Study on cooperative regulation of actin cytoskeletal organization and translation initiation.

高渗透压或葡萄糖剥夺导致酵母中肌动蛋白极化和翻译起始的快速关闭。就像压力一样，服用抗精神病的吩噻嗪类药物或局部麻醉剂也会引起类似的反应。这些药物都具有两亲性结构，并能形成乳剂和渗透细胞膜，表明这些药物具有表面活性剂的相同特性。与这一观点一致，表面活性剂引起的反应类似于抗精神病药物和局部麻醉剂。阳离子表面活性剂苯并氯铵比吩噻嗪具有更强的关闭活性，而阴离子表面活性剂SDS能在不抑制翻译起始的情况下瞬间去极化肌动蛋白，这表明两亲体中的阳离子电荷对细胞关闭很重要。临床药物和低浓度的阳离子表面活性剂在没有细胞膜渗透的情况下导致关闭，这表明这些化合物和压力通过扰动而不是破坏细胞膜激活了关闭。

High osmolarity or glucose deprivation causes rapid shutdowns of both actin polarization and translation initiation in yeast. As like stresses, administration of antipsychotic phenothiazines or local anesthetics causes similar responses. All these drugs have amphiphilic structures, and are able to form emulsions and permeabilize the cell membrane, indicating that the drugs have the same features as a surfactant. Consistent with this notion, surfactants induced responses similar to those of antipsychotic drugs and local anesthetics. Benzethonium chloride, a cationic surfactant, has a more potent shutdown activity than phenothiazines, whereas SDS, an anionic surfactant, transiently depolarized actin without inhibiting translation initiation, indicating that a cationic charge in the amphiphile is important for cellular shutdown. The clinical drugs and the cationic surfactants at low concentrations caused shutdown without membrane permeabilization, suggesting that these compounds and the stresses activate the shutdowns, via perturbation rather than disruption of the cell membrane.