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Photoprotective energy dissipation is a process in which xanthophylls (particularly zeaxanthin and antheraxanthin; Z + A) facilitate the dissipation of excess absorbed light energy as heat. This process can occur in different versions that meet the demands of different environments. Flexible thermal dissipation (qE type) responds to intra-thylakoid pH, is controlled by the PsbS protein, and relaxes rapidly upon darkening at warm temperatures. This flexible, PsbS/ΔpH-dependent dissipation is the predominant form of energy dissipation under environmental conditions favorable for growth, irrespective of plant species. In comparison with short-lived species, perennial evergreens not only have slower growth and lower photosynthetic capacities but also possess higher capacities for flexible thermal dissipation and show greater increases in PsbS level and Z + A in full sun versus moderate growth light intensity. Furthermore, a sustained form of thermal dissipation (qI type) is observed predominantly in photoinhibited evergreens under environmental conditions unfavorable for growth, irrespective of the environmental factor(s) involved. Sustained thermal dissipation is associated with Z + A retention, but is not ΔpH-dependent and does not relax rapidly in darkness even at warm temperatures. The role of PsbS in sustained dissipation versus other factors is discussed. Moreover, a correlation between sustained thermal dissipation in Z + A-retaining photoinhibited leaves and sustained phosphorylation of the photosystem II (PS II) core’s D1 protein is shown. In overwintering Douglas fir, this is associated with an upregulation of an inhibitor (TLP40) of PS II core protein phosphatase. [ABSTRACT FROM AUTHOR]

Both endogenous and exogenous factors are involved in modulating and coordinating gene expression during plant development. Among them are light and plant hormones such as ethylene, cytokinins, abscisic acid, gibberellins, and brassinosteroids. Light and brassinosteroids have received particular attention because of their obvious and pronounced effects on early plant development following seed germination. By contrast, much less is known about the terminal stage of plant development referred to as senescence and the factors controlling this cell death program. Plant hormones such as ethylene and jasmonic acid have, however, been implicated in the initiation and progression of leaf senescence. At all stages of their life cycle, plants are prone to various forms of oxidative stress. Upon illumination, excited tetrapyrroles such as chlorophyll, heme, and their precursors as well as degradation products can transfer their excitation energy onto oxygen, leading to the formation of highly reactive singlet oxygen. Angiosperms being the most highly evolved group of plants must have evolved efficient strategies to prevent the accumulation of such potentially harmful compounds. It is the aim of this chapter to summarize current concepts on the regulation of plant gene expression by light and the plant hormone jasmonic acid, with particular emphasis on the mechanisms by which higher plants prevent photooxidative self-poisoning. Special reference is made to the plastid compartment, which is the major site of tetrapyrrole metabolism and a source of signals that coordinate nuclear gene expression in response to light. [ABSTRACT FROM AUTHOR]

Lipoxygenases are a family of enzymes that dioxygenate unsaturated fatty acids, thus initiating lipoperoxidation of membranes and the synthesis of signaling molecules, or inducing structural and metabolic changes in the cell. This activity is the basis for the critical role of lipoxygenases in a number of pathophysiological conditions, in both animals and plants. In the past few years, a pro-apoptotic effect of lipoxygenase has been reported in different cells and tissues, leading to cell death along unrelated apoptotic pathways. However, anti-apoptotic effects of lipoxygenases have also been reported, often based on the use of enzyme inhibitors. In the present review, the characteristics of the lipoxygenase family and the role of lipoxygenase activation in apoptosis of animal and plant cells are discussed, suggesting a common signal transduction pathway in cell death conserved through the evolution of both kingdoms. In addition, the inhibition of lipoxygenases by antioxidants and its consequences on apoptosis will be presented. [ABSTRACT FROM AUTHOR]

