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Plants often encounter light intensities exceeding the capacity of photosynthesis (excessive light) mainly due to biotic and abiotic factors, which lower CO 2 fixation and reduce light energy sinks. Under excessive light, the photosynthetic electron transport chain generates damaging molecules, hence leading to photooxidative stress and eventually to cell death. In this review, we summarize the mechanisms linking the excessive absorption of light energy in chloroplasts to programmed cell death in plant leaves. We highlight the importance of reactive carbonyl species generated by lipid photooxidation, their detoxification, and the integrating role of the endoplasmic reticulum in the adoption of phototolerance or cell-death pathways. Finally, we invite the scientific community to standardize the conditions of excessive light treatments. Capturing light intensities exceeding the capacity of photosynthesis can lead to cell death in plant leaves. In this review, the authors summarize recent findings on the mechanisms mediating light-induced cell death, highlighting the roles of reactive carbonyl species, the endoplasmic reticulum, and phytohormones in the adoption of phototolerance versus cell-death pathways. [ABSTRACT FROM AUTHOR]

The article discusses a research study which explores the role of carotenoids in Arabidopsis plants. The dihydroactinidiolide and gene expression in Arabidopsis were examined using quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Findings reveal that carotenoid derivative dhA can function as a gene regulator and can play a significant role in the chloroplast retrograde signaling of singlet oxygen (1O2) responsive genes.

Vitamin E is considered a major antioxidant in biomembranes, but little evidence exists for this function in plants under photooxidative stress. Leaf discs of two vitamin E mutants, a tocopherol cyclase mutant (vte1) and a homogentisate phytyl transferase mutant (vte2), were exposed to high light stress at low temperature, which resulted in bleaching and lipid photodestruction. However, this was not observed in whole plants exposed to long-term high light stress, unless the stress conditions were extreme (very low temperature and very high light), suggesting compensatory mechanisms for vitamin E deficiency under physiological conditions. We identified two such mechanisms: nonphotochemical energy dissipation (NPQ) in photosystem II (PSII) and synthesis of zeaxanthin. Inhibition of NPQ in the double mutant vte1 npq4 led to a marked photoinhibition of PSII, suggesting protection of PSII by tocopherols. vte1 plants accumulated more zeaxanthin in high light than the wild type, and inhibiting zeaxanthin synthesis in the vte1 npq1 double mutant resulted in PSII photoinhibition accompanied by extensive oxidation of lipids and pigments. The single mutants npq1, npq4, vte2, and vte1 showed little sensitivity to the stress treatments. We conclude that, in cooperation with the xanthophyll cycle, vitamin E fulfills at least two different functions in chloroplasts at the two major sites of singlet oxygen production: preserving PSII from photoinactivation and protecting membrane lipids from photooxidation. [ABSTRACT FROM AUTHOR]

UV-B and UV-A radiation are natural components of solar radiation that can cause plant stress, as well as induce a range of acclimatory responses mediated by photoreceptors. UV-mediated accumulation of flavonoids and glucosinolates is well documented, but much less is known about UV effects on carotenoid content. Carotenoids are involved in a range of plant physiological processes, including photoprotection of the photosynthetic machinery. UV-induced changes in carotenoid profile were quantified in plants (Arabidopsis thaliana) exposed for up to ten days to supplemental UV radiation under growth chamber conditions. UV induces specific changes in carotenoid profile, including increases in antheraxanthin, neoxanthin, violaxanthin and lutein contents in leaves. The extent of induction was dependent on exposure duration. No individual UV-B (UVR8) or UV-A (Cryptochrome or Phototropin) photoreceptor was found to mediate this induction. Remarkably, UV-induced accumulation of violaxanthin could not be linked to protection of the photosynthetic machinery from UV damage, questioning the functional relevance of this UV response. Here, it is argued that plants exploit UV radiation as a proxy for other stressors. Thus, it is speculated that the function of UV-induced alterations in carotenoid profile is not UV protection, but rather protection against other environmental stressors such as high intensity visible light that will normally accompany UV radiation. [ABSTRACT FROM AUTHOR]

Guanosine pentaphosphate and tetraphosphate (together referred to as ppGpp) are hyperphosphorylated nucleotides found in bacteria and the chloroplasts of plants and algae. In plants and algae artificial ppGpp accumulation can inhibit chloroplast gene expression, and influence photosynthesis, nutrient remobilization, growth, and immunity. However, it is so far unknown whether ppGpp is required for abiotic stress acclimation in plants. Here, we demonstrate that ppGpp biosynthesis is necessary for acclimation to nitrogen starvation in Arabidopsis. We show that ppGpp is required for remodeling the photosynthetic electron transport chain to downregulate photosynthetic activity and for protection against oxidative stress. Furthermore, we demonstrate that ppGpp is required for coupling chloroplastic and nuclear gene expression during nitrogen starvation. Altogether, our work indicates that ppGpp is a pivotal regulator of chloroplast activity for stress acclimation in plants. [ABSTRACT FROM AUTHOR]

Improving yield, nutritional value and tolerance to abiotic stress are major targets of current breeding and biotechnological approaches that aim at increasing crop production and ensuring food security. Metabolic engineering of carotenoids, the precursor of vitamin-A and plant hormones that regulate plant growth and response to adverse growth conditions, has been mainly focusing on provitamin A biofortification or the production of high-value carotenoids. Here, we show that the introduction of a single gene of the carotenoid biosynthetic pathway in different tomato cultivars induced profound metabolic alterations in carotenoid, apocarotenoid and phytohormones pathways. Alterations in isoprenoid- (abscisic acid, gibberellins, cytokinins) and non-isoprenoid (auxin and jasmonic acid) derived hormones together with enhanced xanthophyll content influenced biomass partitioning and abiotic stress tolerance (high light, salt, and drought), and it caused an up to 77% fruit yield increase and enhanced fruit's provitamin A content. In addition, metabolic and hormonal changes led to accumulation of key primary metabolites (e.g. osmoprotectants and antiaging agents) contributing with enhanced abiotic stress tolerance and fruit shelf life. Our findings pave the way for developing a new generation of crops that combine high productivity and increased nutritional value with the capability to cope with climate change-related environmental challenges. [Display omitted] • LYCOPENE β-CYCLASE (LCYB) converts lycopene into β-carotene. • β-carotene, the precursor of apocarotenoids, is located in a metabolic hot spot. • LCYB expression modulates carotenoid, apocarotenoid, and hormone contents in tomato. • Changes in carotenoids and hormones cause biomass partitioning in shoots and fruits. • Changes in carotenoids and hormones enhance stress tolerance and fruit shelf life. [ABSTRACT FROM AUTHOR]

