Dynamics of Mitochondrial Morphology in Apoptosis

Abstract: Mitochondria play an important role in apoptosis by integrating intrinsic and extrinsic apoptotic signals and releasing cytochrome c to initiate caspase cascade. In traditional opinions， there are no changes or nonspecific changes of mitochondrial morphology in early stage of apoptosis. With the discovery of frequent mitochondria fusion and fission in living cells and application of electron tomography plus 3D imaging in cell biology， concept has been renewed in recent years. Mitochondria in cell form a highly interconnected dynamic tubular network and undergo frequent fusion and fission mediated by series of molecules called fusion-fission proteins. The dynamic balance between fusion and fission maintains mitochondrial morphology and function. Once apoptosis is triggered and the balance is perturbed， mitochondrial tubular network will shift to fragmentation and the cristae will become remodeling. These changes are essential for downstream events of apoptosis including cytochrome c release and caspase cascade. Fusion-fission proteins influence the course of apoptosis via controlling mitochondrial morphology and ultrastructure， and may be responsible for apoptosis related disease， such as dominant optic atrophy (DOA) and Charcot-Marie-Tooth neuropathy (CMT). On the other hand， apoptosis-regulating molecules such as Bcl-2 family members can also impact mitochondrial morphology. All these evidences imply significance of mitochondrial morphology in apoptosis and promote mitochondria to a higher position in cell survival and death.

CSTR: 32200.14.cjcb.2006.05.0007