A molecular target for viral killer toxin: TOK1 potassium channels

被引:74
作者
Ahmed, A
Sesti, F
Ilan, N
Shih, TM
Sturley, SL
Goldstein, SAN
机构
[1] Yale Univ, Sch Med, Boyer Ctr Mol Med, Dept Pediat, New Haven, CT 06536 USA
[2] Yale Univ, Sch Med, Boyer Ctr Mol Med, Dept Cellular & Mol Physiol, New Haven, CT 06536 USA
[3] Columbia Univ Coll Phys & Surg, Inst Human Nutr, Dept Physiol, New York, NY 10032 USA
[4] Columbia Univ Coll Phys & Surg, Inst Human Nutr, Dept Pediat, New York, NY 10032 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S0092-8674(00)81659-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:283 / 291
页数:9
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