Carotenoids play a crucial protective role in photosynthetic organisms as quenchers of singlet oxygen (1O2). This function occurs either via a physical mechanism involving thermal energy dissipation or via a chemical mechanism involving direct oxidation of the carotenoid molecule. The latter mechanism can produce a variety of aldehydic or ketonic cleavage products containing a reactive carbonyl group. One such molecule, the volatile β-carotene derivative β-cyclocitral, triggers changes in the expression of 1O2-responsive genes and leads to an enhancement of photooxidative stress tolerance. Thus, besides their well-known functions in light harvesting and photoprotection, carotenoids can also play a role through their nonenzymic oxidation in the sensing and signalling of reactive oxygen species and photooxidative stress in photosynthetic organisms. Enzymic carotenoid oxidation does not seem to play a significant role in this phenomenon. Elucidation of the carotenoid-mediated 1O2 signalling pathway could provide new targets for improving photooxidative stress tolerance of plants. [ABSTRACT FROM AUTHOR]

Tocochromanols (tocopherols, tocotrienols and plastochromanol-8), isoprenoid quinone (plastoquinone-9 and plastoquinol-9) and carotenoids (carotenes and xanthophylls), are lipid-soluble antioxidants in the chloroplasts, which play an important defensive role against photooxidative stress in plants. In this study, the interplay between the antioxidant activities of those compounds in excess light stress was analyzed in wild-type (WT) Arabidopsis thaliana and in a tocopherol cyclase mutant (vte1), a homogentisate phytyl transferase mutant (vte2) and a tocopherol cyclase overexpressor (VTE1oex). The results reveal a strategy of cooperation and replacement between α-tocopherol, plastochromanol-8, plastoquinone-9/plastoquinol-9 and zeaxanthin. In the first line of defense (non-radical mechanism), singlet oxygen is either physically or chemically quenched by α-tocopherol; however, when α-tocopherol is consumed, zeaxanthin and plastoquinone-9/plastoquinol-9 can provide alternative protection against singlet oxygen toxicity by functional replacement of α-tocopherol either by zeaxanthin for the physical quenching or by plastoquinone-9/plastoquinol-9 for the chemical quenching. When singlet oxygen escapes this first line of defense, it oxidizes lipids and forms lipid hydroperoxides, which are oxidized to lipid peroxyl radicals by ferric iron. In the second line of defense (radical mechanism), lipid peroxyl radicals are scavenged by α-tocopherol. After its consumption, plastochromanol-8 overtakes this function. We provide a comprehensive description of the reaction pathways underlying the non-radical and radical antioxidant activities of α-tocopherol, carotenoids, plastoquinone-9/plastoquinol-9 and plastochromanol-8. The interplay between the different plastid lipid-soluble antioxidants in the non-radical and the radical mechanism provides step by step insights into protection against photooxidative stress in higher plants. Image 1 • Interplay between tocochromanols, isoprenoid quinones and carotenoids is crucial to prevent photooxidative stress. • In first line of defense, interplay of α-tocopherol, total plastoquinone-9 and carotenoids protects plant from singlet oxygen. • Singlet oxygen fled from first line of defense oxidize lipids to lipid hydroperoxides which decomposes to peroxyl radical. • In second line of defense, plastochromanol-8 substitutes α-tocopherol's function in its absence to scavenge peroxyl radicals. [ABSTRACT FROM AUTHOR]

Summary: Singlet oxygen (1O2) is a by‐product of photosynthesis that triggers a signalling pathway leading to stress acclimation or to cell death. By analyzing gene expressions in a 1O2‐overproducing Arabidopsis mutant (ch1) under different light regimes, we show here that the 1O2 signalling pathway involves the endoplasmic reticulum (ER)‐mediated unfolded protein response (UPR). ch1 plants in low light exhibited a moderate activation of UPR genes, in particular bZIP60, and low concentrations of the UPR‐inducer tunicamycin enhanced tolerance to photooxidative stress, together suggesting a role for UPR in plant acclimation to low 1O2 levels. Exposure of ch1 to high light stress ultimately leading to cell death resulted in a marked upregulation of the two UPR branches (bZIP60/IRE1 and bZIP28/bZIP17). Accordingly, mutational suppression of bZIP60 and bZIP28 increased plant phototolerance, and a strong UPR activation by high tunicamycin concentrations promoted high light‐induced cell death. Conversely, light acclimation of ch1 to 1O2 stress put a limitation in the high light‐induced expression of UPR genes, except for the gene encoding the BIP3 chaperone, which was selectively upregulated. BIP3 deletion enhanced Arabidopsis photosensitivity while plants treated with a chemical chaperone exhibited enhanced phototolerance. In conclusion, 1O2 induces the ER‐mediated UPR response that fulfils a dual role in high light stress: a moderate UPR, with selective induction of BIP3, is part of the acclimatory response to 1O2, and a strong activation of the whole UPR is associated with cell death. Significance Statement: Singlet oxygen, produced from photosystem II under conditions of excess light energy, triggers the endoplasmic reticulum‐mediated unfolded protein response (UPR), with different UPR levels inducing different physiological responses to light stress. Moderate activation of UPR participates in the acclimation to singlet oxygen, while strong activation leads to cell death. [ABSTRACT FROM AUTHOR]

Carnosic acid, a phenolic diterpene specific to the Lamiaceae family, is highly abundant in rosemary (Rosmarinus officinalis). Despite numerous industrial and medicinal/pharmaceutical applications of its antioxidative features, this compound in planta and its antioxidant mechanism have received little attention, except a few studies of rosemary plants under natural conditions. In vitro analyses, using high-performance liquid chromatography-ultraviolet and luminescence imaging, revealed that carnosic acid and its major oxidized derivative, carnosol, protect lipids from oxidation. Both compounds preserved linolenic acid and monogalactosyldiacylglycerol from singlet oxygen and from hydroxyl radical. When applied exogenously, they were both able to protect thylakoid membranes prepared from Arabidopsis (Arabidopsis thaliana) leaves against lipid peroxidation. Different levels of carnosic acid and carnosol in two contrasting rosemary varieties correlated with tolerance to lipid peroxidation. Upon reactive oxygen species (ROS) oxidation of lipids, carnosic acid was consumed and oxidized into various derivatives, including into carnosol, while carnosol resisted, suggesting that carnosic acid is a chemical quencher of ROS. The antioxidative function of carnosol relies on another mechanism, occurring directly in the lipid oxidation process. Under oxidative conditions that did not involve ROS generation, carnosol inhibited lipid peroxidation, contrary to carnosic acid. Using spin probes and electron paramagnetic resonance detection, we confirmed that carnosic acid, rather than carnosol, is a ROS quencher. Various oxidized derivatives of carnosic acid were detected in rosemary leaves in low light, indicating chronic oxidation of this compound, and accumulated in plants exposed to stress conditions, in parallel with a loss of carnosic acid, confirming that chemical quenching of ROS by carnosic acid takes place in planta. [ABSTRACT FROM AUTHOR]

