Maintain Reactive Oxygen Species Homeostasis Research Articles

BR regulates wheat root salt tolerance by maintaining ROS homeostasis.

Trace amounts of epibrassinolide (EpiBL) could partially rescue wheat root length inhibition in salt-stressed situation by scavenging ROS, and ectopic expression of TaDWF4 or TaBAK1 enhances root salt tolerance in Arabidopsis by balancing ROS level. Salt stress often leads to ion toxicity and oxidative stress, causing cell structure damage and root development inhibition in plants. While prior research indicated the involvement of exogenous brassinosteroid (BR) in plant responses to salt stress, the precise cytological role and the function of BR in wheat root development under salt stress remain elusive. Our study demonstrates that 100mM NaCl solution inhibits wheat root development, but 5nM EpiBL partially rescues root length inhibition by decreasing H2O2 content, oxygen free radical (OFR) content, along with increasing the peroxidase (POD) and catalase (CAT) activities in salt-stressed roots. The qRT-PCR experiment also shows that expression of the ROS-scavenging genes (GPX2 and CAT2) increased in roots after applying BR, especially during salt stress situation. Transcriptional analysis reveals decreased expression of BR synthesis and root meristem development genes under salt stress in wheat roots. Differential expression gene (DEG) enrichment analysis highlights the significant impact of salt stress on various biological processes, particularly "hydrogen peroxide catabolic process" and "response to oxidative stress". Additionally, the BR biosynthesis pathway is enriched under salt stress conditions. Therefore, we investigated the involvement of wheat BR synthesis gene TaDWF4 and BR signaling gene TaBAK1 in salt stress responses in roots. Our results demonstrate that ectopic expression of TaDWF4 or TaBAK1 enhances salt tolerance in Arabidopsis by balancing ROS (Reactive oxygen species) levels in roots.

Genome-wide identification and role of HSFs in antioxidant response of hot water treated zucchini fruit during cold storage

Zucchini squashes are cold-sensitive and vulnerable to chilling injury (CI) resulting from reactive oxygen species (ROS) and hot water (HW) immersing effectively reduce CI symptoms during cold storage. However, mechanism involved in reduced ROS due to HW treatment has not been characterized well. In this study, tender green zucchini fruit were treated with HW for 15 min at 45 ± 1 °C and stored for 15 d at 4 ± 1 °C and above 90 % relative humidity. Results showed substantial reduction in CI index, electrolyte leakage, malonaldehyde (MDA) contents and ROS accumulation along with increased activity of ROS-scavenging enzymes due to HW treatment. To gain insight into the molecular mechanism involved in antioxidant defense system, transcriptomic analysis revealed that heat shock factors (HSF) accumulated due to HW treatment regulated the ROS pathway during cold stress. CpHSFA4a was one of the highly expressed transcription factors (TF) due to HW treatment that regulated the transcription of ROS enzymes related genes. CpHSFA4a bind actively with heat shock element (HSE) in promoter regions of CpSOD, CpCAT, CpAPX1, CpAPX2, and CpAPX3, activated and increased the expression of these genes. In conclusion, HW treatment alleviated the CI by maintaining ROS homeostasis through CpHSFA4a mediated ROS pathway in zucchini squashes during cold storage.

Growth and metabolic differences in the potential of phytoremediation between two hybrid bermudagrasses in roots, stems, and leaves under cadmium stress

