Abstract:Capturing light intensities exceeding the capacity of photosynthesis can lead to cell death in plant leaves. In this review, we summarize recent findings on the mechanisms mediating light-induced cell death, highlighting the role of reactive carbonyl species, of the endoplasmic reticulum and of phytohormones in the adoption of phototolerance versus cell death pathways.
“…The class II TGA factors TGA2, TGA5, and TGA6 recruit SCL14 to the promoters of SCL14 target genes that encode proteins required for detoxification responses ( Fode et al., 2008 ). The SCL14-induced ANAC102 transcription factor is crucial for inducing detoxification-responsive genes ( Christianson et al., 2009 ; D'Alessandro et al., 2020 ). Figure 3 Chloroplast ORS pathways.…”
“…Perhaps βCC-induced SA signaling antagonizes the lipid peroxidation-driven stress responses that are controlled in part by another stress hormone, JA, considering their well-established antagonism ( Thaler et al., 2012 ). How Recent studies also indicate that the SA and JA signaling pathways synergistically aid plants in adapting to high-light stress ( D'Alessandro et al., 2020 ). The synergistic activation of SA and JA signaling pathways has been found to confer basal thermotolerance in Arabidopsis ( Clarke et al., 2009 ).…”
Chloroplasts overproduce reactive oxygen species (ROS) under unfavorable environmental conditions, and these ROS are implicated in both signaling and oxidative damage. There is mounting evidence for their roles in translating environmental fluctuations into distinct physiological responses, but their targets, signaling cascades, and mutualism and antagonism with other stress signaling cascades and within ROS signaling remain poorly understood. Great efforts made in recent years have shed new light on chloroplast ROS-directed plant stress responses, from ROS perception to plant responses, in conditional mutants of
Arabidopsis thaliana
or under various stress conditions. Some articles have also reported the mechanisms underlying the complexity of ROS signaling pathways, with an emphasis on spatiotemporal regulation. ROS and oxidative modification of affected target proteins appear to induce retrograde signaling pathways to maintain chloroplast protein quality control and signaling at a whole-cell level using stress hormones. This review focuses on these seemingly interconnected chloroplast-to-nucleus retrograde signaling pathways initiated by ROS and ROS-modified target molecules. We also discuss future directions in chloroplast stress research to pave the way for discovering new signaling molecules and identifying intersectional signaling components that interact in multiple chloroplast signaling pathways.
“…The class II TGA factors TGA2, TGA5, and TGA6 recruit SCL14 to the promoters of SCL14 target genes that encode proteins required for detoxification responses ( Fode et al., 2008 ). The SCL14-induced ANAC102 transcription factor is crucial for inducing detoxification-responsive genes ( Christianson et al., 2009 ; D'Alessandro et al., 2020 ). Figure 3 Chloroplast ORS pathways.…”
“…Perhaps βCC-induced SA signaling antagonizes the lipid peroxidation-driven stress responses that are controlled in part by another stress hormone, JA, considering their well-established antagonism ( Thaler et al., 2012 ). How Recent studies also indicate that the SA and JA signaling pathways synergistically aid plants in adapting to high-light stress ( D'Alessandro et al., 2020 ). The synergistic activation of SA and JA signaling pathways has been found to confer basal thermotolerance in Arabidopsis ( Clarke et al., 2009 ).…”
Chloroplasts overproduce reactive oxygen species (ROS) under unfavorable environmental conditions, and these ROS are implicated in both signaling and oxidative damage. There is mounting evidence for their roles in translating environmental fluctuations into distinct physiological responses, but their targets, signaling cascades, and mutualism and antagonism with other stress signaling cascades and within ROS signaling remain poorly understood. Great efforts made in recent years have shed new light on chloroplast ROS-directed plant stress responses, from ROS perception to plant responses, in conditional mutants of
Arabidopsis thaliana
or under various stress conditions. Some articles have also reported the mechanisms underlying the complexity of ROS signaling pathways, with an emphasis on spatiotemporal regulation. ROS and oxidative modification of affected target proteins appear to induce retrograde signaling pathways to maintain chloroplast protein quality control and signaling at a whole-cell level using stress hormones. This review focuses on these seemingly interconnected chloroplast-to-nucleus retrograde signaling pathways initiated by ROS and ROS-modified target molecules. We also discuss future directions in chloroplast stress research to pave the way for discovering new signaling molecules and identifying intersectional signaling components that interact in multiple chloroplast signaling pathways.