Distinct ROS signaling pathways initiated by singlet oxygen (¹O2) or superoxide and hydrogen peroxide have been attributed to either cell death or acclimation, respectively. Recent studies have revealed that more complex antagonistic and synergistic relationships exist within and between these pathways. As specific chloroplastic ROS signals are difficult to study, rapid systemic signaling experiments using localized high light (HL) stress or ROS treatments were used in this study to uncouple signals required for direct HL and ROS perception and distal systemic acquired acclimation (SAA). A qPCR approach was chosen to determine local perception and distal signal reception. Analysis of a thylakoidal ascorbate peroxidase mutant (tapx), the ¹O2-retrograde signaling double mutant (ex1/ex2), and an apoplastic signaling double mutant (rbohD/F) revealed that tAPX and EXECUTER 1 are required for both HL and systemic acclimation stress perception. Apoplastic membrane-localized RBOHs were required for systemic spread of the signal but not for local signal induction in directly stressed tissues. Endogenous ROS treatments revealed a very strong systemic response induced by a localized 1 h induction of ¹O2 using the conditional flu mutant. A qPCR time course of ¹O2 induced systemic marker genes in directly and indirectly connected leaves revealed a direct vascular connection component of both immediate and longer term SAA signaling responses. These results reveal the importance of an EXECUTER-dependent ¹O2 retrograde signal for both local and long distance RBOH-dependent acclimation signaling that is distinct from other HL signaling pathways, and that direct vascular connections have a role in spatial-temporal SAA induction. [ABSTRACT FROM AUTHOR]

The circadian clock helps plants measure daylength and adapt to changes in the day-night rhythm. We found that changes in the light-dark regime triggered stress responses, eventually leading to cell death, in leaves of Arabidopsis thaliana plants with reduced cytokinin levels or defective cytokinin signaling. Prolonged light treatment followed by a dark period induced stress and cell death marker genes while reducing photosynthetic efficiency. This response, called circadian stress, is also characterized by altered expression of clock and clock output genes. In particular, this treatment strongly reduced the expression of CIRCADIAN CLOCK ASSOCIATED1 (CCA1) and LATE ELONGATED HYPOCOTYL (LHY). Intriguingly, similar changes in gene expression and cell death were observed in clock mutants lacking proper CCA1 and LHY function. Circadian stress caused strong changes in reactive oxygen species- and jasmonic acid (JA)-related gene expression. The activation of the JA pathway, involving the accumulation of JA metabolites, was crucial for the induction of cell death, since the cell death phenotype was strongly reduced in the jasmonate resistant1 mutant background. We propose that adaptation to circadian stress regimes requires a normal cytokinin status which, acting primarily through the AHK3 receptor, supports circadian clock function to guard against the detrimental effects of circadian stress. [ABSTRACT FROM AUTHOR]

Studies of the singlet oxygen (¹O2)-overproducing flu and chlorina1 (ch1) mutants of Arabidopsis (Arabidopsis thaliana) have shown that ¹O2-induced changes in gene expression can lead to either programmed cell death (PCD) or acclimation. A transcriptomic analysis of the ch1 mutant has allowed the identification of genes whose expression is specifically affected by each phenomenon. One such gene is OXIDATIVE SIGNAL INDUCIBLE1 (OXI1) encoding an AGC kinase that was noticeably induced by excess light energy and ¹O2 stress conditions leading to cell death. Photo-induced oxidative damage and cell death were drastically reduced in the OXI1 null mutant (oxi1) and in the double mutant ch1*oxi1 compared with the wild type and the ch1 single mutant, respectively. This occurred without any changes in the production rate of ¹O2 but was cancelled by exogenous applications of the phytohormone jasmonate. OXI1-mediated ¹O2 signaling appeared to operate through a different pathway from the previously characterized OXI1-dependent response to pathogens and H2O2 and was found to be independent of the EXECUTER proteins. In high-light-stressed plants, the oxi1 mutation was associated with reduced jasmonate levels and with the up-regulation of genes encoding negative regulators of jasmonate signaling and PCD. Our results show that OXI1 is a new regulator of ¹O2-induced PCD, likely acting upstream of jasmonate. [ABSTRACT FROM AUTHOR]

Plant surfaces form the barrier between a plant and its environment. Upon damage, the wound healing process begins immediately and is accompanied by a rapid production of extracellular reactive oxygen species (ROS), essential in deterring pathogens, signalling responses and cell wall restructuring. Although many enzymes produce extracellular ROS, it is unclear if ROS-producing enzymes act synergistically. We characterised the oxidative burst of superoxide (O 2 − ) and hydrogen peroxide (H 2 O 2 ) that follows wounding in pea ( Pisum sativum L.) seedlings. Rates of ROS production were manipulated by exogenous application of enzyme substrates and inhibitors. The results indicate significant roles for di-amine oxidases (DAO) and peroxidases (Prx) rather than NADPH oxidase. The burst of O 2 − was strongly dependent on the presence of H 2 O 2 produced by DAO. Potential substrates released from wounded seedlings included linoleic acid that, upon exogenous application, strongly stimulated catalase-sensitive O 2 − production. Moreover, a 65 kD plasma membrane (PM) guaiacol Prx was found in the secretome of wounded seedlings and showed dependence on linoleic acid for O 2 − production. Lipoxygenases are suggested to modulate O 2 − production by consuming polyunsaturated fatty acids in the apoplast. Overall, a O 2 − -producing mechanism involving H 2 O 2 -derived from DAO, linoleic acid and a PM-associated Prx is proposed. [ABSTRACT FROM AUTHOR]

