Yeast mutants resistant to Bax lethality reveal distinct vacuolar and mitochondrial alterations

Dear Editor,

The Bcl-2 family of proteins is at the core of the metazoan cell death machinery. Bax, a proapoptotic member of this family, is thought to regulate critical control points of cell death in the endoplasmic reticulum (ER) and mitochondria.¹ In mammalian cells, Bax normally resides in the cytoplasm, and only upon apoptotic stimulation does the protein translocate and insert into the mitochondrial membrane and the ER. The regulated insertion of Bax into the outer mitochondrial membrane elicits a number of changes in mitochondrial physiology that include membrane depolarization and the release of apoptosis-promoting factors, such as cytochrome c.²

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