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Perylene derivatives can be stimulated by the hypoxic tumor microenvironment to generate radical anion that is proposed to arouse electron exchange with oxidizing substance, and in turn, realize reactive oxygen species (ROS) burst. Here, three perylene therapeutic agents, PDI‐NI, PDIB‐NI, and PDIC‐NI, are developed and it is found that the minimum lowest unoccupied molecular orbital (LUMO) energy level makes PDIC‐NI most easily accept electrons from the oxidative respiratory chain to form lots of anions, and the resultant maximum ROS generation, establishing an unambiguous mechanism for the formation of perylene radical anions in the cell, presents solid evidence for LUMO energy level determining endogenous ROS burst. Stirringly, PDIC‐NI‐induced ROS generation arouses enhanced mitochondrial oxidative stress and concurrently activates immunogenic cell death (ICD), which not only efficiently kills lung tumor cells but also reprograms immunosuppressive tumor microenvironment, including the cytokine secretion, dendritic cell maturation, as well as cytotoxic T lymphocytes activation, to inhibit the growth of xenografted and metastasis tumor, presenting a proof‐of‐concept demonstration of perylene that acts as an integrated therapeutic agent to well realize hypoxia‐activated chemotherapy with ICD‐induced immunotherapy on lung cancer. This study presents the proof‐of‐concept demonstration that perylene ingeniously employs energy level‐mediated reactive oxygen species burst to reach hypoxia‐activated chemotherapy and immunogenic cell death‐induced immunotherapy on lung cancer.

Plant cell surface pattern-recognition receptors (PRRs) mount pattern-triggered immunity (PTI) by recognizing the typical molecular structures of pathogens, termed pathogen-associated molecular patterns (PAMPs), providing the first line of defence against various phytopathogens. [...]transient expression with 35S::gNbFLS2 and 35S::gNbFLS2:GFP (gNbFLS2, the full-length genomic DNA sequences of NbFLS2s; GFP, coding sequence of green fluorescent protein) revealed that 35S::gNbFLS2-2 and 35S::gNbFLS2-2:GFP can recover the ability to generate ROS bursts in KO1 & 2 after flg22Psy treatment, but 35S::gNbFLS2-1 and 35S::gNbFLS2-1:GFP cannot (Figure 1j). [...]immunoblotting detected the accumulation of NbFLS2-2-GFP (~210 kDa) but did not detect NbFLS2-1-GFP (Figure 1k). Furthermore, no accumulation of target protein was observed in transient expression of the coding sequence of NbFLS2-1 (Figure 1k). [...]the lack of function of NbFLS2-1 may be due to translational level regulation.

Currently, the widely used active form of plant elicitor peptide 1 (PEP1) from Arabidopsis thaliana is composed of 23 amino acids, hereafter AtPEP1(1–23), serving as an immune elicitor. The relatively less conserved N-terminal region in AtPEP family indicates that the amino acids in this region may be unrelated to the function and activity of AtPEP peptides. Consequently, we conducted an investigation to determine the necessity of the nonconserved amino acids in AtPEP1(1–23) peptide for its functional properties. By assessing the primary root growth and the burst of reactive oxygen species (ROS), we discovered that the first eight N-terminal amino acids of AtPEP1(1–23) are not crucial for its functionality, whereas the conserved C-terminal aspartic acid plays a significant role in its functionality. In this study, we identified a truncated peptide, AtPEP1(9–23), which exhibits comparable activity to AtPEP1(1–23) in inhibiting primary root growth and inducing ROS burst. Additionally, the truncated peptide AtPEP1(13–23) shows similar ability to induce ROS burst as AtPEP1(1–23), but its inhibitory effect on primary roots is significantly reduced. These findings are significant as they provide a novel approach to explore and understand the functionality of the AtPEP1(1–23) peptide. Moreover, exogenous application of AtPEP1(13–23) may enhance plant resistance to pathogens without affecting their growth and development. Therefore, AtPEP1(13–23) holds promise for development as a potentially applicable biopesticides.

Banana wilt disease is a typical vascular disease caused by the fungal pathogen Fusarium oxysporum f. sp. cubense 4 ( Foc 4). Pattern recognition receptors in the plant cell membrane can recognize pathogen-associated molecular patterns (PAMPs) to activate multi-layer defense responses, including defense gene expression, stomatal closure, reactive oxygen species (ROS) burst and callose deposition, to limit pathogen growth. In the present study, we found that chitin elicitor receptor kinase 1 (CERK1) was required for the non-host resistance of Arabidopsis thaliana to Foc B2 (a strain of Foc 4). The cerk1 mutant had weaker defense responses after Foc B2 treatment, including lower expression of PAMP- and salicylic acid-responsive genes, no stomatal closure, lower ROS level and less callose deposition, than that of the wild-type plant. Consistent with this, the cerk1 mutant plants exhibited higher susceptibility to non-host pathogen Foc B2. These results suggest the crucial importance of CERK1 in Foc B2-triggered non-host resistance.

This chapter contains sections titled: Phagocytes Generating Reactive Oxygen and Nitrogen Species Reactive Oxygen Species‐The “Respiratory Burst” Reactive Nitrogen Species and Inducible Nitric Oxide Synthase Reactive Oxygen and Nitrogen Species Triggering the Defense Attack Immune Response to Injury and Wound Healing Protection Strategies of Bacteria Parasite Mechanisms to Evade Immune Responses of Fish References

Reactive oxygen species (ROS) play an integral role as signalling molecules in the regulation of numerous biological processes such as growth, development, and responses to biotic and/or abiotic stimuli in plants. To some extent, various functions of ROS signalling are attributed to differences in the regulatory mechanisms of respiratory burst oxidase homologues (RBOHs) that are involved in a multitude of different signal transduction pathways activated in assorted tissue and cell types under fluctuating environmental conditions. Recent findings revealed that stress responses in plants are mediated by a temporal–spatial coordination between ROS and other signals that rely on production of stress-specific chemicals, compounds, and hormones. In this review we will provide an update of recent findings related to the integration of ROS signals with an array of signalling pathways aimed at regulating different responses in plants. In particular, we will address signals that confer systemic acquired resistance (SAR) or systemic acquired acclimation (SAA) in plants.