Singlet oxygen (1O2) is a reactive oxygen species that can function as a stress signal in plant leaves leading to programmed cell death. In microalgae, 1O2 -induced transcriptomic changes result in acclimation to 1O2. Here, using a chlorophyll b –less Arabidopsis thaliana mutant (chlorina1 [ ch1 ]), we show that this phenomenon can also occur in vascular plants. The ch1 mutant is highly photosensitive due to a selective increase in the release of 1O2 by photosystem II. Under photooxidative stress conditions, the gene expression profile of ch1 mutant leaves very much resembled the gene responses to 1O2 reported in the Arabidopsis mutant flu. Preexposure of ch1 plants to moderately elevated light intensities eliminated photooxidative damage without suppressing 1O2 formation, indicating acclimation to 1O2. Substantial differences in gene expression were observed between acclimation and high-light stress: A number of transcription factors were selectively induced by acclimation, and contrasting effects were observed for the jasmonate pathway. Jasmonate biosynthesis was strongly induced in ch1 mutant plants under high-light stress and was noticeably repressed under acclimation conditions, suggesting the involvement of this hormone in 1O2 -induced cell death. This was confirmed by the decreased tolerance to photooxidative damage of jasmonate-treated ch1 plants and by the increased tolerance of the jasmonate-deficient mutant delayed-dehiscence2. [ABSTRACT FROM AUTHOR]

In addition to the linear electron flow, a cyclic electron flow (CEF) around photosystem I occurs in chloroplasts. In CEF, electrons flow back from the donor site of photosystem I to the plastoquinone pool via two main routes: one that involves the Proton Gradient Regulation5 (PGR5)/PGRL1 complex (PGR) and one that is dependent of the NADH dehydrogenase-like complex. While the importance of CEF in photosynthesis and photoprotection has been clearly established, little is known about its regulation. We worked on the assumption of a redox regulation and surveyed the putative role of chloroplastic thioredoxins (TRX). Using Arabidopsis (Arabidopsis thaliana) mutants lacking different TRX isoforms, we demonstrated in vivo that TRXm4 specifically plays a role in the down-regulation of the NADH dehydrogenase-like complex-dependent plastoquinone reduction pathway. This result was confirmed in tobacco (Nicotiana tabacuni) plants overexpressing the TRXm4 orthologous gene. In vitro assays performed with isolated chloroplasts and purified TRXm4 indicated that TRXm4 negatively controls the PGR pathway as well. The physiological significance of this regulation was investigated under steady-state photosynthesis and in the pgr5 mutant background. Lack of TRXm4 reversed the growth phenotype of the pgr5 mutant, but it did not compensate for the impaired photosynthesis and photoinhibition sensitivity. This suggests that the physiological role of TRXm4 occurs in vivo via a mechanism distinct from direct up-regulation of CEF. [ABSTRACT FROM AUTHOR]

1O2 (singlet oxygen) is a reactive O2 species produced from triplet excited chlorophylls in the chloroplasts, especially when plants are exposed to excess light energy. Similarly to other active O2 species, 1O2 has a dual effect: It is toxic, causing oxidation of biomolecules, and it can act as a signal molecule that leads to cell death or to acclimation. Carotenoids are considered to be the main 1O2 quenchers in chloroplasts, and we show here that light stress induces the oxidation of the carotenoid β-carotene in Arabidopsis plants, leading to the accumulation of different volatile derivatives. One such compound, β-cyclocitral, was found to induce changes in the expression of a large set of genes that have been identified as 1O2 responsive genes. In contrast, β-cyclocitral had little effect on the expression of H2O2 gene markers. β-Cyclocitral-induced reprogramming of gene expression was associated with an increased tolerance to photooxidative stress. The results indicate that β-cyclocitral is a stress signal produced in high light that is able to induce defense mechanisms and represents a likely messenger involved in the 1O2 signaling pathway in plants. [ABSTRACT FROM AUTHOR]

Carotenoids are considered to be the first line of defense of plants against singlet oxygen (¹O2) toxicity because of their capacity to quench ¹O2 as well as triplet chlorophylls through a physical mechanism involving transfer of excitation energy followed by thermal deactivation. Here, we show that leaf carotenoids are also able to quench ¹O2 by a chemical mechanism involving their oxidation. In vitro oxidation of β-carotene, lutein, and zeaxanthin by ¹O2 generated various aldehydes and endoperoxides. A search for those molecules in Arabidopsis (Arabidopsis thaliana) leaves revealed the presence of ¹O2-specific endoperoxides ill low-light-grown plants, indicating chronic oxidation of carotenoids by ¹O2. β-Carotene endoperoxide, but not xanthophyll endoperoxide, rapidly accumulated during high-light stress, and this accumulation was correlated with the extent of photosystem (PS) II photoinhibition and the expression of various ¹O2 marker genes. The selective accumulation of β-carotene endoperoxide points at the PSII reaction centers, rather than the PSII chlorophyll antennae, as a major site of ¹O2 accumulation in plants under high-light stress, β-Carotene endoperoxide was found to have a relatively fast turnover, decaying in the dark with a half time of about 6 h. This carotenoid metabolite provides an early index of ¹O2 production in leaves, the occurrence of which precedes the accumulation of fatty acid oxidation products. [ABSTRACT FROM AUTHOR]

Summary Plants, like almost all living organisms, spontaneously emit photons of visible light. We used a highly sensitive, low-noise cooled charge coupled device camera to image spontaneous photon emission (autoluminescence) of plants. Oxidative stress and wounding induced a long-lasting enhancement of plant autoluminescence, the origin of which is investigated here. This long-lived phenomenon can be distinguished from the short-lived chlorophyll luminescence resulting from charge recombinations within the photosystems by pre-adapting the plant to darkness for about 2 h. Lipids in solvent were found to emit a persistent luminescence after oxidation in vitro, which exhibited the same time and temperature dependence as plant autoluminescence. Other biological molecules, such as DNA or proteins, either did not produce measurable light upon oxidation or they did produce a chemiluminescence that decayed rapidly, which excludes their significant contribution to the in vivo light emission signal. Selective manipulation of the lipid oxidation levels in Arabidopsis mutants affected in lipid hydroperoxide metabolism revealed a causal link between leaf autoluminescence and lipid oxidation. Addition of chlorophyll to oxidized lipids enhanced light emission. Both oxidized lipids and plants predominantly emit light at wavelengths higher than 600 nm; the emission spectrum of plant autoluminescence was shifted towards even higher wavelengths, a phenomenon ascribable to chlorophyll molecules acting as luminescence enhancers in vivo. Taken together, the presented results show that spontaneous photon emission imaged in plants mainly emanates from oxidized lipids. Imaging of this signal thus provides a simple and sensitive non-invasive method to selectively visualize and map patterns of lipid oxidation in plants. [ABSTRACT FROM AUTHOR]

