Plants are simultaneously exposed to abiotic and biotic hazards. Here, we show that local and systemic acclimation in Arabidopsis thaliana leaves in response to excess excitation energy (EEE) is associated with cell death and is regulated by specific redox changes of the plastoquinone (PQ) pool. These redox changes cause a rapid decrease of stomatal conductance, global induction of ASCORBATE PEROXIDASE2 and PATHOGEN RESISTANCE1, and increased production of reactive oxygen species (ROS) and ethylene that signals through ETHYLENE INSENSITIVE2 (EIN2). We provide evidence that multiple hormonal/ROS signaling pathways regulate the plant's response to EEE and that EEE stimulates systemic acquired resistance and basal defenses to virulent biotrophic bacteria. In the Arabidopsis LESION SIMULATING DISEASE1 (lsd1) null mutant that is deregulated for EEE acclimation responses, propagation of EEE-induced programmed cell death depends on the plant defense regulators ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4). We find that EDS1 and PAD4 operate upstream of ethylene and ROS production in the EEE response. The data suggest that the balanced activities of LSD1, EDS1, PAD4, and EIN2 regulate signaling of programmed cell death, light acclimation, and holistic defense responses that are initiated, at least in part, by redox changes of the PQ pool.

Although light is essential for photosynthesis, excess light can damage the photosynthetic apparatus and deregulate other cellular processes. Thus, protective integrated regulatory responses that can dissipate excess of absorbed light energy and simultaneously optimize photosynthesis and other cellular processes under variable light conditions can prove highly adaptive. Here, we show that the local and systemic responses to an excess light episode are associated with photoelectrophysiological signaling (PEPS) as well as with changes in nonphotochemical quenching and reactive oxygen species levels. During an excess light incident, PEPS is induced by quantum redox changes in photosystem II and in its proximity and/or by changes in glutathione metabolism in chloroplasts. PEPS is transduced, at least in part, by bundle sheath cells and is light wavelength specific. PEPS systemic propagation speed and action potential are dependent on ASCORBATE PEROXIDASE2 function. Excess light episodes are physiologically memorized in leaves, and the cellular light memory effect is specific for an excess of blue (450 nm) and red (650 nm) light of similar energy. It is concluded that plants possess a complex and dynamic light training and memory system that involves quantum redox, reactive oxygen species, hormonal, and PEPS signaling and is used to optimize light acclimation and immune defenses.

This review confronts the classical view of plant immune defence and light acclimation with recently published data. Earlier findings have linked plant immune defences to nucleotide‐binding site leucine‐rich repeat (NBS‐LRR)‐dependent recognition of pathogen effectors and to the role of plasma membrane‐localized NADPH‐dependent oxidoreductase (AtRbohD), reactive oxygen species (ROS) and salicylic acid (SA). However, recent results suggest that plant immune defence also depends on the absorption of excessive light energy and photorespiration. Rapid changes in light intensity and quality often cause the absorption of energy, which is in excess of that required for photosynthesis. Such excessive light energy is considered to be a factor triggering photoinhibition and disturbance in ROS/hormonal homeostasis, which leads to cell death in foliar tissues. We highlight here the tight crosstalk between ROS‐ and SA‐dependent pathways leading to light acclimation, and defence responses leading to pathogen resistance. We also show that LESION SIMULATING DISEASE 1 (LSD1) regulates and integrates these processes. Moreover, we discuss the role of plastid–nucleus signal transduction, photorespiration, photoelectrochemical signalling and ‘light memory’ in the regulation of acclimation and immune defence responses. All of these results suggest that plants have evolved a genetic system that simultaneously regulates systemic acquired resistance (SAR), cell death and systemic acquired acclimation (SAA).