Bermudagrass (Cynodon) species has been identified as a dominant plant species in cadmium (Cd)-contaminated soils. Objectives of current study were to evaluate Cd tolerance of two hybrid bermudagrass (Cynodon transvaalensis × Cynodon dactylon) cultivars Tifdwarf and Chuannong-3 for urban greening and slope ecological restoration and further to explore the difference in Cd tolerance associated with changes in ion absorption and distribution, antioxidant metabolism, and accumulations of phytochelatins (PCs) and metallothioneins (MTs) in roots, stems, and leaves. After exposure to equal concentration and duration of Cd stress, growth, chlorophyll content, and photochemical efficiency of both cultivars reduced significantly, but Cd-induced these inhibitory effects were more pronounced in Chuannong-3. As compared to Chuannong-3, Tifdwarf maintained significantly higher Cd concentration in roots and lower Cd concentration, bioconcentration factor, and translocation factor in aboveground parts in response to Cd stress. Each plant of Tifdwarf also accumulated more Cd in leaves, stems, and roots than each plant of Chuannong-3 due to larger biomass under Cd stress. Cd stress also significantly inhibited uptake and partitioning of iron, sodium, and potassium in two cultivars. In addition, Tifdwarf exhibited better antioxidant defense for reactive oxygen species (ROS) scavenging than Chuannong-3 under Cd stress, as reflected by higher antioxidant enzyme activities and antioxidant metabolites involved in ascorbic acid (ASA)-glutathione (GSH) cycle. Tifdwarf also accumulated more PCs in leaves, stems, and roots and more MTs in leaves and stems than Chuannong-3, which could help to chelate Cd to reduce cytotoxicity of Cd. Moreover, strong antioxidant property of MTs was beneficial for maintaining ROS homeostasis in plants. Therefore, better Cd tolerance of Tifdwarf could be mainly due to the inhibition of Cd uptake and partitioning, enhanced ASA-GSH cycle, and more accumulations of PCs and MTs. Tifdwarf showed better potential for Cd remediation or urban greening in Cd-polluted soils.

Hepatocellular carcinoma cells downregulate NADH:Ubiquinone Oxidoreductase Subunit B3 to maintain reactive oxygen species homeostasis.

HCC is a leading cause of cancer-related death. The role of reactive oxygen species (ROS) in HCC remains elusive. Since a primary ROS source is the mitochondrial electron transport chain complex Ι and the NADH:ubiquinone Oxidoreductase Subunit B3 (NDUFB3), a complex I subunit, is critical for complex I assembly and regulates the associated ROS production, we hypothesize that some HCCs progress by hijacking NDUFB3 to maintain ROS homeostasis. NDUFB3 in human HCC lines was either knocked down or overexpressed. The cells were then analyzed in vitro for proliferation, migration, invasiveness, colony formation, complex I activity, ROS production, oxygen consumption, apoptosis, and cell cycle. In addition, the in vivo growth of the cells was evaluated in nude mice. Moreover, the role of ROS in the NDUFB3-mediated changes in the HCC lines was determined using cellular and mitochondrion-targeted ROS scavengers. HCC tissues showed reduced NDUFB3 protein expression compared to adjacent healthy tissues. In addition, NDUFB3 knockdown promoted, while its overexpression suppressed, HCC cells' growth, migration, and invasiveness. Moreover, NDUFB3 knockdown significantly decreased, whereas its overexpression increased complex I activity. Further studies revealed that NDUFB3 overexpression elevated mitochondrial ROS production, causing cell apoptosis, as manifested by the enhanced expressions of proapoptotic molecules and the suppressed expression of the antiapoptotic molecule B cell lymphoma 2. Finally, our data demonstrated that the apoptosis was due to the activation of the c-Jun N-terminal kinase (JNK) signaling pathway and cell cycle arrest at G0/G1 phase. Because ROS plays essential roles in many biological processes, such as aging and cancers, our findings suggest that NDFUB3 can be targeted for treating HCC and other human diseases.

Reactive oxygen species are signaling molecules that modulate plant reproduction.

Reactive oxygen species (ROS) can serve as signaling molecules that are essential for plant growth and development but abiotic stress can lead to ROS increases to supraoptimal levels resulting in cellular damage. To ensure efficient ROS signaling, cells have machinery to locally synthesize ROS to initiate cellular responses and to scavenge ROS to prevent it from reaching damaging levels. This review summarizes experimental evidence revealing the role of ROS during multiple stages of plant reproduction. Localized ROS synthesis controls the formation of pollen grains, pollen-stigma interactions, pollen tube growth, ovule development,and fertilization. Plants utilize ROS-producing enzymes such as respiratory burst oxidase homologsand organelle metabolic pathways to generate ROS, while the presence of scavenging mechanisms, including synthesis of antioxidant proteins and small molecules, serves to prevent its escalation to harmful levels. In this review, we summarized the function of ROS and its synthesisand scavenging mechanisms in all reproductive stages from gametophyte development until completion of fertilization. Additionally, we further address the impact of elevated temperatures induced ROS on impairing these reproductive processes and of flavonol antioxidants in maintaining ROS homeostasis to minimize temperature stress to combat the impact of global climate change on agriculture.

