BH3-only protein Bim inhibits activity of antiapoptotic members of Bcl-2 family when expressed in yeast

AbstractProteins of the Bcl-2 family regulate programmed cell death in mammals by promoting the release of cytochrome c from mitochondria in response to various proapoptotic stimuli. The mechanism by which BH3-only members of the family activate multidomain proapoptotic proteins Bax and Bak to form a pore in mitochondrial membranes remains under dispute. We report that cell death promoting activity of BH3-only protein Bim can be reconstituted in yeast when both Bax and antiapoptotic protein Bcl-XL are present, suggesting that Bim likely activates Bax indirectly by inhibiting antiapoptotic proteins