Oxidative Stress and Leaf Senescence

Zentgraf, Ulrike

doi:10.1002/9781119312994.apr0265

Cited by 5 publications

(6 citation statements)

References 124 publications

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“…There are many reports supporting the participation of ROS in the execution of the senescence program, without discrimination of their origin ( Van Breusegem and Dat, 2006 ; Zentgraf, 2007 ; Niewiadomska et al, 2009 ; Sedigheh et al, 2011 ; Jajic et al, 2015 ). ROS may coordinate senescence progress via chloroplast degradation through the activity of ATAF1, a H 2 O 2 -responsive transcriptional regulator that induces expression of the senescence-promoting transcription factor ORESARA1 while repressing the GLK1 gene involved in photosynthesis and chloroplast maintenance ( Garapati et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Expression of a Plastid-Targeted Flavodoxin Decreases Chloroplast Reactive Oxygen Species Accumulation and Delays Senescence in Aging Tobacco Leaves

et al. 2018

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Leaf senescence is a concerted physiological process involving controlled degradation of cellular structures and reallocation of breakdown products to other plant organs. It is accompanied by increased production of reactive oxygen species (ROS) that are proposed to signal cell death, although both the origin and the precise role of ROS in the execution of this developmental program are still poorly understood. To investigate the contribution of chloroplast-associated ROS to natural leaf senescence, we used tobacco plants expressing a plastid-targeted flavodoxin, an electron shuttle flavoprotein present in prokaryotes and algae. When expressed in plants, flavodoxin specifically prevents ROS formation in chloroplasts during stress situations. Senescence symptoms were significantly mitigated in these transformants, with decreased accumulation of chloroplastic ROS and differential preservation of chlorophylls, carotenoids, protein contents, cell and chloroplast structures, membrane integrity and cell viability. Flavodoxin also improved maintenance of chlorophyll-protein complexes, photosynthetic electron flow, CO2 assimilation, central metabolic routes and levels of bioactive cytokinins and auxins in aging leaves. Delayed induction of senescence-associated genes indicates that the entire genetic program of senescence was affected by flavodoxin. The results suggest that ROS generated in chloroplasts are involved in the regulation of natural leaf senescence.

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Section: Discussionmentioning

confidence: 99%

Expression of a Plastid-Targeted Flavodoxin Decreases Chloroplast Reactive Oxygen Species Accumulation and Delays Senescence in Aging Tobacco Leaves

et al. 2018

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“…In this study the general decrease in antioxidative levels during dark-induced senescence was found to be correlated with H 2 O 2 accumulation. The accumulation of H 2 O 2 in leaves is a commonly found effect during dark-induced senescence (Fotopoulos and Kanellis 2013 ; Ding et al 2015 ) and is responsible for the degeneration of lipids, chlorophyll, membranes and organelles and eventually cell death (Mach and Greenberg 2004 ; Zimmermann and Zentgraf 2005 ; Zentgraf 2007 ; Mhamdi et al 2010 ). Further we could demonstrate that H 2 O 2 initially (2 days after dark-induced senescence) accumulated in cell walls, plastids, the cytosol, the tonoplast, and within vacuoles, before symptoms were visible on the leaves.…”

Section: Discussionmentioning

confidence: 99%

“…Reactive oxygen species (ROS) play an important role during these processes as their accumulation during senescence leads to lipid peroxidation, provokes destructive protein modifications, induces mutagenic DNA strand breaks, and causes purine oxidations and protein-DNA-cross links. Furthermore, ROS are involved in senescence through the activation of gene expression, controlling hormone signal transduction and the modulation of specific genes essential for ROS-induced cell death (Mach and Greenberg 2004 ; Zimmermann and Zentgraf 2005 ; Zentgraf 2007 ; Mhamdi et al 2010 ). The accumulation of ROS during senescence is accompanied by a loss of antioxidative capacity in plants and animals (Pastori and del Río 1997 ; Jiménez et al 1998 ; Mach and Greenberg 2004 ; Panchuk et al 2005 ; Palma et al 2006 ; Zimmermann et al 2006 ).…”

Section: Introductionmentioning

confidence: 99%

Compartment-specific investigations of antioxidants and hydrogen peroxide in leaves of Arabidopsis thaliana during dark-induced senescence