The agronomic and physiological traits, drought tolerance indexes, principal component analysis and Ward`s method were applied to assess the differences among 20 wheat genotypes in response to drought. Statistically significant correlation was observed for measured traits. Drought susceptibility index (DSI), stress tolerance index (STI) and stress index (SI) were most useful to identify genotypes differing in their response to drought. Utility of the indexes was confirmed by physiological markers of drought tolerance i.e. membrane injury and leaf water status. Variation of the genotypes in biomass and grain yield during drought stress was also verified by clustering methods. Finally, integration of physiological and statistical methods presented in this work, allows to both, indicate that tolerance to drought in wheat has a common genetic background, and select the most diverse genotypes. Based on the results, we recommend a tool for breeders, useful to select the genotypes resistant and sensitive to drought. Abbreviations: DM: dry matter; DSI: drought susceptibility index; FWC: field water capacity; GY: grain yield; GMP: geometric mean productivity index; H: plant height; LI: leakage index related to membrane injury; M<sub>PRO</sub>: mean productivity index; M<sub>HAR</sub>: harmonic mean index; NoT: number of tillers; NoG, W-1000: number of grains and weight of 1000 grains, respectively; NoL<sub>MT</sub>, NoL<sub>AT</sub>, NoL<sub>T</sub>: number of leaves on main tiller, adventitious tillers and total leaf number, respectively; PCA: principal component analysis; RTC: relative trait change; RWC, RT, WD: relative water content, relative turgidity and water deficit, respectively SI: stress index; SPAD: leaf greening; STI: stress tolerance index; TI: tolerance index; WCA: Ward`s cluster analysis.

Electrical signalling in higher plants is required for the appropriate intracellular and intercellular communication, stress responses, growth and development. In this review, we have focus on recent findings regarding the electrical signalling, as a major regulator of the systemic acquired acclimation (SAA) and the systemic acquired resistance (SAR). The electric signalling on its own cannot confer the required specificity of information to trigger SAA and SAR, therefore, we have also discussed a number of other mechanisms and signalling systems that can operate in combination with electric signalling. We have emphasised the interrelation between ionic mechanism of electrical activity and regulation of photosynthesis, which is intrinsic to a proper induction of SAA and SAR. In a special way, we have summarised the role of non-photochemical quenching and its regulator PsbS. Further, redox status of the cell, calcium and hydraulic waves, hormonal circuits and stomatal aperture regulation have been considered as components of the signalling. Finally, a model of light-dependent mechanisms of electrical signalling propagation has been presented together with the systemic regulation of light-responsive genes encoding both, ion channels and proteins involved in regulation of their activity. Due to space limitations, we have not addressed many other important aspects of hormonal and ROS signalling, which were presented in a number of recent excellent reviews (e.g., Foyer and Noctor, 2013; Vaahtera et al., 2014; Dietz, 2015; Considine et al., 2015; Gilroy et al., 2016; Mignolet-Spruyt et al., 2016).

There is growing evidence that for a comprehensive insight into the function of plant genes, it is crucial to assess their functionalities under a wide range of conditions. In this study, we examined the role of LESION SIMULATING DISEASE1 (LSD1), ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), and PHYTOALEXIN DEFICIENT4 (PAD4) in the regulation of photosynthesis, water use efficiency, reactive oxygen species/hormonal homeostasis, and seed yield in Arabidopsis (Arabidopsis thaliana) grown in the laboratory and in the field. We demonstrate that the LSD1 null mutant (lsd1), which is known to exhibit a runaway cell death in nonpermissive conditions, proves to be more tolerant to combined drought and high-light stress than the wild type. Moreover, depending on growing conditions, it shows variations in water use efficiency, salicylic acid and hydrogen peroxide concentrations, photosystem II maximum efficiency, and transcription profiles. However, despite these changes, lsd1 demonstrates similar seed yield under all tested conditions. All of these traits depend on EDS1 and PAD4. The differences in the pathways prevailing in the lsd1 in various growing environments are manifested by the significantly smaller number of transcripts deregulated in the field compared with the laboratory, with only 43 commonly regulated genes. Our data indicate that LSD1, EDS1, and PAD4 participate in the regulation of various molecular and physiological processes that influence Arabidopsis fitness. On the basis of these results, we emphasize that the function of such important regulators as LSD1, EDS1, and PAD4 should be studied not only under stable laboratory conditions, but also in the environment abounding in multiple stresses.