病毒杀伤毒素的分子靶点：TOK1钾通道。

A molecular target for viral killer toxin: TOK1 potassium channels.

作者信息

Ahmed A, Sesti F, Ilan N, Shih T M, Sturley S L, Goldstein S A

机构信息

Department of Pediatrics, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA.

出版信息

Cell. 1999 Oct 29;99(3):283-91. doi: 10.1016/s0092-8674(00)81659-1.

DOI:10.1016/s0092-8674(00)81659-1

PMID:10555144

Abstract

Killer strains of S. cerevisiae harbor double-stranded RNA viruses and secrete protein toxins that kill virus-free cells. The K1 killer toxin acts on sensitive yeast cells to perturb potassium homeostasis and cause cell death. Here, the toxin is shown to activate the plasma membrane potassium channel of S. cerevisiae, TOK1. Genetic deletion of TOK1 confers toxin resistance; overexpression increases susceptibility. Cells expressing TOK1 exhibit toxin-induced potassium flux; those without the gene do not. K1 toxin acts in the absence of other viral or yeast products: toxin synthesized from a cDNA increases open probability of single TOK1 channels (via reversible destabilization of closed states) whether channels are studied in yeast cells or X. laevis oocytes.

摘要

酿酒酵母的杀伤菌株携带双链RNA病毒，并分泌可杀死无病毒细胞的蛋白质毒素。K1杀伤毒素作用于敏感酵母细胞，扰乱钾离子稳态并导致细胞死亡。在此研究中，该毒素被证明可激活酿酒酵母的质膜钾离子通道TOK1。TOK1基因的缺失赋予了毒素抗性；过表达则增加了易感性。表达TOK1的细胞表现出毒素诱导的钾离子通量；而没有该基因的细胞则没有。K1毒素在没有其他病毒或酵母产物的情况下发挥作用：从cDNA合成的毒素增加了单个TOK1通道的开放概率（通过可逆地破坏关闭状态），无论通道是在酵母细胞还是非洲爪蟾卵母细胞中进行研究。