Peroxiredoxins (Prx) constitute a group of recently identified peroxidases that detoxify a broad range of peroxides in distinct subcellular compartments, including chloroplasts. They are ubiquitously expressed in all organisms, i.e. bacteria, fungi, and animals, as well as in cyanobacteria and plants, in which they frequently represent a considerable fraction of total cellular and organellar protein. At least seven prx genes are expressed in leaves of Arabidopsis. The gene products of four of them are targeted to chloroplasts. Five genes encoding (putative) Prx are found in Synechocystis sp. PCC 6803. Based on such circumstantial evidence, as well as biochemical analysis and observations on photosynthetic organisms with modified levels of Prx, it has been established that a subset of Prx plays a role in the context of photosynthesis. The conclusion is further strengthened by studies that showed a modulation of prx gene expression in response to photosynthetic activity. This chapter describes the properties of peroxiredoxins in general and focuses on the role of Prx in protecting the photosynthetic apparatus from oxidative damage and, possibly, in redox signaling in photooxygenic cells. [ABSTRACT FROM AUTHOR]

The chloroplast proteome is encoded by genes that reside in both the chloroplast and the nucleus. This separation of genetic material necessitates a system for coordinating the expression of genes that reside in each compartment. Because the overwhelming majority of genes that encode chloroplast proteins reside in the nucleus, the regulation of nuclear genes by developmental and environmental cues plays a dominant role in chloroplast development and function. However, the chloroplast is not indifferent to its own protein composition. In fact, the chloroplast generates signals that have dramatic effects on the expression of nuclear genes that encode particular chloroplast proteins. Currently it is known that plastids produce at least a few distinct signals during chloroplast development that are required for proper expression of particular nuclear genes that encode components of the photosynthetic machinery. In response to certain environmental signals, mature chloroplasts send additional signals that regulate nuclear gene expression. The molecular nature of most of these plastid-to-nucleus signaling pathways is not well established. However, a number of studies have suggested that accumulation of certain chlorophyll precursors within plastids is a signal that regulates nuclear gene expression during chloroplast development and during the diurnal cycle. Future work in this area should provide detailed molecular information on the influence of chlorophyll synthesis and other plastid-localized metabolism on nuclear gene expression and howplants utilize this formof interorganellar communication during their lifecycles. [ABSTRACT FROM AUTHOR]

The chloroplast is the most important biosynthetic compartment of a green plant cell, being the site of photosynthesis and aspects of carbon, sulfur, and nitrogen assimilation as well as other pathways. At the same time, the complex enzymatic machinery of the organelle is a key target for photooxidative stress. The chloroplast contains an evolutionarily conserved set of genes and a specially adaptable gene expression machinery that is in close physical proximity to the photosynthetic apparatus, i.e. the primary source of reactive oxygen species. This adaptability somehow links the rapid gene expression response to the activity status of photosynthetic electron transport and accompanying redox reactions. In this chapter, we address the following questions: (i) which plastid gene products are subject to redox control? (ii) which stage(s) of organellar gene expression are redox-controlled? and (iii) what are the mechanisms and mediators involved? [ABSTRACT FROM AUTHOR]

Ascorbate, glutathione, and tocopherol are the three major low molecular weight antioxidants of plant cells. While tocopherol is hydrophobic and is found only in lipid membranes, ascorbate and glutathione are hydrophilic, accumulating to high concentrations in the chloroplast stroma and other compartments of the plant cell. Ascorbate and glutathione not only limit photo-oxidative damage but can also act independently as signal-transducing molecules regulating defense gene expression. Both metabolites transmit information concerning oxidative load and redox-buffering capacity. Ascorbate modifies the expression of chloroplast genes. Net glutathione synthesis during stress restores the cellular redox state and allows orchestration of systemic acquired resistance. The degree of redox coupling between these antioxidants has profound implications for regulation, function, and signaling associated with the two major energy-generating systems, i.e. photosynthesis and respiration. Tocopherol fulfills an essential protective function, counter-acting the harmful effects of singlet oxygen production at photosystem II. Ascorbate reduces and thus regenerates oxidized tocopherol, but flux through this reaction is not sufficient to maintain the reduced tocopherol pool under high light stress. This may be because tocopherol regeneration draws on the ascorbate pool of the chloroplast lumen, which may be depleted under stress. Moreover, while glutathione always reduces oxidized ascorbate (dehydroascorbate), the degree of coupling between the ascorbate and glutathione redox couples is variable. The flexibility of coupling between these antioxidant pools is crucial to differential redox signaling, particularly by ascorbate and glutathione. [ABSTRACT FROM AUTHOR]