Auxin-responsive ROS homeostasis genes display dynamic expression pattern during rice crown root primordia morphogenesis

Reactive oxygen species (ROS) are generated continuously as a by-product of aerobic metabolism in plants. While excessive ROS cause oxidative stresses in cells, they act as signaling molecules when maintained at an optimum concentration through the dynamic equilibrium of ROS metabolizing mechanisms to regulate growth, development and response to environmental stress. Auxin and its crosstalk with other signaling cascades are crucial for maintaining ROS homeostasis and orchestrating root architecture but dissecting the underlying mechanism requires detailed investigation at the molecular level. Rice fibrous root system is primarily composed of shoot-derived adventitious roots (also called crown roots). Here, we uncover auxin-ROS cross-talk during initiation and growth of rice roots. Potassium iodide treatment changes ROS levels that results in an altered rice root architecture. We reveal that auxin induction recover root growth and development defects by recouping level of hydrogen peroxide. By comparing global datasets previously generated by auxin induction and laser capture microdissection-RNA sequencing, we identify the redox-related antioxidants genes from peroxidase, glutathione reductase, glutathione S-transferase, and thioredoxin reductase families whose expression is regulated by the auxin signaling and also display dynamic expression patterns during crown root primordia morphogenesis. The auxin-mediated differential transcriptome data were validated by quantifying expression levels of a set of genes upon auxin induction. Further, in-depth spatio-temporal expression pattern analysis by RNA in situ hybridization shows the spatially restricted expression of selected genes in the developing crown root primordia. Together, our findings uncover molecular components of auxin-ROS crosstalk involved in root organogenesis.

The Snf5-Hsf1 transcription module synergistically regulates stress responses and pathogenicity by maintaining ROS homeostasis in Sclerotinia sclerotiorum.

The SWI/SNF complex is guided to the promoters of designated genes by its co-operator to activate transcription in a timely and appropriate manner to govern development, pathogenesis, and stress responses in fungi. Nevertheless, knowledge of the complexes and their co-operator in phytopathogenic fungi is still fragmented. We demonstrate that the heat shock transcription factor SsHsf1 guides the SWI/SNF complex to promoters of heat shock protein (hsp) genes and antioxidant enzyme genes using biochemistry and pharmacology. This is accomplished through direct interaction with the complex subunit SsSnf5 under heat shock and oxidative stress. This results in the activation of their transcription and mediates histone displacement to maintain reactive oxygen species (ROS) homeostasis. Genetic results demonstrate that the transcription module formed by SsSnf5 and SsHsf1 is responsible for regulating morphogenesis, stress tolerance, and pathogenicity in Sclerotinia sclerotiorum, especially by directly activating the transcription of hsp genes and antioxidant enzyme genes counteracting plant-derived ROS. Furthermore, we show that stress-induced phosphorylation of SsSnf5 is necessary for the formation of the transcription module. This study establishes that the SWI/SNF complex and its co-operator cooperatively regulate the transcription of hsp genes and antioxidant enzyme genes to respond to host and environmental stress in the devastating phytopathogenic fungi.

Flavonoids are involved in salt tolerance through ROS scavenging in the halophyte Atriplex canescens.

The content of flavonoids could increase in A. canescens under saline conditions. Overexpression of AcCHI in transgenic A. thaliana promotes flavonoid biosynthesis, thereby functioning in the tolerance of transgenic plants to salt and osmotic stress by maintaining ROS homeostasis. Atriplex canescens is a halophytic forage shrub with excellent adaptation to saline environment. Our previous study showed that a large number of genes related to the biosynthesis of flavonoids in A. canescens were significantly up-regulated by NaCl treatments. However, it remains unclear whether flavonoids are involved in A. canescens response to salinity. In this study, we found that the accumulation of flavonoids significantly increased in either the leaves or roots of A. canescens seedling under 100 and 300mM NaCl treatments. Correspondingly, AcCHS, AcCHI and AcF3H, which encode three key enzymes (chalcone synthases (CHS), chalcone isomerase (CHI), and flavanone 3-hydroxylase (F3H), respectively) of flavonoids biosynthesis, were significantly induced in the roots or leaves of A. canescens by 100 or 300mM NaCl. Then, we generated the transgenic Arabidopsis thaliana overexpressing AcCHI and found that transgenic plants accumulated more flavonoids through enhancing the pathway of flavonoids biosynthesis. Furthermore, overexpression of AcCHI conferred salt and osmotic stress tolerance in transgenic A. thaliana. Contrasted with wild-type A. thaliana, transgenic lines grew better with greater biomass, less H2O2 content as well as lower relative plasma permeability in either salt or osmotic stress conditions. In conclusion, our results indicate that flavonoids play an important role in A. canescens response to salt stress through reactive oxygen species (ROS) scavenging and the key enzyme gene AcCHI in flavonoids biosynthesis pathway of A. canescens has the potential to improve the stress tolerance of forages and crops.

