2007
DOI: 10.1016/j.tplants.2007.01.005
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Mitochondrial redox biology and homeostasis in plants

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Cited by 458 publications
(321 citation statements)
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References 103 publications
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“…Lower capacity of complex I-deficient mutant cells to reoxidize cellular NADH must limit the rate of catabolic pathways (Krebs cycle, glycolysis and acetate assimilation). In photosynthetic organisms, reducing equivalents generated by photosynthetic electron transfer chain can in part be consumed by the mitochondrial respiratory chain, owing to metabolic exchanges between the two organelles (reviewed in Cardol et al, 2011;Noctor et al, 2007). This process can be mediated by the activity of the malate-aspartate shuttle (Noguchi and Yoshida, 2008), whose genes are present in Chlamydomonas (Merchant et al, 2007).…”
Section: Discussionmentioning
confidence: 99%
“…Lower capacity of complex I-deficient mutant cells to reoxidize cellular NADH must limit the rate of catabolic pathways (Krebs cycle, glycolysis and acetate assimilation). In photosynthetic organisms, reducing equivalents generated by photosynthetic electron transfer chain can in part be consumed by the mitochondrial respiratory chain, owing to metabolic exchanges between the two organelles (reviewed in Cardol et al, 2011;Noctor et al, 2007). This process can be mediated by the activity of the malate-aspartate shuttle (Noguchi and Yoshida, 2008), whose genes are present in Chlamydomonas (Merchant et al, 2007).…”
Section: Discussionmentioning
confidence: 99%
“…Inhibition of Complex I by inhibitors, such as rotenone, or by loss of subunits as in the mutants described above leads to problems with primary metabolism in the affected plants (reviewed in Noctor et al, 2007). The primary entry point for electrons into the electron transport chain is missing, leading to a loss in ATP synthesis and an initial buildup of unoxidized NADH.…”
Section: The Effects Of a Loss Of Complex I Activitymentioning
confidence: 99%
“…Deficiency in Complex I function has been associated with various human diseases, including neurodegenerative diseases, and the aging process (Adam-Vizi and Chinopoulos, 2006;Janssen et al, 2006). In plants, this complex is still the major entry point under normal conditions, even though the electron transport chain is potentially more complicated due to the presence of alternative NAD(P)H dehydrogenases and alternative oxidase (reviewed in Noctor et al, 2007). Due to these alternative pathways, the plant mitochondrial respiratory chain has been a popular target for biochemical studies.…”
Section: Introductionmentioning
confidence: 99%
“…Thirdly, the available evidence suggests that the many kinetic constraints on metabolic carbon flow are exquisitely coordinated (Raghavendra & Padmasree 2003;Noctor, De Paepe & Foyer 2006;Rasmusson & Escobar 2007). Any effective model of respiration should at least attempt to capture this coordination.…”
Section: Some Thoughts On the Nature Of Our Modelmentioning
confidence: 99%
“…This could be done from the bottom up, by explicitly describing the many regulatory 'throttles' available to plant cells -for example, control of mitochondrial electron transport and reactions of glycolysis by adenylates, negative feedback inhibition of mitochondrial NAD(P)H dehydrogenases by NADH, redox regulation of alternative oxidase, and inactivation of pyruvate decarboxylase in the light by phosphorylation. We refer readers to the several excellent reviews and textbooks on the subject (Buchanan et al 2000;Atkin & Tjoelker 2003;Noctor et al 2006;Plaxton & Podesta 2006;Rasmusson & Escobar 2007;Lambers et al 2008). Our model captures this coordination from the top down, by applying a single synthetic hypothesis, rather than by attempting to describe this vast array of regulatory processes.…”
Section: Some Thoughts On the Nature Of Our Modelmentioning
confidence: 99%