Ezrin, a membrane–actin cytoskeleton linker, which participates in epithelial cell morphogenesis, is held inactive in the cytoplasm through an intramolecular interaction. Phosphatidylinositol 4,5-bisphosphate (PIP2) binding and the phosphorylation of threonine 567 (T567) are involved in the activation process that unmasks both membrane and actin binding sites. Here, we demonstrate that ezrin binding to PIP2, through its NH2-terminal domain, is required for T567 phosphorylation and thus for the conformational activation of ezrin in vivo. Furthermore, we found that the T567D mutation mimicking T567 phosphorylation bypasses the need for PIP2 binding for unmasking both membrane and actin binding sites. However, PIP2 binding and T567 phosphorylation are both necessary for the correct apical localization of ezrin and for its role in epithelial cell morphogenesis. These results establish that PIP2 binding and T567 phosphorylation act sequentially to allow ezrin to exert its cellular functions.

ERM (Ezrin, Radixin, Moesin) proteins are membrane-cytoskeleton linkers that regulate the structure and the function of specific domains of the plasma membrane. ERM proteins are expressed in all metazoan analyzed so far. Genetic analysis of ERM protein functions has recently been performed simultaneously in three different organisms, mouse, Drosophila melanogaster and C. elegans. These studies have revealed a remarkable conservation of the protein functions through evolution. Moreover they have shed light on the crucial role these proteins play in various physiological processes that occur in epithelial cells.

Contamination of the marine environment following the accident in the Fukushima Dai-ichi nuclear power plant represented the most important artificial radioactive release flux into the sea ever known. The radioactive marine pollution came from atmospheric fallout onto the ocean, direct release of contaminated water from the plant and transport of radioactive pollution from leaching through contaminated soil. In the immediate vicinity of the plant (less than 500 m), the seawater concentrations reached 68,000 Bq.L(-1) for (134)Cs and (137)Cs, and exceeded 100,000 Bq.L(-1) for (131)I in early April. Due to the accidental context of the releases, it is difficult to estimate the total amount of radionuclides introduced into seawater from data obtained in the plant. An evaluation is proposed here, based on measurements performed in seawater for monitoring purposes. Quantities of (137)Cs in seawater in a 50-km area around the plant were calculated from interpolation of seawater measurements. The environmental halftime of seawater in this area is deduced from the time-evolution of these quantities. This halftime appeared constant at about 7 days for (137)Cs. These data allowed estimation of the amount of principal marine inputs and their evolution in time: a total of 27 PBq (12 PBq-41 PBq) of (137)Cs was estimated up to July 18. Even though this main release may be followed by residual inputs from the plant, river runoff and leakage from deposited sediments, it represents the principal source-term that must be accounted for future studies of the consequences of the accident on marine systems. The (137)Cs from Fukushima will remain detectable for several years throughout the North Pacific, and (137)Cs/(134)Cs ratio will be a tracer for future studies.