Abstract: The cellular redox balance seems an important modulator under heavy metal stress. While for other heavy metals these processes are well studied, oxidative stress related responses are also known to be triggered under uranium stress but information remains limited. This study aimed to further unravel the mechanisms by which plants respond to uranium stress. Seventeen-day-old Arabidopsis thaliana seedlings, grown on a modified Hoagland solution under controlled conditions, were exposed to 0, 0.1, 1, 10 and 100 μM uranium for 1, 3 and 7 days. While in Part I of this study oxidative stress related responses in the roots were discussed, this second Part II discusses oxidative stress related responses in the leaves and general conclusions drawn from the results of the roots and the leaves will be presented. As several responses were already visible following 1 day exposure, when uranium concentrations in the leaves were negligible, a root-to-shoot signaling system was suggested in which plastids could be important sensing sites. While lipid peroxidation, based on the amount of thiobarbituric acid reactive compounds, was observed after exposure to 100 μM uranium, affecting membrane structure and function, a transient concentration dependent response pattern was visible for lipoxygenase initiated lipid peroxidation. This transient character of uranium stress responses in leaves was emphasized by results of lipoxygenase (LOX2) and antioxidative enzyme transcript levels, enzyme capacities and glutathione concentrations both in time as with concentration. The ascorbate redox balance seemed an important modulator of uranium stress responses in the leaves as in addition to the previous transient responses, the total ascorbate concentration and ascorbate/dehydroascorbate redox balance increased in a concentration and time dependent manner. This could represent either a slow transient response or a stable increase with regard to plant acclimation to uranium stress. [Copyright &y& Elsevier]

Methionine oxidation to methionine sulfoxide (MetSO) is reversed by two types of methionine sulfoxide reductases (MSRs), A and B, specific to MetSO S- and R-diastereomers, respectively. Two MSRB isoforms, MSRB1 and MSRB2, are present in chloroplasts of Arabidopsis thaliana. To assess their physiological role, we characterized Arabidopsis mutants knockout for the expression of MSRB1, MSRB2 or both genes. Measurements of MSR activity in leaf extracts revealed that the two plastidial MSRB enzymes account for the major part of leaf peptide MSR capacity. Under standard conditions of light and temperature, plants lacking one or both plastidial MSRBs do not exhibit any phenotype, regarding growth and development. In contrast, we observed that the concomitant absence of both proteins results in a reduced growth for plants cultivated under high light or low temperature. In contrast, double mutant lines restored for MSRB2 expression display no phenotype. Under environmental constraints, the MetSO level in leaf proteins is higher in plants lacking both plastidial MSRBs than in Wt plants. The absence of plastidial MSRBs is associated with an increased chlorophyll a/b ratio, a reduced content of Lhca1 and Lhcb1 proteins and an impaired photosynthetic performance. Finally, we show that MSRBs are able to use as substrates, oxidized cpSRP43 and cpSRP54, the two main components involved in the targeting of Lhc proteins to the thylakoids. We propose that plastidial MSRBs fulfil an essential function in maintaining vegetative growth of plants during environmental constraints, through a role in the preservation of photosynthetic antennae. [ABSTRACT FROM AUTHOR]

Increasing aridity in the Mediterranean region will result in longer and recurrent drought. These changes could strongly modify plant defenses, endangering tree survival. We investigate the response of chemical defenses from central and specialized metabolism in Quercus pubescens Willd. to future Mediterranean drought using a long-term drought experiment in natura where trees have been submitted to amplified drought (~ -30% annual precipitation) since April 2012. We focused on leaf metabolites including chlorophylls and carotenoids (central metabolism) and flavonols (specialized metabolism). Measurements were performed in summer from 2016 to 2022. Amplified drought led to higher concentrations of total photosynthetic pigments over the 2016-2022 period. However, it also led to lower AZ/VAZ and flavonol concentrations. Additionally, chemical defenses of Q. pubescens responded to previous precipitation where low precipitation 1 year and/or 2 years preceding sampling was associated to low concentrations of VAZ, flavonol and high neoxanthin concentrations. Our study indicates that the decline of flavonol concentration under long-term drought is counterbalanced by a higher production of several central metabolites. Such results are potentially due to an adjustment in tree metabolism, highlighting the importance of performing long-term experimental studies in natura for assessing drought legacy effects and thus forest adaptation to climate change., (© 2024. The Author(s).)

Environmental abiotic constraints are known to reduce plant growth. This effect is largely due to the inhibition of cell division in the leaf and root meristems caused by perturbations of the cell cycle machinery. Progression of the cell cycle is regulated by CDK kinases whose phosphorylation activities are dependent on cyclin proteins. Recent results have emphasized the role of inhibitors of the cyclin-CDK complexes in the impairment of the cell cycle and the resulting growth inhibition under environmental constraints. Those cyclin-CDK inhibitors (CKIs) include the KRP and SIAMESE families of proteins. This review presents the current knowledge on how CKIs respond to environmental changes and on the role played by one subclass of CKIs, the SIAMESE RELATED proteins (SMRs), in the tolerance of plants to abiotic stresses. The SMRs could play a central role in adjusting the balance between growth and stress defenses in plants exposed to environmental stresses., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Braat and Havaux.)

With climate change, an aggravation in summer drought is expected in the Mediterranean region. To assess the impact of such a future scenario, we compared the response of Quercus pubescens, a drought-resistant deciduous oak species, to long-term amplified drought (AD) (partial rain exclusion in natura for 10 years) and natural drought (ND). We studied leaf physiological and physico-chemical trait responses to ND and AD over the seasonal cycle, with a focus on chemical traits including major groups of central (photosynthetic pigments and plastoquinones) and specialized (tocochromanols, phenolic compounds, and cuticular waxes) metabolites. Seasonality was the main driver of all leaf traits, including cuticular triterpenoids, which were highly concentrated in summer, suggesting their importance to cope with drought and thermal stress periods. Under AD, trees not only reduced CO 2 assimilation (-42%) in summer and leaf concentrations of some phenolic compounds and photosynthetic pigments (carotenoids from the xanthophyll cycle) but also enhanced the levels of other photosynthetic pigments (chlorophylls, lutein, and neoxanthin) and plastochromanol-8, an antioxidant located in chloroplasts. Overall, the metabolomic adjustments across seasons and drought conditions reinforce the idea that Q. pubescens is highly resistant to drought although significant losses of antioxidant defenses and photoprotection were identified under AD., (© 2023 Society for Experimental Biology and John Wiley & Sons Ltd.)

