Reactive Oxygen Species in Plant Cell Death

Breusegem, Frank Van; Dat, James F.

doi:10.1104/pp.106.078295

Cited by 837 publications

(518 citation statements)

References 74 publications

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“…Increased production of NO and/or H 2 O 2 in plants responding to abiotic stresses can cause cell death (Brüne 2003; Gao et al 2008;Breusegem and Dat 2006;Arasimowicz et al 2012;Domingos et al 2015). Our present study showed that SO 2 toxicity was decreased by scavengers of NO or H 2 O 2 and could be completely reversed when NO and H 2 O 2 scavengers were both present.…”

Section: Discussionsupporting

confidence: 56%

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

Bai

Xue

et al. 2017

Environ Sci Pollut Res

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NO and H 2 O 2 have been implicated as important signals in biotic and abiotic stress responses of plants to the environment. Previously, we have shown that SO 2 exposure increased the levels of NO and H 2 O 2 in plant cells. We hypothesize that, as signaling molecules, NO and H 2 O 2 mediate SO 2 -caused toxicity. In this paper, we show that SO 2 hydrates caused guard cell death in a concentration-dependent manner in the concentration range of 0.25 to 6 mmol L −1 , which was associated with elevation of intracellular NO, H 2 O 2 , and Ca 2+ levels in Vicia faba guard cells. NO donor SNP enhanced SO 2 toxicity, while NO scavenger c-PTIO and NO synthesis inhibitors L-NAME and tungstate significantly prevented SO 2 toxicity. ROS scavenger ascorbic acid (AsA) and catalase (CAT), Ca 2+ chelating agent EGTA, and Ca 2+ channel inhibitor LaCl 3 also markedly blocked SO 2 toxicity. In addition, both c-PTIO and AsA could completely block SO 2 -induced elevation of intracellular Ca 2+ level. Moreover, c-PTIO efficiently blocked SO 2 -induced H 2 O 2 elevation, and AsA significantly blocked SO 2 -induced NO elevation. These results indicate that extra NO and H 2 O 2 are produced and accumulated in SO 2 -treated guard cells, which further activate Ca 2+ signaling to mediate SO 2 toxicity. Our findings suggest that both NO and H 2 O 2 contribute to SO 2 toxicity via Ca 2+ signaling.

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Section: Discussionsupporting

confidence: 56%

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

Bai

Xue

et al. 2017

Environ Sci Pollut Res

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“…Lipid peroxidation releases H 2 O 2 , which can then trigger PCD (Van Breusegem and Dat, 2006;Keunen et al, 2013). The identity of the genes activated or upregulated in the barley ETCs over the period 10 to 12 DAP (Thiel et al, 2012) suggests that redox homeostasis occurs during late ETC development when transfer cell architecture is established.…”

Section: Inulin-type Fructans Accumulate In Transfer Cell Tissuesmentioning

confidence: 99%

“…Cells that actively mediate transport processes produce substantial quantities of ROS (Luthje et al, 2013). The hydroxyl radical ( c OH), thought to be the most reactive ROS (Van Breusegem and Dat, 2006;Gadjev et al, 2008), is formed by the Fenton reaction from hydrogen peroxide ( Figure 7B; Fenton, 1894). The interaction of sugars with the hydroxyl radical is thought to involve a hydrogen transfer from a sugar C-H bond (Hernandez-Marin and Martínez, 2012).…”

Section: Oligosaccharides React With Hydroxyl Radicalsmentioning

confidence: 99%

Spatio-Temporal Dynamics of Fructan Metabolism in Developing Barley Grains

et al. 2014

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Barley (Hordeum vulgare) grain development follows a series of defined morphological and physiological stages and depends on the supply of assimilates (mainly sucrose) from the mother plant. Here, spatio-temporal patterns of sugar distributions were investigated by mass spectrometric imaging, targeted metabolite analyses, and transcript profiling of microdissected grain tissues. Distinct spatio-temporal sugar balances were observed, which may relate to differentiation and grain filling processes. Notably, various types of oligofructans showed specific distribution patterns. Levan-and graminan-type oligofructans were synthesized in the cellularized endosperm prior to the commencement of starch biosynthesis, while during the storage phase, inulin-type oligofructans accumulated to a high concentration in and around the nascent endosperm cavity. In the shrunken endosperm mutant seg8, with a decreased sucrose flux toward the endosperm, fructan accumulation was impaired. The tight partitioning of oligofructan biosynthesis hints at distinct functions of the various fructan types in the young endosperm prior to starch accumulation and in the endosperm transfer cells that accomplish the assimilate supply toward the endosperm at the storage phase.

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“…In high doses, ROS can be very harmful to living cells, ultimately leading to induction of cell death (Van Breusegem and Dat, 2006). In order to avoid the damage caused by ROS, aerobic organisms developed an antioxidant machinery to control the levels of different reactive species.…”

Section: Introductionmentioning

confidence: 99%

Modulation of host ROS metabolism is essential for viral infection of a bloom-forming coccolithophore in the ocean

et al. 2016

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The cosmopolitan coccolithophore Emiliania huxleyi is a unicellular eukaryotic alga responsible for vast blooms in the ocean. These blooms have immense impact on large biogeochemical cycles and are terminated by a specific large double-stranded DNA E. huxleyi virus (EhV, Phycodnaviridae). EhV infection is accompanied by induction of hallmarks of programmed cell death and production of reactive oxygen species (ROS). Here we characterized alterations in ROS metabolism and explored its role during infection. Transcriptomic analysis of ROS-related genes predicted an increase in glutathione (GSH) and H 2 O 2 production during infection. In accordance, using biochemical assays and specific fluorescent probes we demonstrated the overproduction of GSH during lytic infection. We also showed that H 2 O 2 production, rather than superoxide, is the predominant ROS during the onset of the lytic phase of infection. Using flow cytometry, confocal microscopy and multispectral imaging flow cytometry, we showed that the profound co-production of H 2 O 2 and GSH occurred in the same subpopulation of cells but at different subcellular localization. Positively stained cells for GSH and H 2 O 2 were highly infected compared with negatively stained cells. Inhibition of ROS production by application of a peroxidase inhibitor or an H 2 O 2 scavenger inhibited host cell death and reduced viral production. We conclude that viral infection induced remodeling of the host antioxidant network that is essential for a successful viral replication cycle. This study provides insight into viral replication strategy and suggests the use of specific cellular markers to identify and quantify the extent of active viral infection during E. huxleyi blooms in the ocean.

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Reactive Oxygen Species in Plant Cell Death

Cited by 837 publications

References 74 publications

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

Spatio-Temporal Dynamics of Fructan Metabolism in Developing Barley Grains

Modulation of host ROS metabolism is essential for viral infection of a bloom-forming coccolithophore in the ocean

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