This perspective advocates a holistic view of photoinhibition from the molecule to the biosphere; a view that integrates many biophysical and biochemical processes in antennae and reaction centers of the photosystems that, when acting in concert, allow plants to respond to diverse and dynamic light conditions in many different environments. We take the general view that photoinhibition refers to a reduction in the efficiency of light use in the photosynthetic apparatus (Kok, 1956). Since the 1970s, biochemical, ecophysiological, and genetic studies of photosynthetic functions in strong light, in vivo and in situ, and their interactions with biotic and abiotic stresses, have significantly advanced our understanding of photoinhibition. We trace some origins of the idea then, that slow dark reactions, such as growth, CO2 assimilation, photorespiration, and photosynthetic electron transport, ultimately limit light use in photosynthesis, and thus determine whether light is in excess and the magnitude of “excitation pressure” in the photosynthetic apparatus at any moment. This and other ideas are followed through studies of photoacclimation in leaves of plants and algae from diverse terrestrial and marine environments. We highlight two currently interesting possibilities for the photoprotective dissipation of “excitation pressure” that reduce the efficiency of photosynthesis by changes in structure and function of antenna pigment-protein complexes and in the populations of functional and non-functional PS II centers. We conclude by briefly considering challenges presented now by the discovery of “gain of function”, very high light resistant (VHLR) mutants of Chlamydomonas, by the accessory lutein-epoxide cycle, and by technologies for remote sensing of photoinhibition in the field. [ABSTRACT FROM AUTHOR]

In the last few years, it has become apparent that reactive oxygen species (ROS) have important roles as signaling intermediaries in a large number of cellular processes, especially in relation to plants’ interactions with their environment. A complex network of low molecular weight antioxidants, ROS scavenging enzymes, and enzymes that maintain antioxidant pools are required to control the levels of ROS in all subcellular compartments. The coordinated regulation of this network by ROS themselves and stress-associated hormones such as salicylic acid, abscisic acid, and jasmonic acid reveals that antioxidant metabolism is central to considerations of how signaling networks are regulated. Furthermore, it is becoming apparent that key antioxidants such as glutathione and ascorbate are involved in the regulation of stress hormone-directed signaling pathways without any interaction with ROS. Therefore ROS and antioxidants may be key points at which the coordination of different signaling pathways is achieved. These issues are considered in this chapter. [ABSTRACT FROM AUTHOR]

Cyclic electron transport around photosystem I has been proposed to play dual roles in the regulation of photosynthetic electron transport: down-regulating PS II and adjusting the ATP/NADPH ratio. Recent molecular genetics revealed that cyclic electron flow is essential for normal photosynthesis and growth. The water-water-cycle would also play a role similar to cyclic electron transport, in addition to the effective scavenging of reactive oxygen species generated in PS I. Though their rates of electron flux are lower than that of linear electron transport at steady state, these alternative electron flows are indispensable for acute responses to environmental changes and stress. Recent biochemical and molecular studies at the protein and gene level have clarified the components participating in the alternative electron transport. These new findings, including the dual functions of cyclic electron flow and the water-water cycle, and their respective roles in stress responses, are discussed in this chapter. [ABSTRACT FROM AUTHOR]

The activity of photosystem II (PS II) is severely restricted by a variety of environmental factors and, under environmental stress, is determined by the balance between the rate of damage to PS II and the rate of the repair of damaged PS II. The effects of environmental stress on damage and repair can be examined separately and it appears that, while light can damage PS II directly, most types of environmental stress act primarily by inhibiting the repair of PS II. Studies in cyanobacteria have demonstrated that repair-inhibiting conditions include oxidative stress, salt stress, and low-temperatures stress, each of which suppresses the de novo synthesis of proteins, in particular the D1 protein, which is required for the repair of PS II. The synergistic effects of combinations of different types of environmental stress suggest that it is the repair process that determines the sensitivity of PS II to specific environmental conditions. [ABSTRACT FROM AUTHOR]

