Investigation of bax-induced release of cytochrome c from yeast mitochondria permeability of mitochondrial membranes, role of VDAC and ATP requirement.

摘要: Recent studies that attempt to explore the action of pro- and anti-apoptotic proteins bcl2 family demonstrate crucial role relocalization cytochrome c from mitochondrial intermembrane space cytosol. This early event apoptosis can be mimicked in yeast Saccharomyces cerevisiae following expression bax. In mammalian mitochondria, mechanism is thought involve opening so-called permeability transition pore. We show this paper: (a) bax-induced release does not any inner membrane but involves a general alteration outer macromolecules. suggests an required for yeast. (b) The outer-membrane voltage-dependent anion channel (VDAC), putative component pore, involved or prevention by bcl-xL. (c) Bax devoid its C-terminal hydrophobic α-helix as efficient full-length bax allow c, demonstrating segment protein membrane-targeting. (d) finally observe on requires presence ATP both vitro vivo, it shown directly increases amount inserted mitochondria.