Salinity stress is the major abiotic stress that affects crop production and productivity as it has a multifarious negative effect on the growth and development of the plant. Salinity stress stimulates the accumulation of reactive oxygen species (ROS) which is toxic to cells at higher concentrations. At lower concentrations, these molecules help in the mitigation of salinity stress through a series of signal transduction mechanisms. The respiratory burst by NADPH oxidase leads to an increase in ROS generation. It is a key signalling node in the plant gene network and helps to integrate the signal transduction with ROS signalling. Reactive nitrogen species (RNS) are free radical and non-radical reactive molecules that are also produced under salinity stress and lead to nitrosative stress by regulating SOS, MAPK dependent, Ca 2+ dependent and G-protein dependent pathways. The reactive sulphur species (RSS) is a strong oxidizing agent that preferably attacks the thiol functional group. Activation of the different signalling components like ROS, RNS, RSS, SOS, Calcium, MAPK signalling and cross-talk between different signalling pathways and phytohormones have been considered as the main mechanism for ion homeostasis and Na + exclusion at the cellular level. These reactive species and their interaction upregulate the gene expression and phosphorylation level of different membrane transporters viz., PM H + -ATPase and Na + / H + antiporter which might endure salinity tolerance in plants. This review aims to describe the interplay/crosstalk amongst reactive species and phytohormones under salinity stress. Moreover, mechanistic insight of reactive species-mediated stress regulation and the response has also been discussed which will be helpful for the development of stress-tolerant cultivars.

Cadmium (Cd) is considered to be one of the most toxic pollutants persistent in soil for thousands of years and is ranked on seventh position among all environmental pollutants. The higher concentration of Cd in plants inhibits their growth and metabolism and further enters the food chain. Cd toxicity initiates redox actions in plants by inducing oxidative stress through the production of free radicals. It alters mineral uptake by disturbing water potential or affects the microbial population in soils, opening and closing of stomata, transpiration, photosynthesis, antioxidant levels, sugar metabolism and productivities. It also causes chlorosis, mineral deficiencies, inhibition of nitrate reductase activity and ammonia assimilation in several plant species. The plants have adopted a number of mechanisms to facilitate reduction in the amount of ROS. They possess series of antioxidative defence responses to scavenge reactive oxygen species (ROS) levels. Furthermore, specific mechanisms such as such as efflux, immobilization, stabilization, complexation, sequestration and detoxification are generally observed to combat the Cd stresses. Moreover, endogenous phytohormonal signalling during stressed conditions within plants has also been focussed. Cd stimulates various hormonal signalling pathways and regulates many physiological processes in plants that in turn ameliorate Cd stress. Strikingly, phytohormones play an imperative role during signal transduction pathway along with regulating overall growth and development of plants under toxic conditions. Moreover, plant hormones boost antioxidant activities and plummet oxidative damage from plants along with maintaining cellular homeostasis. This review encompasses the ecotoxicological aspects of Cd within plants and plant responses to tackle such adversities.

Root hair polar growth is endogenously controlled by auxin and sustained by oscillating levels of reactive oxygen species (ROS). These cells extend several hundred-fold their original size toward signals important for plant survival. Although their final cell size is of fundamental importance, the molecular mechanisms that control it remain largely unknown. Here we show that ROS production is controlled by the transcription factor RSL4, which in turn is transcriptionally regulated by auxin through several auxin response factors (ARFs). In this manner, auxin controls ROS-mediated polar growth by activating RSL4, which then up-regulates the expression of genes encoding NADPH oxidases (also known as RESPIRATORY BURST OXIDASE HOMOLOG proteins) and class III peroxidases, which catalyze ROS production. Chemical or genetic interference with ROS balance or peroxidase activity affects root hair final cell size. Overall, our findings establish amolecular link between auxin and ROS-mediated polar root hair growth.

Reactive oxygen species (ROS) produced by the NADPH oxidase, respiratory burst oxidase homolog (RBOH), trigger signal transduction in diverse biological processes in plants. However, the functions of RBOH homologs in rice (Oryza sativa) and other gramineous plants are poorly understood. Ethylene induces the formation of lysigenous aerenchyma, which consists of internal gas spaces created by programmed cell death of cortical cells, in roots of gramineous plants under oxygen-deficient conditions. Here, we report that, in rice, one RBOH isoform (RBOHH) has a role in ethylene-induced aerenchyma formation in roots. Induction of RBOHH expression under oxygen-deficient conditions was greater in cortical cells than in cells of other root tissues. In addition, genes encoding group I calcium-dependent protein kinases (CDPK5 and CDPK13) were strongly expressed in root cortical cells. Coexpression of RBOHH with CDPK5 or CDPK13 induced ROS production in Nicotiana benthamiana leaves. Inhibitors of RBOH activity or cytosolic calcium influx suppressed ethylene-induced aerenchyma formation. Moreover, knockout of RBOHH by CRISPR/Cas9 reduced ROS accumulation and inducible aerenchyma formation in rice roots. These results suggest that RBOHH-mediated ROS production, which is stimulated by CDPK5 and/or CDPK13, is essential for ethylene-induced aerenchyma formation in rice roots under oxygen-deficient conditions.