Polyethyleneimine-coated MXene quantum dots improve cotton tolerance to Verticillium dahliae by maintaining ROS homeostasis

Verticillium dahliae is a soil-borne hemibiotrophic fungal pathogen that threatens cotton production worldwide. In this study, we assemble the genomes of two V. dahliae isolates: the more virulence and defoliating isolate V991 and nondefoliating isolate 1cd3-2. Transcriptome and comparative genomics analyses show that genes associated with pathogen virulence are mostly induced at the late stage of infection (Stage II), accompanied by a burst of reactive oxygen species (ROS), with upregulation of more genes involved in defense response in cotton. We identify the V991-specific virulence gene SP3 that is highly expressed during the infection Stage II. V. dahliae SP3 knock-out strain shows attenuated virulence and triggers less ROS production in cotton plants. To control the disease, we employ polyethyleneimine-coated MXene quantum dots (PEI-MQDs) that possess the ability to remove ROS. Cotton seedlings treated with PEI-MQDs are capable of maintaining ROS homeostasis with enhanced peroxidase, catalase, and glutathione peroxidase activities and exhibit improved tolerance to V. dahliae. These results suggest that V. dahliae trigger ROS production to promote infection and scavenging ROS is an effective way to manage this disease. This study reveals a virulence mechanism of V. dahliae and provides a means for V. dahliae resistance that benefits cotton production.

Modified atmosphere packaging delays postharvest leaf senescence of Chinese flowering cabbage via suppressing chloroplast dismantling and alleviating mitochondrial oxidative damage

Onset of leaf senescence comes with biomolecule degradation and cellular organelle degeneration. Here, we examined the efficacy of modified atmosphere packaging (MAP) on reactive oxygen species (ROS) metabolism and ultrastructural changes of chloroplasts and mitochondria in Chinese flowering cabbage leaves during storage at 20 ± 1 ℃. MAP delayed chloroplast dismantling along with lower chlorophyll reduction and Fv/Fm ratio. Furthermore, the integrity of mitochondrial ultrastructure was maintained by MAP treatment during leaf senescence. MAP treatment also lowered accumulation of ROS and maintained higher levels of key components and enzyme activity of ascorbate–glutathione cycle, as well as expression of BrAPX5, BrGR, BrDHAR1 and BrMDHAR2. Additionally, MAP-treated cabbage leaves showed higher activity of peroxidase, superoxide dismutase, catalase and encoding gene expressions. Collectively, above findings suggest that MAP treatment could suppress chloroplast dismantling and maintain ROS homeostasis to mitigate mitochondrial oxidative damage and sustain mitochondrial structure, thereby postponing senescence of Chinese flowering cabbage.

Naked Mole-Rat Cortex Maintains Reactive Oxygen Species Homeostasis During In Vitro Hypoxia or Ischemia and Reperfusion.

Neuronal injury during acute hypoxia, ischemia, and following reperfusion are partially attributable to oxidative damage caused by deleterious fluctuations of reactive oxygen species (ROS). In particular, mitochondrial superoxide (O2•-) production is believed to upsurge during lowoxygen conditions and also following reperfusion, before being dismutated to H2O2 and released into the cell. However, disruptions of redox homeostasis may be beneficially attenuated in the brain of hypoxia-tolerant species, such as the naked mole-rat (NMR, Heterocephalus glaber). As such, we hypothesized that ROS homeostasis is better maintained in the brain of NMRs during severe hypoxic/ ischemic insults and following reperfusion. We predicted that NMR brain would not exhibit substantial fluctuations in ROS during hypoxia or reoxygenation, unlike previous reports from hypoxiaintolerant mouse brain. To test this hypothesis, we measured cortical ROS flux using corrected total cell fluorescence measurements from live brain slices loaded with the MitoSOX red superoxide (O2•-) indicator or chloromethyl 2',7'-dichlorodihydrofluorescein diacetate (CM-H2-DCFDA; which fluoresces with whole-cell hydrogen peroxide (H2O2) production) during various low-oxygen treatments, exogenous oxidative stress, and reperfusion. We found that NMR cortex maintained ROS homeostasis during low-oxygen conditions, while mouse cortex exhibited a ~40% increase and a ~30% decrease in mitochondrial O2•- and cellular H2O2 production, respectively. Mitochondrial ROS homeostasis in NMRs was only disrupted following sodium cyanide application, which was similarly observed in mice. Our results suggest that NMRs have evolved strategies to maintain ROS homeostasis during acute bouts of hypoxia and reoxygenation, potentially as an adaptation to life in an intermittently hypoxic environment.

