ArticleThe Plant cell2003
Leaf mitochondria modulate whole cell redox homeostasis, set antioxidant capacity, and determine stress resistance through altered signaling and diurnal regulation.
Article in The Plant cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.
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Who cites it
170 citing papers in PubMed, 513 citations in OpenAlex.
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- The biogenesis and regulation of the plant oxidative phosphorylation system.Plant physiology · 2023Review
- Submergence Stress Alters the Expression of Clock Genes and Configures New Zeniths and Expression of Outputs inInternational journal of molecular sciences · 2023Article
- Genome-wide characterization of L-aspartate oxidase genes in wheat and their potential roles in the responses to wheat disease and abiotic stresses.Frontiers in plant science · 2023Article
- Mitochondrial Complex I Disruption Causes Broad Reorchestration of Plant Lipidome Including Chloroplast Lipids.International journal of molecular sciences · 2022Article
- Redox status of the plant cell determines epigenetic modifications under abiotic stress conditions and during developmental processes.Journal of advanced research · 2022Review
110 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the role of plant mitochondria in the regulation of cellular redox homeostasis and stress resistance, we exploited a Nicotiana sylvestris mitochondrial mutant. The cytoplasmic male-sterile mutant (CMSII) is impaired in complex I function and displays enhanced nonphosphorylating rotenone-insensitive [NAD(P)H dehydrogenases] and cyanide-insensitive (alternative oxidase) respiration. Loss of complex I function is not associated with increased oxidative stress, as shown by decreased leaf H(2)O(2) and the maintenance of glutathione and ascorbate content and redox state. However, the expression and activity of several antioxidant enzymes are modified in CMSII. In particular, diurnal patterns of alternative oxidase expression are lost, the relative importance of the different catalase isoforms is modified, and the transcripts, protein, and activity of cytosolic ascorbate peroxidase are enhanced markedly. Thus, loss of complex I function reveals effective antioxidant crosstalk and acclimation between the mitochondria and other organelles to maintain whole cell redox balance. This reorchestration of the cellular antioxidative system is associated with higher tolerance to ozone and Tobacco mosaic virus.
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