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Does apoptosis‐inducing factor (AIF) have both life and death functions in cells?
Author(s) -
Porter Alan G.,
Urbano Alexander G.L.
Publication year - 2006
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.20444
Subject(s) - apoptosis inducing factor , microbiology and biotechnology , mitochondrion , programmed cell death , biology , neurodegeneration , apoptosis , fragmentation (computing) , nucleus , cytoplasm , dna fragmentation , genetics , pathology , medicine , caspase , ecology , disease
Apoptosis‐inducing factor (AIF) is expelled from mitochondria after some apoptotic stimuli and translocates to the nucleus, which may contribute to DNA and nuclear fragmentation in some non‐physiological mammalian cell deaths. Conversely, the requirement for mitochondrial AIF in oxidative phosphorylation and energy generation provides a plausible explanation for the embryonic lethality or neurodegeneration that has been found in different AIF‐deficient mouse models. These findings may help illuminate the ability of mitochondrial AIF to suppress cytoplasmic stress granule formation and to promote the tumorigenic growth of cancer cells. AIF is ideally located in the mitochondrion to perform a vital normal function in energy production. Once it translocates to the nucleus, however, the cell might die either of energy failure or nuclear fragmentation (or both). We propose that the main function of AIF is to support energy production in both normal and transformed cell physiology, whereas nuclear‐translocated AIF might contribute to stress‐induced or pathological cell death in certain scenarios. BioEssays 28: 834–843, 2006. © 2006 Wiley Periodicals, Inc.