Mitochondrial Stress Signaling Promotes Cellular Adaptations

Barbour, Jayne A.; Turner, Nigel

doi:10.1155/2014/156020

Cited by 76 publications

(55 citation statements)

References 136 publications

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“…This result suggests that not only is nuclear DNA damage verification an important cell cycle checkpoint, but organellar DNA damage verification is as well. Because mitochondrial dysfunction is efficiently signaled to the nucleus (Van Aken et al, 2009;De Clercq et al, 2013), mitochondrial DNA stress is also likely to cause a retrograde signal affecting nuclear gene expression (Barbour and Turner, 2014) and to affect plant development as such. In animals, a mitochondrial damage checkpoint during the cell cycle has been proposed because mitochondrial dysfunction leads to cell cycle arrest, cellular senescence, and tumorigenic phenotype (reviewed in Singh, 2006;van Gisbergen et al, 2015).…”

Section: Importance Of Mitochondrial Proteins In Plant Growthmentioning

confidence: 99%

The Mitochondrial DNA (mtDNA)-Associated Protein SWIB5 Influences mtDNA Architecture and Homologous Recombination

et al. 2017

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In addition to the nucleus, mitochondria and chloroplasts in plant cells also contain genomes. Efficient DNA repair pathways are crucial in these organelles to fix damage resulting from endogenous and exogenous factors. Plant organellar genomes are complex compared with their animal counterparts, and although several plant-specific mediators of organelle DNA repair have been reported, many regulators remain to be identified. Here, we show that a mitochondrial SWI/SNF (nucleosome remodeling) complex B protein, SWIB5, is capable of associating with mitochondrial DNA (mtDNA) in Arabidopsis thaliana. Gain-and loss-of-function mutants provided evidence for a role of SWIB5 in influencing mtDNA architecture and homologous recombination at specific intermediate-sized repeats both under normal and genotoxic conditions. SWIB5 interacts with other mitochondrial SWIB proteins. Gene expression and mutant phenotypic analysis of SWIB5 and SWIB family members suggests a link between organellar genome maintenance and cell proliferation. Taken together, our work presents a protein family that influences mtDNA architecture and homologous recombination in plants and suggests a link between organelle functioning and plant development.

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Section: Importance Of Mitochondrial Proteins In Plant Growthmentioning

confidence: 99%

The Mitochondrial DNA (mtDNA)-Associated Protein SWIB5 Influences mtDNA Architecture and Homologous Recombination

et al. 2017

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“…More fission leads to more fragmented and smaller mitochondria, which are easily detected as damaged mitochondria and are degraded by mitophagy. Lower mitochondrial membrane potential diminishes fusion and promotes fission and mitophagy [22]. Unbalanced fusion leads to mitochondrial elongation while unbalanced fission leads to excessive mitochondrial fragmentation, both of which can lead to impaired mitochondrial functions (Fig.…”

Section: Mitochondrial Fission Fusion and Autophagy (Mitophagy)mentioning

confidence: 99%

“…Fatty acids have a role in regulating the activity of MPT pore which links lipids with mitochondrial dysfunction as well as with mitochondrial degradation (Fig. 4) [22]. Mitophagy mediated by MPT pore can also be induced by Drp1 translocation from cytosol to mitochondria.…”

Section: Mitochondrial Fission Fusion and Autophagy (Mitophagy)mentioning

confidence: 99%

Abnormal Glucose Metabolism in Alzheimer’s Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches

et al. 2015

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Diminished glucose metabolism accompanies many neurodegenerative diseases including Alzheimer’s disease. An understanding of the relation of these metabolic changes to the disease will enable development of novel therapeutic strategies. Following a metabolic challenge, cells generally conserve energy to preserve viability. This requires activation of many cellular repair/regenerative processes such as mitophagy/autophagy and fusion/fission. These responses may diminish cell function in the long term. Prolonged fission induces mitophagy/autophagy which promotes repair but if prolonged progresses to mitochondrial degradation. Abnormal glucose metabolism alters protein signaling including the release of proteins from the mitochondria or migration of proteins from the cytosol to the mitochondria or nucleus. This overview provides an insight into the different mechanisms of autophagy/mitophagy and mitochondrial dynamics in response to the diminished metabolism that occurs with diseases, especially neurodegenerative diseases such as Alzheimer's disease. The review discusses multiple aspects of mitochondrial responses including different signaling proteins and pathways of mitophagy and mitochondrial biogenesis. Improving cellular bioenergetics and mitochondrial dynamics will alter protein signaling and improve cellular/mitochondrial repair and regeneration. An understanding of these changes will suggest new therapeutic strategies.

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“…Multiple studies of preeclampsia and IUGR have shown increases in mitochondrial content [16,[19][20][21][22], indicating placental mitochondrial biogenesis is initiated in reaction to adverse conditions [23].…”

Section: Introductionmentioning

confidence: 99%

Changes in mitochondrial respiration in the human placenta over gestation

et al. 2017

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Respiration and mitochondrial content alter over gestation/with labour. Decreased respiration at 11 weeks and increased mitochondrial content at 12-13 weeks may relate to onset of maternal blood flow, and increased respiration as a result of labour may be an adaptation to ischaemia-reperfusion. At term, mitochondria were more susceptible to changes in respiratory function relative to first trimester when cultured in vitro, perhaps reflecting changes in metabolic demands as gestation progresses. Metabolic plasticity of placental mitochondria has relevance to placenta-mediated diseases.

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Mitochondrial Stress Signaling Promotes Cellular Adaptations

Cited by 76 publications

References 136 publications

The Mitochondrial DNA (mtDNA)-Associated Protein SWIB5 Influences mtDNA Architecture and Homologous Recombination

The Mitochondrial DNA (mtDNA)-Associated Protein SWIB5 Influences mtDNA Architecture and Homologous Recombination

Abnormal Glucose Metabolism in Alzheimer’s Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches

Changes in mitochondrial respiration in the human placenta over gestation

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