D ezrin从LLC-PK 1上皮细胞。我们发现T567 A ezrin与细胞骨架的相关性很差，但能够形成寡聚体。与此相反，T567 D ezrin与细胞骨架，但其分布从低聚物转移到单体在膜上。此外，生产T567 D ezrin诱导形成的板状伪足，膜皱褶，和微绒毛簇。T567 A和T567 D ezrin均影响多细胞上皮结构的发育。总的来说，这些结果表明，磷酸化的ERM蛋白在这个保守的苏氨酸调节从膜结合的寡聚体的活性单体，诱导和富含肌动蛋白的膜投影的一部分的过渡。
ERM (ezrin, radixin, moesin) proteins act as linkers between the plasma membrane and the actin cytoskeleton. An interaction between their NH2- and COOH-terminal domains occurs intramolecularly in closed monomers and intermolecularly in head-to-tail oligomers. In vitro, phosphorylation of a conserved threonine residue (T567 in ezrin) in the COOH-terminal domain of ERM proteins disrupts this interaction. Here, we have analyzed the role of this phosphorylation event in vivo, by deriving stable clones producing wild-type, T567A, and T567D ezrin from LLC-PK1 epithelial cells. We found that T567A ezrin was poorly associated with the cytoskeleton, but was able to form oligomers. In contrast, T567D ezrin was associated with the cytoskeleton, but its distribution was shifted from oligomers to monomers at the membrane. Moreover, production of T567D ezrin induced the formation of lamellipodia, membrane ruffles, and tufts of microvilli. Both T567A and T567D ezrin affected the development of multicellular epithelial structures. Collectively, these results suggest that phosphorylation of ERM proteins on this conserved threonine regulates the transition from membrane-bound oligomers to active monomers, which induce and are part of actin-rich membrane projections.
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影响因子：
4.8
作者：
Oshiro, N;Fukata, Y;Kaibuchi, K
通讯作者：
Kaibuchi, K
DOI：
10.1006/bbrc.1996.1410
发表时间：
1996-09-24
影响因子：
3.1
作者：
Nakamura, F;Amieva, MR;Furthmayr, H
通讯作者：
Furthmayr, H
影响因子：
64.5
作者：
Pearson, MA;Reczek, D;Karplus, PA
通讯作者：
Karplus, PA
DOI：
10.1083/jcb.120.1.129
发表时间：
1993-01
期刊：
The Journal of cell biology
影响因子：
--
作者：
Algrain M;Turunen O;Vaheri A;Louvard D;Arpin M
通讯作者：
Arpin M
影响因子：
3.3
作者：
Nakamura, F;Huang, LQ;Furthmayr, H
通讯作者：
Furthmayr, H