This Chapter provides highlights on the mechanism of a photosystem II (PS II) damage and repair cycle in chloroplasts. Photo-oxidative damage to the PS II reaction center is a phenomenon that occurs in every organism of oxygenic photosynthesis. Through the process of evolution, an elaborate repair mechanism was devised, one that rectifies this presumably unavoidable and irreversible photoinhibition and restores the PS II charge separation activity. The repair process entails several enzymatic reactions for the selective removal and replacement of the inactivated D1/32 kD reaction center protein (the chloroplast-encoded psbA gene product) from the massive (>1,000 kD) H2O-oxidizing and O2-evolving PS II holocomplex. This repair process is unique in the annals of biology; nothing analogous in complexity and specificity has been reported in other biological systems. Elucidation of the repair mechanism may reveal the occurrence of hitherto unknown regulatory and catalytic reactions for the selective in situ replacement of specific proteins from within multi-protein complexes. This may not only have significant applications in photosynthesis and agriculture but also in medicine and other fields. [ABSTRACT FROM AUTHOR]

Understanding the role of the xanthophyll cycle and elucidating the mechanisms of antenna quenching through the non-photochemical dissipation of excess absorbed energy in the photoprotection of the photochemical apparatus continues to be a major focus of photosynthetic research. In addition to antenna quenching, there is evidence for the non-photochemical dissipation of excess energy through the PS II reaction center. Hence, this photoprotective mechanism is called reaction center quenching. One technique to assess reaction center quenching is photosynthetic thermoluminescence. This technique represents a simple but powerful probe of PS II photochemistry that measures the light emitted due to the reversal of PS II charge separation through the thermally-dependent recombination of the negative charges stabilized on QA− and QB− on the acceptor side of PS II with the positive charges accumulated in the S2- and S3-states of the oxygen evolving complex. Changes in the temperature maxima for photosynthetic thermoluminescence may reflect changes in redox potentials of recombining species within PS II reaction centers. Exposure of Synechococcus sp. PCC 7942, Pinus sylvestris L., Arabidopsis thaliana, and Chlamydomonas reinhardtii to either low temperatures or to high light induces a significant downshift in the temperature maxima for S2QB−B− and S3QB− recombinations relative to S2QA− and S3QA− recombinations. These shifts in recombination temperatures are indicative of lower activation energy for the S2Q−B redox pair recombination and a narrowing of the free energy gap between QA and QB electron acceptors. This, in turn, is associated with a decrease in the overall thermoluminescence emission. We propose that environmental factors such as high light and low temperature result in an increased population of reduced QA (QA−), that is, increased excitation pressure, facilitating non-radiative P680+QA− radical pair recombination within the PS II reaction center. The underlying molecular mechanisms regulating reaction center quenching appear to be species dependent. We conclude that reaction center quenching and antenna quenching are complementary mechanisms that may function to photoprotect PS II to different extents in vivo depending on the species as well as the environmental conditions to which the organism is exposed. [ABSTRACT FROM AUTHOR]

Photoprotection seems to be an intrinsic property of light-harvesting systems, and an interesting question to address is whether the light-harvesting or the photoprotection function was the “original” function, and which function evolved subsequently. It appears that the cyanobacterial one-helix proteins, the presumed ancestors to the LHC proteins, were not designed as antenna proteins but were involved in photoprotection and /or pigment metabolism. Some intermediate steps (two- and four-helix proteins) also seem to have photoprotective functions. The antenna function appeared later in evolution, and many different LHC proteins with somewhat diversified functions arose. To some extent, this happened before the lineages leading to Chlamydomonas and higher plants separated, but further diversification also took place following the split, and some of the proteins may have evolved in a direction away from optimizing light harvesting. When the evolution of feedback de-excitation is put into this evolutionary scheme, it is likely that xanthophyll conversions, that evolved previously to optimize photoprotection, were starting to be used as indicators of light stress and regulators of antenna function. [ABSTRACT FROM AUTHOR]

Plants have diverse defense mechanisms against high light stress. Plants can reduce absorption of light energy through chloroplast avoidance and antenna size reduction. However, the capacity of the avoidance and the antenna size reduction for protection is limited, so that plants often absorb more energy than they can use. Therefore, plants need mechanisms to deal with this excess absorbed light energy, such as harmless thermal dissipation by feedback de-excitation. The transthylakoid pH gradient, xanthophyll cycle, PsbS, and other light-harvesting complex proteins are required for this thermal dissipation. In addition, alternative electron transport allows electrons to pass to acceptors other than CO2, thereby relieving overreduction of electron transport components in high light conditions. To detoxify reactive oxygen species that are inevitably produced during high light stress, plants have antioxidants including carotenoids, ascorbate, and tocopherols. In spite of these photoprotective mechanisms, photodamage may still occur, and efficient repair of damaged systems could be a photoprotective mechanism. In this chapter, recently published molecular genetics studies on each step of photoprotection have been reviewed. Genes required for each defense mechanism that have been identified thus far are introduced, and cloned genes that can possibly be related to photoprotection are discussed. [ABSTRACT FROM AUTHOR]

