Abstract
Commitment to apoptotic cell death occurs at the mitochondria and is regulated by BCL-2 family proteins localized to this organelle. However, BIK, a resident protein of the endoplasmic reticulum, inhibits mitochondrial BCL-2 proteins to promote apoptosis. In a recent paper in the JBC, Osterlund et al. investigated this conundrum. Surprisingly, they discovered that these endoplasmic reticulum and mitochondrial proteins moved toward each other and met at the contact site between the two organelles, thereby forming a 'bridge to death'.