New regulatory functions in plant development and environmental stress responses have recently emerged for a number of apocarotenoids produced by enzymatic or nonenzymatic oxidation of carotenoids. β-Cyclocitric acid (β-CCA) is one such compound derived from β-carotene, which triggers defense mechanisms leading to a marked enhancement of plant tolerance to drought stress. We show here that this response is associated with an inhibition of root growth affecting both root cell elongation and division. Remarkably, β-CCA selectively induced cell cycle inhibitors of the SIAMESE-RELATED (SMR) family, especially SMR5, in root tip cells. Overexpression of the SMR5 gene in Arabidopsis induced molecular and physiological changes that mimicked in large part the effects of β-CCA. In particular, the SMR5 overexpressors exhibited an inhibition of root development and a marked increase in drought tolerance which is not related to stomatal closure. SMR5 up-regulation induced changes in gene expression that strongly overlapped with the β-CCA-induced transcriptomic changes. Both β-CCA and SMR5 led to a down-regulation of many cell cycle activators (cyclins, cyclin-dependent kinases) and a concomitant up-regulation of genes related to water deprivation, cellular detoxification, and biosynthesis of lipid biopolymers such as suberin and lignin. This was correlated with an accumulation of suberin lipid polyesters in the roots and a decrease in nonstomatal leaf transpiration. Taken together, our results identify the β-CCA-inducible and drought-inducible SMR5 gene as a key component of a stress-signaling pathway that reorients root metabolism from growth to multiple defense mechanisms leading to drought tolerance., (© The Author(s) 2023. Published by Oxford University Press on behalf of National Academy of Sciences.)

Greenhouse gas (GHG) emissions have created a global climate crisis which requires immediate interventions to mitigate the negative effects on all aspects of life on this planet. As current agriculture and land use contributes up to 25% of total GHG emissions, plant scientists take center stage in finding possible solutions for a transition to sustainable agriculture and land use. In this article, the PlantACT! (Plants for climate ACTion!) initiative of plant scientists lays out a road map of how and in which areas plant scientists can contribute to finding immediate, mid-term, and long-term solutions, and what changes are necessary to implement these solutions at the personal, institutional, and funding levels., Competing Interests: Declaration of interests No interests are declared., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

The degree of unsaturation of plant lipids is high, making them sensitive to oxidation. They thus constitute primary targets of reactive oxygen species and oxidative stress. Moreover, the hydroperoxides generated during lipid peroxidation decompose in a variety of secondary products which can propagate oxidative stress or trigger signaling mechanisms. Both primary and secondary products of lipid oxidation are helpful markers of oxidative stress in plants. This chapter describes a number of methods that have been developed to measure those biomarkers and signals, with special emphasis on the monitoring of photooxidative stress. Depending on their characteristics, those lipid markers provide information not only on the oxidation status of plant tissues but also on the origin of lipid peroxidation, the localization of the damage, or the type of reactive oxygen species involved., (© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Plants, like most living organisms, spontaneously emit photons of visible light. This ultraweak endogenous chemiluminescence is linked to the oxidative metabolism, with lipid peroxidation constituting a major source of photons in plants. We imaged this signal using a very sensitive cooled CCD camera and analysed its spectral characteristics using bandpass interference filters. In vitro oxidation of lipids induced luminescence throughout the visible spectrum (450−850 nm). However, luminescence in the red spectral domain (>640 nm) occurred first, then declined in parallel with the appearance of the emission in the blue-green (<600 nm). This temporal separation suggests that the chemical species emitting in the blue-green are secondary products, possibly deriving from the red light-emitting species. This conversion did not seem to occur in planta because spontaneous chemiluminescence from plant tissues (leaves, roots) occurred only in the red/far-red light domain (>640 nm), peaking at 700−750 nm. The spectrum of plant chemiluminescence was independent of chlorophyll. The in vivo signal was modulated by cellular detoxification mechanisms and by changes in the concentration of singlet oxygen in the tissues, although the singlet oxygen luminescence bands did not appear as major bands in the spectra. Our results indicate that the intensity of endogenous chemiluminescence from plant tissues is determined by the balance between the formation of luminescent species through secondary reactions involving lipid peroxide-derived intermediates, including singlet oxygen, and their elimination by metabolizing processes. The kinetic aspects of plant chemiluminescence must be taken into account when using the signal as an oxidative stress marker.

Arabidopsis plants were grown from seeds at different photon flux densities (PFDs) of white light ranging from 65 to 800 µmol photons m -2  s -1 . Increasing PFD brought about a marked accumulation of plastoquinone (PQ) in leaves. However, the thylakoid photoactive PQ pool, estimated to about 700 pmol mg -1 leaf dry weight, was independent of PFD; PQ accumulation in high light mostly occurred in the photochemically non-active pool (plastoglobules, chloroplast envelopes) which represented up to 75% of total PQ. The amounts of PSII reaction center (on a leaf dry weight basis) also were little affected by PFD during growth, leading to a constant PQ/PSII ratio at all PFDs. Boosting PQ biosynthesis by overexpression of a solanesyl diphosphate-synthesizing enzyme strongly enhanced the PQ levels, particularly at high PFDs. Again, this accumulation occurred exclusively in the non-photoactive PQ pool. Mutational suppression of the plastoglobular ABC1K1 kinase led to a selective reduction of the thylakoid PQ pool size to ca. 400 pmol mg -1 in a large range of PFDs, which was associated with a restriction of the photosynthetic electron flow. Our results show that photosynthetic acclimation to light intensity does not involve modulation of the thylakoid PQ pool size or the amounts of PSII reaction centers. There appears to be a fixed amount of PQ molecules for optimal interaction with PSII and efficient photosynthesis, with the extra PQ molecules being stored outside the thylakoid membranes, implying a tight regulation of PQ distribution within the chloroplasts., (© 2021. The Author(s), under exclusive licence to Springer Nature B.V.)

