Mitochondrial Dynamics: Functional Link with Apoptosis

Figure 2

Relation between mitochondrial structural changes and the release of IMS-stored apoptogenic factors. During apoptosis in wild-type cells, mitochondrial fragmentation normally occurs concomitantly with MOMP, cristae disorganization, and subsequent release of the IMS-stored apoptogenic factors (e.g., cytochrome 𝑐, smac/DIABLO, HtrA2/omi). Mitochondrial fission facilitates these reactions (State I). In contrast, elongated but cristae-disrupted mitochondria (i.e., Drp1- and OPA1-double RNAi cells; Drp1-KO and OPA1 RNAi cells) exhibit a significant delay only in the cytochrome 𝑐 release in response to apoptotic stimuli, because of the absence of mitochondrial fragmentation. Of note, however, MOM targeting and oligomeric assembly of Bax and the release of the IMS-soluble Smac/DIABLO normally proceed (State II). State III: presumed MOM permeabilized state in the absence of both cristae disorganization and mitochondrial fragmentation. MOMP: mitochondrial outer membrane permeabilization.