Wednesday, 15 October 2014

OPA1‐dependent cristae modulation is essential for cellular adaptation to metabolic demand

OPA1 mediates fusion of the inner mitochondrial membrane and is also involved in cristae remodelling. Maintenance of the cristae structure requires oligomerization of OPA1 because disruption of OPA1 oligomers is necessary for cristae opening and cytochrome c release.

In this paper, they observe that OPA1 dynamically regulates cristae shape and that OPA1 is required for resistance against starvation-induced cell death, and that these processes are independent of mitochondrial fusion (a mutant of OPA1 that does oligomerize but has no fusion activity is still able to maintain cristae structure).

They also show that some group of mitochondrial solute carriers (SLC25A) interacts with OPA1. These SLC25A transporters can sense changes in energy substrate availability. So if there are changes in energy substrate levels, SLC25A transporters respond to this and in turn interact with OPA1 which modulates cristae structure (which regulates assembly of ATP synthases) to respond to the change in energy substrate availability. All of this is independent of OPA1's role in fusion.

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