Use of mitochondrial electron transport mutants to evaluate the effects of redox state on photosynthesis, stress tolerance and the integration of carbon/nitrogen metabolism
Identifieur interne : 000032 ( France/Analysis ); précédent : 000031; suivant : 000033Use of mitochondrial electron transport mutants to evaluate the effects of redox state on photosynthesis, stress tolerance and the integration of carbon/nitrogen metabolism
Auteurs : Graham Noctor [France] ; Christelle Dutilleul [France] ; Rosine De Paepe [France] ; Christine H. Foyer [Royaume-Uni]Source :
- Journal of Experimental Botany [ 0022-0957 ] ; 2004-01-01.
English descriptors
- KwdEn :
- Teeft :
- Alternative oxidase, Amino, Amino acids, Ammonia, Annual review, Chloroplast, Cmsii, Cmsii mitochondria, Cycle activity, Dehydrogenase, Dutilleul, Electron transport chain, Experimental botany, Foyer, Gene expression, Kromer, Leaf metabolism, Leaf mitochondria, Major nadh, Malate, Metabolism, Mitochondrial, Mitochondrial electron transport, Mitochondrial electron transport chain, Mitochondrial redox state, Mitochondrion, Mutant, Nadh, National academy, Ndin, Nicotiana, Nicotiana sylvestris, Nitrogen assimilation, Nitrogen metabolism, Noctor, Nuclear gene expression, Other components, Oxidative, Pathway, Photorespiration, Photorespiratory, Photosynthesis, Photosynthetic, Photosynthetic capacity, Physiologia plantarum, Physiology, Plant physiology, Plant science, Reactive oxygen species, Redox, Redox interactions, Redox state, Reductant, Reduction state, Respiration, Sabar, Stress resistance, Stress tolerance, Sucrose synthesis, Sylvestris, Unpublished results, Wild type.
Abstract
Primary leaf metabolism requires the co‐ordinated production and use of carbon skeletons and redox equivalents in several subcellular compartments. The role of the mitochondria in leaf metabolism has long been recognized, but it is only recently that molecular tools and mutants have become available to evaluate cause‐and‐effect relationships. In particular, analysis of the CMSII mutant of Nicotiana sylvestris, which lacks functional complex I, has provided information on the role of mitochondrial electron transport in leaf function. The essential feature of CMSII is the absence of a major NADH sink, i.e. complex I. This necessitates re‐adjustment of whole‐cell redox homeostasis, gene expression, and also influences metabolic pathways that use pyridine nucleotides. In air, CMSII is not able to use its photosynthetic capacity as well as the wild type. The mutant shows up‐regulation of the leaf antioxidant system, lower leaf contents of reactive oxygen species, and enhanced stress resistance. Lastly, the loss of a major mitochondrial dehydrogenase has important repercussions for the integration of primary carbon and nitrogen metabolism, causing distinct changes in leaf organic acid profiles, and also affecting downstream processes such as the biosynthesis of the spectrum of leaf amino acids.
Url:
DOI: 10.1093/jxb/erh021
Affiliations:
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<term>Annual review</term>
<term>Chloroplast</term>
<term>Cmsii</term>
<term>Cmsii mitochondria</term>
<term>Cycle activity</term>
<term>Dehydrogenase</term>
<term>Dutilleul</term>
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<term>Experimental botany</term>
<term>Foyer</term>
<term>Gene expression</term>
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<term>Leaf metabolism</term>
<term>Leaf mitochondria</term>
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<term>Malate</term>
<term>Metabolism</term>
<term>Mitochondrial</term>
<term>Mitochondrial electron transport</term>
<term>Mitochondrial electron transport chain</term>
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<term>Nadh</term>
<term>National academy</term>
<term>Ndin</term>
<term>Nicotiana</term>
<term>Nicotiana sylvestris</term>
<term>Nitrogen assimilation</term>
<term>Nitrogen metabolism</term>
<term>Noctor</term>
<term>Nuclear gene expression</term>
<term>Other components</term>
<term>Oxidative</term>
<term>Pathway</term>
<term>Photorespiration</term>
<term>Photorespiratory</term>
<term>Photosynthesis</term>
<term>Photosynthetic</term>
<term>Photosynthetic capacity</term>
<term>Physiologia plantarum</term>
<term>Physiology</term>
<term>Plant physiology</term>
<term>Plant science</term>
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<term>Redox</term>
<term>Redox interactions</term>
<term>Redox state</term>
<term>Reductant</term>
<term>Reduction state</term>
<term>Respiration</term>
<term>Sabar</term>
<term>Stress resistance</term>
<term>Stress tolerance</term>
<term>Sucrose synthesis</term>
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<front><div type="abstract" xml:lang="en">Primary leaf metabolism requires the co‐ordinated production and use of carbon skeletons and redox equivalents in several subcellular compartments. The role of the mitochondria in leaf metabolism has long been recognized, but it is only recently that molecular tools and mutants have become available to evaluate cause‐and‐effect relationships. In particular, analysis of the CMSII mutant of Nicotiana sylvestris, which lacks functional complex I, has provided information on the role of mitochondrial electron transport in leaf function. The essential feature of CMSII is the absence of a major NADH sink, i.e. complex I. This necessitates re‐adjustment of whole‐cell redox homeostasis, gene expression, and also influences metabolic pathways that use pyridine nucleotides. In air, CMSII is not able to use its photosynthetic capacity as well as the wild type. The mutant shows up‐regulation of the leaf antioxidant system, lower leaf contents of reactive oxygen species, and enhanced stress resistance. Lastly, the loss of a major mitochondrial dehydrogenase has important repercussions for the integration of primary carbon and nitrogen metabolism, causing distinct changes in leaf organic acid profiles, and also affecting downstream processes such as the biosynthesis of the spectrum of leaf amino acids.</div>
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