Because they are highly unsaturated, plant lipids are sensitive to oxidation and constitute a primary target of reactive oxygen species. Therefore, quantification of lipid peroxidation provides a pertinent approach to evaluating oxidative stress in plants. Here, we describe a simple method to measure upstream products of the peroxidation of the major polyunsaturated fatty acids in plants, namely, linolenic acid (C18:3) and linoleic acid (C18:2). The method uses conventional HPLC with UV detection to measure hydroxy C18:3 and C18:2 after reduction of their respective hydroperoxides. The described experimental approach requires low amounts of plant material (a few hundred milligrams), monitors oxidation of both membrane and free fatty acids, and can discriminate between enzymatic and non-enzymatic lipid peroxidation., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature.)

Recently, we published a set of tobacco lines expressing the Daucus carota (carrot) DcLCYB1 gene with accelerated development, increased carotenoid content, photosynthetic efficiency, and yield. Because of this development, DcLCYB1 expression might be of general interest in crop species as a strategy to accelerate development and increase biomass production under field conditions. However, to follow this path, a better understanding of the molecular basis of this phenotype is essential. Here, we combine OMICs (RNAseq, proteomics, and metabolomics) approaches to advance our understanding of the broader effect of LCYB expression on the tobacco transcriptome and metabolism. Upon DcLCYB1 expression, the tobacco transcriptome (~2,000 genes), proteome (~700 proteins), and metabolome (26 metabolites) showed a high number of changes in the genes involved in metabolic processes related to cell wall, lipids, glycolysis, and secondary metabolism. Gene and protein networks revealed clusters of interacting genes and proteins mainly involved in ribosome and RNA metabolism and translation. In addition, abiotic stress-related genes and proteins were mainly upregulated in the transgenic lines. This was well in line with an enhanced stress (high light, salt, and H 2 O 2 ) tolerance response in all the transgenic lines compared with the wild type. Altogether, our results show an extended and coordinated response beyond the chloroplast (nucleus and cytosol) at the transcriptome, proteome, and metabolome levels, supporting enhanced plant growth under normal and stress conditions. This final evidence completes the set of benefits conferred by the expression of the DcLCYB1 gene, making it a very promising bioengineering tool to generate super crops., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Moreno, Martinez-Jaime, Kosmacz, Sokolowska, Schulz, Fischer, Luzarowska, Havaux and Skirycz.)

Plastoquinone-9 (PQ-9) is an essential component of photosynthesis that carries electrons in the linear and alternative electron transport chains, and is also a redox sensor that regulates state transitions and gene expression. However, a large fraction of the PQ pool is located outside the thylakoid membranes, in the plastoglobules and the chloroplast envelopes, reflecting a wider range of functions beyond electron transport. This review describes new functions of PQ in photoprotection, as a potent antioxidant, and in chloroplast metabolism as a cofactor in the biosynthesis of chloroplast metabolites. It also focuses on the essential need for tight environmental control of PQ biosynthesis and for active exchange of this compound between the thylakoid membranes and the plastoglobules. Through its multiple functions, PQ connects photosynthesis with metabolism, light acclimation, and stress tolerance., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

β-cyclocitral is a volatile short-chain apocarotenoid generated by enzymatic or non-enzymatic oxidation of the carotenoid β-carotene. β-cyclocitral has recently emerged as a new bioactive compound in various organisms ranging from plants and cyanobacteria to fungi and animals. In vascular plants, β-cyclocitral and its direct oxidation product, β-cyclocitric acid, are stress signals that accumulate under unfavorable environmental conditions such as drought or high light. Both compounds regulate nuclear gene expression through several signaling pathways, leading to stress acclimation. In cyanobacteria, β-cyclocitral functions as an inhibitor of competing microalgae and as a repellent against grazers. As a volatile compound, this apocarotenoid plays also an important role in intra-species and inter-species communication. This review summarizes recent findings on the multiple roles of β-cyclocitral and of some of its derivatives., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Photosynthesis is an essential pathway providing the chemical energy and reducing equivalents that sustain higher plant metabolism. It relies on sunlight, which is an inconstant source of energy that fluctuates in both intensity and spectrum. The fine and rapid tuning of the photosynthetic apparatus is essential to cope with changing light conditions and increase plant fitness. Recently PROTON GRADIENT REGULATION 6 (PGR6-ABC1K1), an atypical plastoglobule-associated kinase, was shown to regulate a new mechanism of light response by controlling the homeostasis of photoactive plastoquinone (PQ). PQ is a crucial electron carrier existing as a free neutral lipid in the photosynthetic thylakoid membrane. Perturbed homeostasis of PQ impairs photosynthesis and plant acclimation to high light. Here we show that a homologous kinase, ABC1K3, which like PGR6-ABC1K1 is associated with plastoglobules, also contributes to the homeostasis of the photoactive PQ pool. Contrary to PGR6-ABC1K1, ABC1K3 disfavors PQ availability for photosynthetic electron transport. In fact, in the abc1k1/abc1k3 double mutant the pgr6 ( abc1k1 ) the photosynthetic defect seen in the abc1k1 mutant is mitigated. However, the PQ concentration in the photoactive pool of the double mutant is comparable to that of abc1k1 mutant. An increase of the PQ mobility, inferred from the kinetics of its oxidation in dark, contributes to the mitigation of the pgr6 ( abc1k1 ) photosynthetic defect. Our results also demonstrate that ABC1K3 contributes to the regulation of other mechanisms involved in the adaptation of the photosynthetic apparatus to changes in light quality and intensity such as the induction of thermal dissipation and state transitions. Overall, we suggests that, besides the absolute concentration of PQ, its mobility and exchange between storage and active pools are critical for light acclimation in plants., (Copyright © 2020 Pralon, Collombat, Pipitone, Ksas, Shanmugabalaji, Havaux, Finazzi, Longoni and Kessler.)