The RhWRKY33a-RhPLATZ9 regulatory module delays petal senescence by suppressing rapid reactive oxygen species accumulation in rose flowers.

Redox homeostasis in plant cells is critical for maintaining normal growth and development because reactive oxygen species (ROS) can function as signaling molecules or toxic compounds. However, how plants fine-tune redox homeostasis during natural or stress-induced senescence remains unclear. Cut roses (Rosa hybrida), an economically important ornamental product worldwide, often undergo stress-induced precocious senescence at the post-harvest bud stage. Here, we identified RhPLATZ9, an age- and dehydration-induced PLATZ (plant AT-rich sequence and zinc-binding) protein, and determined that it functions as a transcriptional repressor in rose flowers during senescence. We also showed that RhWRKY33a regulates RhPLATZ9 expression during flower senescence. RhPLATZ9-silenced flowers and RhWRKY33a-silenced flowers showed accelerated senescence, with higher ROS contents than the control. By contrast, overexpression of RhWRKY33a or RhPLATZ9 delayed flower senescence, and overexpression in rose calli showed lower ROS accumulation than the control. RNA-sequencing analysis revealed that apoplastic NADPH oxidase genes (RhRbohs) were enriched among the upregulated differentially expressed genes in RhPLATZ9-silenced flowers compared to wild-type flowers. Yeast one-hybrid assays, electrophoretic mobility shift assays, dual luciferase assays and chromatin immunoprecipitation quantitative PCR confirmed that the RhRbohD gene is a direct target of RhPLATZ9. These findings suggest that the RhWRKY33a-RhPLATZ9-RhRbohD regulatory module acts as a brake to help maintain ROS homeostasis in petals and thus antagonize age- and stress-induced precocious senescence in rose flowers.

Suppression of the HOS1 Gene Affects the Level of ROS Depending on Light and Cold.

The E3 ubiquitin-protein ligase HOS1 is an important integrator of temperature information and developmental processes. HOS1 is a negative regulator of plant cold tolerance, and silencing HOS1 leads to increased cold tolerance. In the present work, we studied ROS levels in hos1Cas9Arabidopsis thaliana plants, in which the HOS1 gene was silenced by disruption of the open reading frame via CRISPR/Cas9 technology. Confocal imaging of intracellular reactive oxygen species (ROS) showed that the hos1 mutation moderately increased levels of ROS under both low and high light (HL) conditions, but wild-type (WT) and hos1Cas9 plants exhibited similar ROS levels in the dark. Visualization of single cells did not reveal differences in the intracellular distribution of ROS between WT and hos1Cas9 plants. The hos1Cas9 plants contained a high basal level of ascorbic acid, maintained a normal balance between reduced and oxidized glutathione (GSH and GSSG), and generated a strong antioxidant defense response against paraquat under HL conditions. Under cold exposure, the hos1 mutation decreased the ROS level and substantially increased the expression of the ascorbate peroxidase genes Apx1 and Apx2. When plants were pre-exposed to cold and further exposed to HL, the expression of the NADPH oxidase genes RbohD and RbohF was increased in the hos1Cas9 plants but not in WT plants. hos1-mediated changes in the level of ROS are cold-dependent and cold-independent, which implies different levels of regulation. Our data indicate that HOS1 is required to maintain ROS homeostasis not only under cold conditions, but also under conditions of both low and high light intensity. It is likely that HOS1 prevents the overinduction of defense mechanisms to balance growth.

