Premium
Intersection of mitochondrial fission and fusion machinery with apoptotic pathways: Role of Mcl‐1
Author(s) -
Morciano Giampaolo,
Pedriali Gaia,
Sbano Luigi,
Iannitti Tommaso,
Giorgi Carlotta,
Pinton Paolo
Publication year - 2016
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1111/boc.201600019
Subject(s) - mitochondrial fission , microbiology and biotechnology , biology , mitochondrion , mitochondrial fusion , intermembrane space , mfn2 , apoptosis , apoptosome , cytosol , dnaja3 , mitochondrial apoptosis induced channel , mitochondrial intermembrane space , programmed cell death , dnm1l , mfn1 , cytochrome c , mitochondrial dna , caspase , genetics , bacterial outer membrane , biochemistry , escherichia coli , gene , enzyme
Mitochondria actively contribute to apoptotic cell death through mechanisms including the loss of integrity of the outer mitochondrial membrane, the release of intermembrane space proteins, such as cytochrome c, in the cytosol and the caspase cascade activation. This process is the result of careful cooperation not only among members of the Bcl‐2 family but also dynamin‐related proteins. These events are often accompanied by fission of the organelle, thus linking mitochondrial dynamics to apoptosis. Emerging evidences are suggesting a fine regulation of mitochondrial morphology by Bcl‐2 family members and active participation of fission–fusion proteins in apoptosis. The debate whether in mitochondrial morphogenesis the role of Bcl‐2 family members is functionally distinct from their role in apoptosis is still open and, above all, which morphological changes are associated with cell death sensitisation. This review will cover the findings on how the mitochondrial fission and fusion machinery may intersect apoptotic pathways focusing on recent advances on the key role played by Mcl‐1.