Which came first, the cytochrome c release or the mitochondrial fission?
Which came first, the cytochrome c release or the mitochondrial fission?
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DOI:
10.1038/sj.cdd.4401985
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发表时间:
2006-08-01
影响因子:
12.4
通讯作者:
Youle, R. J.
中科院分区:
文献类型:
--
作者:
Martinou, J-C;Youle, R. J.
Mitochondria play a crucial role in apoptosis triggered by many stimuli. They integrate death signals through Bcl-2 family members and coordinate caspase activation through the release of apoptogenic factors, such as cytochrome c, as a result of the outer mitochondrial membrane becoming permeable. At the same time, mitochondria fragment and their internal ultrastructure is altered. Here, we attempt to summarize current views of the mechanism that leads to mitochondrial fission during apoptosis and the role that this event plays in this process.Mitochondria are essential for life of eukaryotic cells as they are the main source of energy. Depending on the cell type and the metabolic demands, these organelles can adopt various shapes from long, tubular and filamentous to small and punctiform. 1 Their morphology is dynamically remodeled for a large part by continuous events of fission and fusion. The protein machineries responsible for mitochondrial fusion and fission are described in Box 1. When fusion events overcome fission events, then mitochondria are elongated whereas they are punctiform when fission events are predominant. In most cell types, including primary and transformed cells, mitochondria are predominantly elongated and densely packed in the perinuclear region. However, in primary hepatocytes, they are punctiform and evenly distributed within the cell. 2 Mitochondria are also essential for apoptosis triggered by many stimuli. When cells undergo apoptosis, the morphology of mitochondria changes resulting in small, round and more numerous organelles. The observation that the morphology of mitochondria is altered during cell death is not new. More than 50 years ago, well before the seminal description of apoptosis by Kerr et al., 3 Roullier4 observed a reduction in mitochondrial volume during cell death. This phenomenon was not reported by Kerr et al. 3 who may not have been able to determine in detail the length of