Application of novel techniques for the characterization of in vivo protein phosphorylation has revealed sixteen distinct phosphorylation sites in ten integral and two peripheral proteins in photosynthetic thylakoid membranes. In addition to phosphorylation of the photosystem II (PS II) proteins D1, D2, CP43, and PsbH, and the light-harvesting antenna polypeptides LHCII and CP29, phosphorylation has been found in photosystem I (PS I) protein PsaD and in two recently identified proteins TSP9 and TMP14. The accumulated knowledge favors an involvement of reversible phosphorylation in adaptive stress responses and cellular signaling, but not in direct regulation of photosynthetic activities like electron transfer or oxygen evolution. Enhancement of PS II protein phosphorylation by abiotic stress maintains the integrity of PS II before it migrates to the stroma regions of the thylakoids where dephosphorylation and subsequent protein turnover take place. Specific dephosphorylation of the D1, D2, and CP43 polypeptides is performed by a heat shock-inducible protein phosphatase intrinsic to the thylakoid membrane. The phosphatase activity is regulated by the lumenal peptidyl-prolyl isomerase TLP40. This regulation may coordinate the protein folding activity of TLP40 in the lumen with the protein dephosphorylation at the opposite side of the thylakoid membrane. Reversible phosphorylation of LHCII in vivo is under complex redox and metabolic control and is probably involved in regulation of the size of the PS II antennae. Cold- and high light-induced phosphorylation of CP29 may facilitate photoprotective energy dissipation by changing PS II-LHCII interactions under stress conditions. Phosphorylation of PsaD protein could be involved in regulation of PS I stability and ferredoxin reduction by PS I. The light-induced phosphorylation of TSP9, followed by its release from thylakoids, is implicated in plant cell signaling. The exact physiological roles of the protein phosphorylation events in thylakoids should be revealed by studies with appropriate mutants of plants and algae. [ABSTRACT FROM AUTHOR]

This chapter summarizes the effects of excessive solar radiation on aquatic primary producers with an emphasis on macroalgae. The introductory paragraphs deal with the aquatic environment and the specific implications for sessile algae and their vertical distribution on the coast. Macroalgae are exposed to dramatically changing irradiances and complicated light patterns governed by the diel solar cycle, the tidal rhythm, and changing cloud cover. The following sections concentrate on the phenomenon of photoinhibition with specific reference to in situ measurements with as little disturbance of the specimens on site as possible. Despite its low percentage contribution in solar radiation, short wavelength ultraviolet is a major component in photoinhibition of algae in their natural habitat. Fast kinetics of fluorescence parameters demonstrates the rapid adaptation of the organisms to their changing photic environment. Early developmental stages are more prone to inhibitory effects of excessive solar radiation. Pigment bleaching and resynthesis are important consequences of solar exposure. Macroalgae have developed several strategies for protection against excessive light stress. UV-absorbing substances, which they share with cyanobacteria and phytoplankton, limit the amount of UV photons reaching the photosynthetic apparatus and the nucleus. They include carotenoids, mycosporine-like amino acids, as well as several chemically not yet identified substances. In addition, the fast turnover of the D1 protein in photosystem II allows rapid recovery from photoinhibition. [ABSTRACT FROM AUTHOR]

Some of the more frequent abiotic stresses in plants are limited availability of nutrients and water, as well as salinity. All these situations occur both in natural habitats and in crops. Stressed plants often experience decreases in photosynthetic rates, whereas they still harvest sunlight. Environmental stresses such as those may decrease the efficiency with which solar energy is harvested and used by plants in photosynthetic reactions. This feature is what the scientific community has often called photoinhibition. Some researchers tacitly assume that photoinhibition may result from photodamage, whereas others believe that it is more the integration of a series of regulatory and protective adjustments. The aim of this review is to summarize the current knowledge concerning photoinhibition- and photoprotection-related processes under nutrient deficiencies, drought, and salinity stress, and to discuss the role that photoinhibition could play under such environmental stresses. [ABSTRACT FROM AUTHOR]

