Journal
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
Volume 1817, Issue 10, Pages 1886-1893Publisher
ELSEVIER
DOI: 10.1016/j.bbabio.2012.05.001
Keywords
Mitochondrion; OPA1; PARL; Heat shock response; Cytochrome c release; Apoptosis
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Funding
- Dulbecco-Telethon Institute
- Telethon Italy [S02016]
- AIRC
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The mitochondria-shaping protein optic atrophy 1 (OPA1) has genetically distinguishable roles in mitochondrial morphology and apoptosis. The latter depends on the presenilin associated rhomboid like (PARL) protease, essential for the accumulation of a soluble intermembrane space form of OPA1 (IMS-OPA1). Here we show that OPA1 and PARL participate in the heat shock response, a stereotypical cellular process of adaptation to thermal stress. Upon heat shock, long forms of OPA1 are lost and mitochondria fragment. However. mitochondrial fusion is dispensable to maintain viability, whereas IMS-OPA1 is required. Upon conditioning a process of mild heat shock and recovery IMS-OPA1 accumulates, OPA1 oligomers increase and mitochondria release less cytochrome c, ultimately resulting in cellular resistance to subsequent apoptotic inducers. In Parl(-/-) cells accumulation of IMS-OPA1 is blunted and conditioning fails to protect from cytochrome c release and apoptosis. Thus, the OPA1/PARL dependent pathway of cristae remodeling is implicated in heat shock. This article is part of a Special Issue entitled: 17th European Bioenergetics Conference (EBEC 2012). (C) 2012 Elsevier B.V. All rights reserved.
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