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1.  Mitochondrial Cristae Shape Determines Respiratory Chain Supercomplexes Assembly and Respiratory Efficiency 
Cell  2013;155(1):160-171.
Summary
Respiratory chain complexes assemble into functional quaternary structures called supercomplexes (RCS) within the folds of the inner mitochondrial membrane, or cristae. Here, we investigate the relationship between respiratory function and mitochondrial ultrastructure and provide evidence that cristae shape determines the assembly and stability of RCS and hence mitochondrial respiratory efficiency. Genetic and apoptotic manipulations of cristae structure affect assembly and activity of RCS in vitro and in vivo, independently of changes to mitochondrial protein synthesis or apoptotic outer mitochondrial membrane permeabilization. We demonstrate that, accordingly, the efficiency of mitochondria-dependent cell growth depends on cristae shape. Thus, RCS assembly emerges as a link between membrane morphology and function.
Graphical Abstract
Highlights
•Dissociation of cristae remodeling from OMM permeabilization•Cristae shape determines assembly of respiratory chain supercomplexes•Efficiency of mitochondrial respiration and cellular growth depends on cristae shape
The ability to perturb cristae shape without affecting other key aspects of mitochondrial physiology reveals that membrane shape influences supercomplex assembly and stability to regulate mitochondrial respiration and cellular respiratory growth. Quaternary structures such as supercomplexes therefore emerge as a link between membrane morphology and function.
doi:10.1016/j.cell.2013.08.032
PMCID: PMC3790458  PMID: 24055366
2.  Mitochondrial elongation during autophagy 
Autophagy  2011;7(10):1251-1253.
Mitochondrial morphological and structural changes play a role in several cellular processes, including apoptosis. We recently reported that mitochondrial elongation is also critical to sustain cell viability during macroautophagy. During macroautophagy unopposed mitochondrial fusion leads to organelle elongation both in vitro and in vivo. Longer mitochondria are protected from being degraded and possess more cristae where activity of the ATP synthase is increased, optimizing ATP production in times of nutrient restriction.
doi:10.4161/auto.7.10.16771
PMCID: PMC3242616  PMID: 21743300
mitochondria; autophagy; fusion; cAMP; PKA; DRP-1; cell death
3.  During autophagy mitochondria elongate, are spared from degradation and sustain cell viability 
Nature cell biology  2011;13(5):589-598.
Summary
A plethora of cellular processes, including apoptosis, depend on regulated changes in mitochondrial shape and ultrastructure. Scarce is our understanding of the role of mitochondria and of their morphology during autophagy, a bulk degradation and recycling process of eukaryotic cells’ constituents. Here we show that mitochondrial morphology determines the cellular response to macroautophagy. When autophagy is triggered, mitochondria elongate in vitro and in vivo. Upon starvation cellular cAMP levels increase and protein kinase A (PKA) becomes activated. PKA in turn phosphorylates the pro-fission dynamin related protein 1 (DRP1) that is therefore retained in the cytoplasm, leading to unopposed mitochondrial fusion. Elongated mitochondria are spared from autophagic degradation, possess more cristae, increase dimerization and activity of ATP synthase, and maintain ATP production. When elongation is genetically or pharmacologically blocked, mitochondria conversely consume ATP, precipitating starvation-induced death. Thus, regulated changes in mitochondrial morphology determine the fate of the cell during autophagy.
doi:10.1038/ncb2220
PMCID: PMC3088644  PMID: 21478857

Results 1-3 (3)