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Figure 2 The principal features of photosynthetic electron transport under high light stress that lead to the production of ROS in chloroplasts and peroxisomes. Two elec- tron sinks can be used to alleviate the negative consequences of overreduction of the photosynthetic electron chain: (a) the reduction of oxygen by PSI that generates su- peroxide and H2Oz, and (b) the Rubisco oxygenase reaction and the photorespiratory pathway that lead to H2O2 generation within the peroxisome. Under light stress, in- creasing amounts of singlet oxygen are produced within PSII. Bold arrows show the main routes of electron transport. Key enzymes discussed in the text are shown in encir- cled numbers: 1) superoxide dismutase, 2) Rubisco, 3) glycolate oxidase, 4) catalase, and 5) ascorbate peroxidase.

Figure 2 The principal features of photosynthetic electron transport under high light stress that lead to the production of ROS in chloroplasts and peroxisomes. Two elec- tron sinks can be used to alleviate the negative consequences of overreduction of the photosynthetic electron chain: (a) the reduction of oxygen by PSI that generates su- peroxide and H2Oz, and (b) the Rubisco oxygenase reaction and the photorespiratory pathway that lead to H2O2 generation within the peroxisome. Under light stress, in- creasing amounts of singlet oxygen are produced within PSII. Bold arrows show the main routes of electron transport. Key enzymes discussed in the text are shown in encir- cled numbers: 1) superoxide dismutase, 2) Rubisco, 3) glycolate oxidase, 4) catalase, and 5) ascorbate peroxidase.

Related Figures (4)

Figure 1 Generation of different ROS by energy transfer or sequential univalent reduction of ground state triplet oxygen.
Figure 1 Generation of different ROS by energy transfer or sequential univalent reduction of ground state triplet oxygen.
Figure 3 The principal modes of enzymatic ROS scavenging by superoxide dis- mutase (SOD), catalase (CAT), the ascorbate-glutathione cycle, and the glutathione peroxidase (GPX) cycle. SOD converts hydrogen superoxide into hydrogen perox- ide. CAT converts hydrogen peroxide into water. Hydrogen peroxide is also converted into water by the ascorbate- glutathione cycle. The reducing agent in the first reaction catalyzed by ascorbate peroxidase (A PX ) is ascorbate, which oxidizes into monodehy- droascorbate (MDA). MDA reductase (MDAR) reduces MDA into ascorbate with the help of NAD(P)H. Dehydroascorbate (DHA) is produced spontaneously by MDA and can be reduced to ascorbate by DHA reductase (DHAR) with the help of GSH that is oxidized to GSSG. The cycle closes with glutathione reductase (GR) converting GSSG back into GSH with the reducing agent NAD(P)H. The GPX cycle converts hydrogen peroxide into water using reducing equivalents from GSH. Oxidized GSSG is again converted into GSH by GR and the reducing agent NAD(P)H.
Figure 3 The principal modes of enzymatic ROS scavenging by superoxide dis- mutase (SOD), catalase (CAT), the ascorbate-glutathione cycle, and the glutathione peroxidase (GPX) cycle. SOD converts hydrogen superoxide into hydrogen perox- ide. CAT converts hydrogen peroxide into water. Hydrogen peroxide is also converted into water by the ascorbate- glutathione cycle. The reducing agent in the first reaction catalyzed by ascorbate peroxidase (A PX ) is ascorbate, which oxidizes into monodehy- droascorbate (MDA). MDA reductase (MDAR) reduces MDA into ascorbate with the help of NAD(P)H. Dehydroascorbate (DHA) is produced spontaneously by MDA and can be reduced to ascorbate by DHA reductase (DHAR) with the help of GSH that is oxidized to GSSG. The cycle closes with glutathione reductase (GR) converting GSSG back into GSH with the reducing agent NAD(P)H. The GPX cycle converts hydrogen peroxide into water using reducing equivalents from GSH. Oxidized GSSG is again converted into GSH by GR and the reducing agent NAD(P)H.
Figure 4 Schematic depiction of cellular ROS sensing and signaling mechanisms. ROS sensors such as membrane-localized histidine kinases can sense extracellular and intracellular ROS. Intracellular ROS can also influence the ROS-induced mito- gen-activated protein kinase (MAPK) signaling pathway through inhibition of MAPK phosphatases (PPases) or downstream transcription factors. Whereas MAP kinases regulate gene expression by altering transcription factor activity through phosphorylation of serine and threonine residues, ROS regulation occurs by oxida- tion of cysteine residues.
Figure 4 Schematic depiction of cellular ROS sensing and signaling mechanisms. ROS sensors such as membrane-localized histidine kinases can sense extracellular and intracellular ROS. Intracellular ROS can also influence the ROS-induced mito- gen-activated protein kinase (MAPK) signaling pathway through inhibition of MAPK phosphatases (PPases) or downstream transcription factors. Whereas MAP kinases regulate gene expression by altering transcription factor activity through phosphorylation of serine and threonine residues, ROS regulation occurs by oxida- tion of cysteine residues.
Figure 5 Different roles of ROS under conditions of (a) pathogen attack or (b) abi- otic stress. Upon pathogen attack, receptor-induced signaling activates plasma mem- brane or apoplast-localized oxidases that produce superoxide radicals (07) that are highly toxic and can help to kill the invading pathogen. On the other hand, 07 is rapidly dismutated into hydrogen peroxide, which, in contrast to superoxide, can readily cross the plasma membrane. Intracellular ROS levels increase due not only to extracellular production of ROS but also by downregulation of ROS scavenging mechanisms. Overall, ROS amounts increase to critical levels and induce pro- grammed cell death (PCD). During abiotic stress, ROS production occurs mainly in chloroplasts and mitochondria at the sites of electron transport, increasing intracellu- lar ROS amounts to toxic levels. The cellular response encompasses upregulation of ROS scavenging mechanisms to detoxify increased amounts of ROS.
Figure 5 Different roles of ROS under conditions of (a) pathogen attack or (b) abi- otic stress. Upon pathogen attack, receptor-induced signaling activates plasma mem- brane or apoplast-localized oxidases that produce superoxide radicals (07) that are highly toxic and can help to kill the invading pathogen. On the other hand, 07 is rapidly dismutated into hydrogen peroxide, which, in contrast to superoxide, can readily cross the plasma membrane. Intracellular ROS levels increase due not only to extracellular production of ROS but also by downregulation of ROS scavenging mechanisms. Overall, ROS amounts increase to critical levels and induce pro- grammed cell death (PCD). During abiotic stress, ROS production occurs mainly in chloroplasts and mitochondria at the sites of electron transport, increasing intracellu- lar ROS amounts to toxic levels. The cellular response encompasses upregulation of ROS scavenging mechanisms to detoxify increased amounts of ROS.
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