Energetic requirements and bioenergetic modulation of mitochondrial morphology and dynamics

Sauvanet, Cécile; Duvezin-Caubet, Stéphane; Rago, Jean‐Paul di; Rojo, Manuel

doi:10.1016/j.semcdb.2009.12.006

Cited by 94 publications

(85 citation statements)

References 62 publications

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“…68 Of note, our data were obtained in cells containing the same mutation and were grown in identical culture conditions therefore minimizing the factors that strongly influence bioenergetic status, morphology and dynamics of mitochondria. 28,69 Therefore, the differences observed in mtQC and bioenergetics are due to the respective cell-type specificity.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial quality control: Cell-type-dependent responses to pathological mutant mitochondrial DNA

et al. 2016

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Pathological mutations in the mitochondrial DNA (mtDNA) produce a diverse range of tissue-specific diseases and the proportion of mutant mitochondrial DNA can increase or decrease with time via segregation, dependent on the cell or tissue type. Previously we found that adenocarcinoma (A549.B2) cells favored wild-type (WT) mtDNA, whereas rhabdomyosarcoma (RD.Myo) cells favored mutant (m3243G) mtDNA. Mitochondrial quality control (mtQC) can purge the cells of dysfunctional mitochondria via mitochondrial dynamics and mitophagy and appears to offer the perfect solution to the human diseases caused by mutant mtDNA. In A549.B2 and RD.Myo cybrids, with various mutant mtDNA levels, mtQC was explored together with macroautophagy/autophagy and bioenergetic profile. The 2 types of tumor-derived cell lines differed in bioenergetic profile and mitophagy, but not in autophagy. A549.B2 cybrids displayed upregulation of mitophagy, increased mtDNA removal, mitochondrial fragmentation and mitochondrial depolarization on incubation with oligomycin, parameters that correlated with mutant load. Conversely, heteroplasmic RD.Myo lines had lower mitophagic markers that negatively correlated with mutant load, combined with a fully polarized and highly fused mitochondrial network. These findings indicate that pathological mutant mitochondrial DNA can modulate mitochondrial dynamics and mitophagy in a cell-type dependent manner and thereby offer an explanation for the persistence and accumulation of deleterious variants.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial quality control: Cell-type-dependent responses to pathological mutant mitochondrial DNA

et al. 2016

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“…Listeria may act similarly, explaining MAVS-independent activation of the innate immune response (53). Given that bioenergetics affect mitochondrial shape, and vice-versa (2,49), it is likely that mitochondrial localization of innate immunity components serves to coordinate innate immune responses with cellular energy levels via sensing of mitochondrial morphology and function. How innate immunity components and the fission/ The mitochondrial membrane potential ΔΨ of HeLa cells was measured in a plate-based TMRE-release assay.…”

Section: Discussionmentioning

confidence: 99%

“…They have emerged as important integrators of several signaling cascades (1). Fusion and fission of mitochondria occurs constantly, regulating their size and subcellular distribution and reflecting their functional state (1,2). Disturbance of mitochondrial dynamics leads to pathological conditions exacerbated in tissues with high metabolic demand such as neuronal or muscle tissues (3).…”

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confidence: 99%

Listeria monocytogenes transiently alters mitochondrial dynamics during infection

Stavru

Bouillaud

Sartori

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

211

214

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Mitochondria are essential and highly dynamic organelles, constantly undergoing fusion and fission. We analyzed mitochondrial dynamics during infection with the human bacterial pathogen Listeria monocytogenes and show that this infection profoundly alters mitochondrial dynamics by causing transient mitochondrial network fragmentation. Mitochondrial fragmentation is specific to pathogenic Listeria monocytogenes, and it is not observed with the nonpathogenic Listeria innocua species or several other intracellular pathogens. Strikingly, the efficiency of Listeria infection is affected in cells where either mitochondrial fusion or fission has been altered by siRNA treatment, highlighting the relevance of mitochondrial dynamics for Listeria infection. We identified the secreted pore-forming toxin listeriolysin O as the bacterial factor mainly responsible for mitochondrial network disruption and mitochondrial function modulation. Together, our results suggest that the transient shutdown of mitochondrial function and dynamics represents a strategy used by Listeria at the onset of infection to interfere with cellular physiology.bacterial infection | calcium influx | bioenergetics

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“…On the other hand, fission would either generate small mitochondria that can be delivered to distant regions of the cell where energy is required, as the synaptic boutons in neuronal axons, or would allow the segregation of pre-existing mitochondria between daughter cells during mitosis (Nakada et al, 2001;Skulachev, 2001;Detmer and Chan, 2007;Twig et al, 2008a). Pioneering works from several laboratories have described some of the proteins involved in the fusion and fission events, amongst which the best characterized are: mitofusin1 and mitofusin 2 (Mfn1, Mfn2), that are involved in the fusion of the outer mitochondrial membrane; OPA1, that mediates mitochondrial inner membrane fusion; and Drp1, known to be essential for mitochondrial fission (reviewed in Chen and Chan, 2009;Sauvanet et al, 2010). Mutations in genes encoding proteins involved in mitochondrial dynamics have been reported and linked to neurodegeneration (Weber and Reichert, 2010).…”

Section: Alterations In Mitochondrial Dynamicsmentioning

confidence: 99%

Mitochondrial respiratory chain dysfunction: Implications in neurodegeneration

Morán

Moreno-Lastres

Marín-Buera

et al. 2012

Free Radical Biology and Medicine

144

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For decades mitochondria have been considered static round shaped organelles in charge of energy production. On the contrary, they are highly dynamic cellular components that undergo continuous cycles of fusion and fission influenced, for instance, by oxidative stress, cellular energy requirements, or the cell cycle state. New important functions beyond energy production have been attributed to mitochondria, such as the regulation of cell survival due to their role in the modulation of apoptosis, autophagy and aging. Primary mitochondrial diseases due to mutations in genes involved in these new mitochondrial functions, and the implication of mitochondrial dysfunction in multifactorial human pathologies like cancer, Alzheimer's and Parkinson's diseases, or diabetes has been demonstrated. Therefore, mitochondria are set at a central point of the equilibrium between health and disease, and a better understanding of mitochondrial functions will open new fields to explore the role of these mitochondrial pathways in human pathologies. The present review will dissect the relationships between the activity and assembly defects of the mitochondrial respiratory chain, oxidative damage, and alterations in mitochondrial dynamics, with special focus at their implications in neurodegeneration.

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Energetic requirements and bioenergetic modulation of mitochondrial morphology and dynamics

Cited by 94 publications

References 62 publications

Mitochondrial quality control: Cell-type-dependent responses to pathological mutant mitochondrial DNA

Mitochondrial quality control: Cell-type-dependent responses to pathological mutant mitochondrial DNA

Listeria monocytogenes transiently alters mitochondrial dynamics during infection

Mitochondrial respiratory chain dysfunction: Implications in neurodegeneration

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