| First Author | Sanjuán Szklarz LK | Year | 2012 |
| Journal | Biochim Biophys Acta | Volume | 1817 |
| Issue | 10 | Pages | 1886-93 |
| PubMed ID | 22579715 | Mgi Jnum | J:188075 |
| Mgi Id | MGI:5439076 | Doi | 10.1016/j.bbabio.2012.05.001 |
| Citation | Sanjuan Szklarz LK, et al. (2012) The antiapoptotic OPA1/Parl couple participates in mitochondrial adaptation to heat shock. Biochim Biophys Acta 1817(10):1886-93 |
| abstractText | 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). |