The photosynthetic apparatus is exquisitely adapted to capture light energy and convert it into reduced carbon compounds while also protecting against the potential deleterious effects of excessive excitation energy. The latter is achieved through fine regulation of thermal energy dissipation over multiple time scales and in response to many different environmental stresses. Over short time scales in the absence of additional stress, control is exerted through pH regulation of the enzymatic conversion of violaxanthin to zeaxanthin (and its return to violaxanthin) and engagement of zeaxanthin in thermal energy dissipation. Under more extreme exposure to excess light (transfer of shade leaves to high light or the imposition of additional stresses in the presence of high light), greater levels of zeaxanthin are retained and may also be maintained in a dissipative configuration even in darkness. Engagement of zeaxanthin in thermal energy dissipation lowers the maximal efficiency of photosystem II (PS II) as the excess excitation energy is diverted away from the reaction centers and harmlessly released as heat. Thus, maximal PS II efficiency exhibits decreases and increases with varying degrees of light absorption. Under prolonged and/or pronounced exposure to excess light, maximal PS II efficiency can furthermore exhibit nocturnally sustained decreases as the potential for photoprotective zeaxanthin-dependent energy dissipation is maintained. Zeaxanthin-dependent energy dissipation that is sustained at moderate temperatures is also typically accompanied by downregulation of photosynthesis, including photosynthetic electron transport. Decreases in photosynthetic electron transport presumably lower the likelihood of electrons reducing molecular oxygen to superoxide, and sustained zeaxanthin-dependent energy dissipation mitigates the formation of singlet excited oxygen. Thus, while sustained decreases in maximal PS II efficiency and photosynthetic capacity are key characteristics of photoinhibition, they are also the features that provide powerful photoprotection against the formation of toxic reactive oxygen species. [ABSTRACT FROM AUTHOR]

The chloroplast-coded D1 protein of Photosystem II (PS II) is the major membrane protein synthesized within the plastid. It is involved in light-dependent electron transport, is a major target for photosynthesis herbicides and is universal to oxygenic phototrophs. The defining feature of D1 is its rapid turnover in spite of its being a structural component of the PS II reaction center core. Processing of nascent D1 precursor (33.5–34 kDa) occurs on unstacked stromal lamellae. The mature protein (32 kDa) then migrates to the grana where an initial scission occurs producing a 23 kDa N-terminal degradation fragment. Post-translational and reversible palmitoylation and phosphorylation accompany the protein along its life cycle. Both anabolism and catabolism of D1 are photoregulated, with synthesis coupled to phosphorylation but degradation coupled to PS II electron transport. Dephosphorylation of D1, in turn, is regulated by PS I excitation. Thus, the phosphorylation state of the protein is sensitive to the relative energy distribution between the two photosystems. Beyond redox regulation of D1 phosphorylation, an internal, circadian clock exerts overriding control. Two photosensitizers are involved in D1 degradation: chlorophyll pigments in the visible and far-red regions of the spectrum, and plastosemiquinone in the UV-B region. D1 degradation in visible light is a process only marginally overlapping with photoinhibition and overwhelmingly associated with fluences limiting for photosynthesis. Mixing physiological levels of visible and UV-B radiances leads to synergistic effects such that above a critical threshold of UV-B, the D1 as well as its sister protein, D2, both are targeted for accelerated degradation. These and other D1 protein studies, mainly carried out with intact Spirodela plants during the past 25 years in the authors’ laboratories, are presented in a historical perspective. [ABSTRACT FROM AUTHOR]

This is an account of my personal and professional life as a student of the violaxanthin-antheraxanthin-zeaxanthin scheme for the xanthophyll cycle in higher plants. I had no early vision of becoming a scientist, but one circumstance led to another, and what began as a random walk ultimately developed into a life-long study of the biochemistry, physiology, and function of the xanthophyll cycle. The circumstances and people with whom I shared this path are described, with special attention given to the early developments. [ABSTRACT FROM AUTHOR]