The α-toxin activates intracellular caspases independently of transmembrane death receptor proteins, and can induce release of cytochrome c from isolated mitochondria. In both cases, however, the mechanism is likely to be indirect. Pores formed by α-toxin are unlikely to be big enough to allow either entry of α-toxin into the cell or exit of cytochrome c from mitochondria. Thus, apoptosis may be triggered by loss of monovalent ions through the plasma membrane pores. In addition, if the bacterium gains access to the inside of the cell, the intracellular α-toxin may form pores in mitochondria that activate a process leading to cytochrome c release. ▪

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