Milne J C, Collier R J
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Mol Microbiol. 1993 Nov;10(3):647-53. doi: 10.1111/j.1365-2958.1993.tb00936.x.
Protective antigen (PA) of anthrax toxin forms ion-conductive channels in planar lipid bilayers and liposomes under acidic pH conditions. We show here that PA has a similar permeabilizing action on the plasma membranes of CHO-K1 and three other mammalian cell lines (J774A.1, RAW264.7 and Vero). Changes in membrane permeability were evaluated by measuring the efflux of the K+ analogue, 86Rb+, from prelabelled cells, and the influx of 22Na+. The permeabilizing activity of PA was limited to a proteolytically activated form (PAN) and was dependent on acidic pH for membrane insertion (optimal at pH 5.0), but not for sustained ion flux. The flux was reduced in the presence of several known channel blockers: tetrabutyl-, tetrapentyl-, and tetrahexylammonium bromides. PAN facilitated the membrane translocation of anthrax edema factor under the same conditions that induced changes in membrane permeability to ions. These results indicate that PAN permeabilizes cellular membranes under conditions that are believed to prevail in the endosomal compartment of toxin-sensitive cells; and they provide a basis for more detailed studies of the relationship between channel formation and translocation of toxin effector moieties in vivo.
炭疽毒素的保护性抗原(PA)在酸性pH条件下可在平面脂质双层和脂质体中形成离子传导通道。我们在此表明,PA对CHO-K1以及其他三种哺乳动物细胞系(J774A.1、RAW264.7和Vero)的质膜具有类似的通透作用。通过测量预标记细胞中K+类似物86Rb+的外流以及22Na+的内流来评估膜通透性的变化。PA的通透活性仅限于蛋白水解激活形式(PAN),并且依赖于酸性pH进行膜插入(在pH 5.0时最佳),但不依赖于持续的离子通量。在几种已知的通道阻滞剂存在下,通量降低:四丁基、四戊基和四己基溴化铵。在诱导膜对离子通透性变化的相同条件下,PAN促进了炭疽水肿因子的膜转位。这些结果表明,PAN在被认为在毒素敏感细胞的内体区室中普遍存在 的条件下使细胞膜通透;并且它们为更详细研究体内通道形成与毒素效应部分转位之间的关系提供了基础。