Expression of Bax in yeast affects not only the mitochondria but also vacuolar integrity and intracellular protein traffic

被引：12

作者：

Dimitrova, I

Toby, GG

Tili, E

Strich, R

Kampranis, SC

Makrisa, AM

机构：

[1] Mediterranean Agron Inst Chania, Dept Nat Prod, Khania 73100, Greece

[2] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA

[3] Univ Penn, Sch Med, Philadelphia, PA 19104 USA

[4] Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA

来源：

FEBS LETTERS | 2004年 / 566卷 / 1-3期

关键词：

programmed cell death; yeast; Bax; glutathione S-transferase; mitochondria; vacuole;

D O I：

10.1016/j.febslet.2004.04.012

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：

Bax-induced lethality in yeast is accompanied by morphological changes in mitochondria, giving rise to a reduced number of swollen tubules. Although these changes are completely abolished upon coexpression of the Bax inhibitor, Bcl-2, coexpression of Bax with Bax inhibiting-glutathione S-transferase (BI-GST) leads to aggregation, but not fusion of the mitochondria. In addition, Bax affects the integrity of yeast vacuoles, resulting in the disintegration and eventual loss of the organelles, and the disruption of intracellular protein traffic. While Bcl-2 coexpression only partially corrects this phenotype, coexpression of BI-GST fully restores the organelles, indicating a different mode of protection exerted by Bcl-2 and BI-GST. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：100 / 104

页数：5

共 29 条

[1] An ARL1 mutation affected autophagic cell death in yeast, causing a defect in central vacuole formation [J].