β-Cyclocitral (β-CC) is a volatile compound deriving from 1 O 2 oxidation of β-carotene in plant leaves. β-CC elicits a retrograde signal, modulating 1 O 2 -responsive genes and enhancing tolerance to photooxidative stress. Here, we show that β-CC is converted into water-soluble β-cyclocitric acid (β-CCA) in leaves. This metabolite is a signal that enhances plant tolerance to drought by a mechanism different from known responses such as stomatal closure, osmotic potential adjustment, and jasmonate signaling. This action of β-CCA is a conserved mechanism, being observed in various plant species, and it does not fully overlap with the β-CC-dependent signaling, indicating that β-CCA induces only a branch of β-CC signaling. Overexpressing SCARECROW-LIKE14 (SCL14, a regulator of xenobiotic detoxification) increased drought tolerance and potentiated the protective effect of β-CCA, showing the involvement of the SCL14-dependent detoxification in the phenomenon. β-CCA is a bioactive apocarotenoid that could potentially be used to protect crop plants against drought., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)

Light utilization is finely tuned in photosynthetic organisms to prevent cellular damage. The dissipation of excess absorbed light energy, a process termed nonphotochemical quenching (NPQ), plays an important role in photoprotection. Little is known about the sustained or slowly reversible form(s) of NPQ and whether they are photoprotective, in part due to the lack of mutants. The Arabidopsis thaliana suppressor of quenching1 ( soq1 ) mutant exhibits enhanced sustained NPQ, which we term qH. To identify molecular players involved in qH, we screened for suppressors of soq1 and isolated mutants affecting either chlorophyllide a oxygenase or the chloroplastic lipocalin, now renamed plastid lipocalin (LCNP). Analysis of the mutants confirmed that qH is localized to the peripheral antenna (LHCII) of photosystem II and demonstrated that LCNP is required for qH, either directly (by forming NPQ sites) or indirectly (by modifying the LHCII membrane environment). qH operates under stress conditions such as cold and high light and is photoprotective, as it reduces lipid peroxidation levels. We propose that, under stress conditions, LCNP protects the thylakoid membrane by enabling sustained NPQ in LHCII, thereby preventing singlet oxygen stress., (© 2018 American Society of Plant Biologists. All rights reserved.)

Carotenoids are known to play important roles in plants as antioxidants, accessory light-harvesting pigments, and attractants for pollinators and seed dispersers. A new function for carotenoids has recently emerged, which relates to the response of plants to environmental stresses. Reactive oxygen species, especially singlet oxygen, produced in the chloroplasts under stress conditions, can oxidize carotenoids leading to a variety of oxidized products, including aldehydes, ketones, endoperoxides and lactones. Some of those carotenoid derivatives, such as volatile β-cyclocitral, derived from the oxidation of β-carotene, are reactive electrophile species that are bioactive and can induce changes in gene expression leading to acclimation to stress conditions. This review summarizes the current knowledge on the non-enzymatic oxidation of carotenoids, the bioactivity of the resulting cleavage compounds and their functions as stress signals in plants., (© 2013 The Author The Plant Journal © 2013 John Wiley & Sons Ltd.)

Under stress conditions that bring about excessive absorption of light energy in the chloroplasts, the formation of singlet oxygen ( (1)O2) can be strongly enhanced, triggering programmed cell death. However, the (1)O2 signaling pathway can also lead to acclimation to photooxidative stress, when (1)O2 is produced in relatively low amounts. This acclimatory response is associated with a strong downregulation of the jasmonate biosynthesis pathway and the maintenance of low jasmonate levels, even under high light stress conditions that normally induce jasmonate synthesis. These findings suggest a central role for this phytohormone in the orientation of the (1)O2 signaling pathway toward cell death or acclimation. This conclusion is confirmed here in an Arabidopsis double mutant obtained by crossing the (1)O2-overproducing mutant ch1 and the jasmonate-deficient mutant dde2. This double mutant was found to be constitutively resistant to (1)O2 stress and to display a strongly stimulated growth rate compared with the single ch1 mutant. However, the involvement of other phytohormones, such as ethylene, cannot be excluded.

Lipid droplets are ubiquitous cellular structures in eukaryotes and are required for lipid metabolism. Little is currently known about plant lipid droplets other than oil bodies. Here, we define dual roles for chloroplast lipid droplets (plastoglobules) in energy and prenylquinone metabolism. The prenylquinones--plastoquinone, plastochromanol-8, phylloquinone (vitamin K(1)), and tocopherol (vitamin E)--are partly stored in plastoglobules. This work shows that NAD(P)H dehydrogenase C1 (NDC1) (At5g08740), a type II NAD(P)H quinone oxidoreductase, associates with plastoglobules. NDC1 reduces a plastoquinone analog in vitro and affects the overall redox state of the total plastoquinone pool in vivo by reducing the plastoquinone reservoir of plastoglobules. Finally, NDC1 is required for normal plastochromanol-8 accumulation and is essential for vitamin K(1) production.

The photosynthetic apparatus, especially the electron transport chain imbedded in the thylakoid membrane, is one of the main targets of cold and heat stress in plants. Prompt and delayed fluorescence emission originating from photosystem II have been used, most often separately, to monitor the changes induced in the photosynthetic membranes during progressive warming or cooling of a leaf sample. Thermofluorescence of F (0) and F (M) informs on the effects of heat on the chlorophyll antennae and the photochemical centers, thermoluminescence on the stabilization and movements of charges and Delayed Light Emission on the permeability of the thylakoid membranes to protons and ions. Considered together and operated simultaneously, these techniques constitute a powerful tool to characterize the effect of thermal stress on intact photosynthetic systems and to understand the mechanisms of constitutive or induced tolerance to temperature stresses.

Thellungiella halophila seedlings grown on a solid substrate for 25 days on standard medium were challenged with NaCl. Growth, tissue hydration, ion accumulation, photosynthesis, lipid peroxidation and antioxidant enzymatic activities were studied on rosette leaves. Three accessions of Arabidopsis thaliana were cultivated under the same conditions. During the first two weeks of salt treatment, the growth of T. halophila leaves was restricted by NaCl. No significant difference appeared between T. halophila and A. thaliana concerning biomass deposition, or hydric and ionic parameters. However, all A. thaliana plants displayed foliar damage, and died during the third week of salt (50mM NaCl) treatment. Almost all (94%) T. halophila plants remained alive, but did not display any sign of altered physiological condition. Tissue hydration, chlorophyll content, stomatal conductance, photosynthetic quantum yield, and photosynthetic rate were very similar to those of control plants. Lipid peroxidation, estimated from thermoluminescence, was very low and insensitive to salt treatment. Only slight changes occurred in antioxidant enzymatic activities (SOD, several peroxidases, and catalase). From the absence of physiological disorder symptoms, we infer that salt was efficiently compartmentalized in leaf vacuoles. In salt-treated A. thaliana, the photosynthetic quantum yield was diminished, and lipid peroxidation was augmented. These observations reinforce the conclusion that T. halophila could accumulate salt in its leaves without damage, in contrast to A. thaliana.