Luschin-Ebengreuth

Zechmann

2016

Acta Physiol Plant

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The aim of this study was to gain insight into the compartment-specific roles of ascorbate and glutathione in leaf senescence in Arabidopsis thaliana. The subcellular distribution of ascorbate, glutathione, and hydrogen peroxide (H2O2) was analyzed by transmission electron microscopy and correlated with the activity of antioxidative enzymes in wildtype plants and the ascorbate- and glutathione-deficient mutants vtc2-1 and pad2-1, respectively. Both mutants showed earlier and stronger senescence than the wildtype indicating the importance of a functioning ascorbate and glutathione cycle in the induction and regulation of senescence. Glutathione levels dropped drastically and up to 93 % in all cell compartments of wildtype plants and the vtc2-1 mutant within the first day of dark-induced senescence while ascorbate contents remained unchanged until the very end. Glutathione contents in mitochondria of pad2-1 mutants decreased more slowly over the first 7 days than compared to the other plants indicating an important role of glutathione in mitochondria in this mutant during senescence. The strongest decrease (84 %) of glutathione contents in wildtype plants at this time point was found in mitochondria indicating an important role of mitochondria for the induction of senescence and cell death events. Due to the general decrease of the antioxidative capacity, a strong accumulation of H2O2 was observed in cell walls, plastids, and the cytosol in all plants. Activities of glutathione reductase, dehydroascorbate reductase and catalase were strongly reduced while ascorbate peroxidase and monodehydroascorbate reductase were increased. The initial rapid drop of glutathione levels seemed to be the trigger for senescence, while ascorbate appeared to be the key factor in regulating senescence through controlling H2O2 levels by the oxidation of reduced ascorbate to monodehydroascorbate and the subsequent reduction to ascorbate by monodehydroascorbate reductase.Electronic supplementary materialThe online version of this article (doi:10.1007/s11738-016-2150-6) contains supplementary material, which is available to authorized users.

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“…In summary, these findings highlight the importance of peroxisomal NO metabolism under abiotic stress conditions in plants. ROS production in plant cells shows dramatic increases during senescence and under biotic and abiotic stress (Zentgraf 2007 ). Within this scenario, H 2 O 2 plays a key role.…”

Section: Mysterious Messengers: Peroxisomes In Signalling and Antivirmentioning

confidence: 99%

The peroxisome: an update on mysteries 2.0

Islinger

Voelkl

Fahimi

et al. 2018

Histochem Cell Biol

244

227

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Peroxisomes are key metabolic organelles, which contribute to cellular lipid metabolism, e.g. the β-oxidation of fatty acids and the synthesis of myelin sheath lipids, as well as cellular redox balance. Peroxisomal dysfunction has been linked to severe metabolic disorders in man, but peroxisomes are now also recognized as protective organelles with a wider significance in human health and potential impact on a large number of globally important human diseases such as neurodegeneration, obesity, cancer, and age-related disorders. Therefore, the interest in peroxisomes and their physiological functions has significantly increased in recent years. In this review, we intend to highlight recent discoveries, advancements and trends in peroxisome research, and present an update as well as a continuation of two former review articles addressing the unsolved mysteries of this astonishing organelle. We summarize novel findings on the biological functions of peroxisomes, their biogenesis, formation, membrane dynamics and division, as well as on peroxisome–organelle contacts and cooperation. Furthermore, novel peroxisomal proteins and machineries at the peroxisomal membrane are discussed. Finally, we address recent findings on the role of peroxisomes in the brain, in neurological disorders, and in the development of cancer.

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Oxidative Stress and Leaf Senescence

Abstract: The sections in this article areIntroductionAntioxidative Capacity, Oxidative Stress and Life SpanAntioxidantsROSSignalingRole of Different Cell CompartmentsConcluding Remarks

Cited by 5 publications

References 124 publications

Expression of a Plastid-Targeted Flavodoxin Decreases Chloroplast Reactive Oxygen Species Accumulation and Delays Senescence in Aging Tobacco Leaves

Expression of a Plastid-Targeted Flavodoxin Decreases Chloroplast Reactive Oxygen Species Accumulation and Delays Senescence in Aging Tobacco Leaves

Compartment-specific investigations of antioxidants and hydrogen peroxide in leaves of Arabidopsis thaliana during dark-induced senescence

The peroxisome: an update on mysteries 2.0

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