“…Oxidation of membrane lipids gives rise to reactive carbonyl species, of which many are cytotoxic and readily respond to proteins (D'Alessandro et al, 2020;Johansson et al, 2004). Strategies to control their accumulation by overexpressing detoxifying enzymes have been successful in improving stress tolerance and are discussed below.…”
Section: Oxidative Posttranslational Modifications and Damagementioning
Originally conceived as harmful metabolic byproducts, reactive oxygen species (ROS) are now recognized as an integral part of numerous cellular programs. Thanks to their diverse physicochemical properties, compartmentalized production, and tight control exerted by the antioxidant machinery they activate signaling pathways that govern plant growth, development, and defense. Excessive ROS levels are often driven by adverse changes in environmental conditions, ultimately causing oxidative stress. The associated negative impact on cellular constituents have been a major focus of decade-long research efforts to improve the oxidative stress resilience by boosting the antioxidant machinery in model and crop species. We highlight the role of enzymatic and non-enzymatic antioxidants as integral factors of multiple signaling cascades beyond their mere function to prevent oxidative damage under adverse abiotic stress conditions.
“…Chloroplast ROS, byproducts of photosynthesis, are accountable for the photodamage of chloroplast macromolecules, such as proteins, lipids, and nucleic acids [20][21][22][23][24]. These harmful ROS produced in chloroplasts include singlet oxygen ( 1 O 2 ), superoxide anion (O 2 − ), hydrogen peroxide (H 2 O 2 ), and hydroxyl radical (HO•) [16,25,26].…”
“…Since the various foliar metabolisms significantly rely on chloroplasts, it is indisputable that the ROS-driven chloroplast photodamage will negatively affect plant productivity, especially under fluctuating, severe, and long-lasting stress conditions. However, independent studies have revealed that chloroplast ROS can be beneficial for plants to adapt to distinct stress factors by triggering various signaling pathways from the stressed chloroplasts back to the nucleus, collectively referred to as operational retrograde signaling (ORS) [22,27,28]. For instance, the ROS-driven oxidation of proteins and an antioxidant compound (β-carotene) were found to be integral for activating ORS pathways in response to external stimuli, such as high light, cold, drought, and herbivores, thereby linking chloroplast photodamage to signaling [23,[29][30][31].…”
Low and high temperatures are life-threatening stress factors, diminishing plant productivity. One of the earliest responses of plants to stress is a rapid burst of reactive oxygen species (ROS) in chloroplasts. Widespread efforts over the past decade shed new light on the chloroplast as an environmental sensor, translating the environmental fluctuation into varying physiological responses by utilizing distinct retrograde (chloroplast-to-nucleus) signals. Recent studies have unveiled that chloroplasts mediate a similar unfolded/misfolded/damaged protein response (cpUPR) as observed in the endoplasmic reticulum and mitochondria. Although observing cpUPR is not surprising since the chloroplast is a prime organelle producing harmful ROS, the intertwined relationship among ROS, protein damage, and chloroplast protein quality controls (cpPQCs) with retrograde signaling has recently been reported. This finding also gives rise to critical attention on chloroplast proteins involved in cpPQCs, ROS detoxifiers, transcription/translation, import of precursor proteins, and assembly/maturation, the deficiency of which compromises chloroplast protein homeostasis (proteostasis). Any perturbation in the protein may require readjustment of proteostasis by transmitting retrograde signal(s) to the nucleus, whose genome encodes most of the chloroplast proteins involved in proteostasis. This review focuses on recent findings on cpUPR and chloroplast-targeted FILAMENTOUS TEMPERATURE-SENSITIVE H proteases involved in cpPQC and retrograde signaling and their impacts on plant responses to temperature stress.
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