Exogenous melatonin enhances tomato heat resistance by regulating photosynthetic electron flux and maintaining ROS homeostasis

Heat stress reduces plant growth and reproduction and increases agricultural risks. As a natural compound, melatonin modulates broad aspects of the responses of plants to various biotic and abiotic stresses. However, regulation of the photosynthetic electron transfer, reactive oxygen species (ROS) homeostasis and the redox state of redox-sensitive proteins in the tolerance to heat stress induced by melatonin remain largely unknown. The oxygen evolution complex activity on the electron-donating side of photosystem II (PSII) is inhibited, and the electron transfer process from QA to QB on the electron-accepting side of PSII is inhibited. In this case, heat stress decreased the chlorophyll content, carbon assimilation rate, PSII activity, and the proportion of light absorbed by tomato seedlings during electron transfer. The ROS burst led to the breakdown of the PSII core protein. However, exogenous melatonin increased the net photosynthetic rate by 11.3% compared with heat stress, substantially reducing the restriction of photosynthetic systems induced by heat stress. Additionally, melatonin reduces the oxidative damage to PSII by balancing electron transfer on the donor, reactive center, and acceptor sides. Melatonin was used under heat stress to increase the activity of the antioxidant enzyme and preserve ROS equilibrium. In addition, redox proteomics also showed that melatonin controls the redox levels of proteins involved in photosynthesis, and stress and defense processes, which enhances the expression of oxidative genes. In conclusion, melatonin via controlling the photosynthetic electron transport and antioxidant, melatonin increased tomato heat stress tolerance and aided plant growth.

The plant peptide hormone phytosulfokine promotes somatic embryogenesis by maintaining redox homeostasis in Cunninghamia lanceolata.

Somatic embryogenesis (SE) is widely used for studying the mechanisms of embryo development. However, little is known about the underlying mechanisms, especially in woody plants. Previous studies have established an SE system for Chinese fir (Cunninghamia lanceolata), but this system is genotype-dependent, which limits its application in practice. Here, we found that phytosulfokine (PSK), a plant peptide hormone, can not only increase SE efficiency, but also establish SE in recalcitrant genotypes of C.lanceolata. Proembryogenic mass (PEM) browning and determination of hydrogen peroxide (H2 O2 ) content by 2',7'-dichlorofluorescein staining indicated that a reactive oxygen species (ROS) burst occurred rapidly after PEMs were transferred to SE induction medium. Transcriptome analysis and quantitative reverse transcriptase-PCR validation showed that PSK treatment helped to maintain ROS homeostasis by decreasing the activity of peroxidases in early SE induction. This PSK-regulated redox microenvironment might be helpful to induce expression of SE-related genes like WOX2 in early SE induction. Further analyses suggested that PSK promotes SE induction in C. lanceolata partially through decreasing H2 O2 levels, which is necessary but not sufficient for SE induction in recalcitrant genotypes of C. lanceolata. Furthermore, heterologous overexpression of ClPSK in Arabidopsis led to enhanced SE induction and resistance to H2 O2 stress. Taken together, our study reveals a biological function for the plant peptide hormone PSK, extends our knowledge about SE in woody trees, and provides a valuable tool for establishing an efficient and genotype-independent SE system in C. lanceolata and other coniferous trees.

Protein l-isoAspartyl Methyltransferase (PIMT) and antioxidants in plants.

All life forms, including plants, accumulate reactive oxygen species (ROS) as a byproduct of metabolism; however, environmental stresses, including abiotic stresses and pathogen attacks, cause enhanced accumulation of ROS in plants. The increased accumulation of ROS often causes oxidative damage to cells. Organisms are able to maintain levels of ROS below permissible limits by several mechanisms, including efficient antioxidant systems. In addition to antioxidant systems, recent studies suggest that protein l-isoaspartyl methyltransferase (PIMT), a highly conserved protein repair enzyme across evolutionary diverse organisms, plays a critical role in maintaining ROS homeostasis by repairing isoaspartyl-mediated damage to antioxidants in plants. Under stress conditions, antioxidant proteins undergo spontaneous isoaspartyl (isoAsp) modification which is often detrimental to protein structure and function. This reduces the catalytic action of antioxidants and disturbs the ROS homeostasis of cells. This chapter focuses on PIMT and its interaction with antioxidants in plants, where PIMT constitutes a secondary level of protection by shielding a primary level of antioxidants from dysfunction and permitting them to guard during unfavorable situations.

The phloem lectin PP2-A1 enhances aphid resistance by affecting aphid behavior and maintaining ROS homeostasis in cucumber plants

Aphid (Aphis gossypii Glover) attack frequently results in a significant loss of output and deterioration of fruit quality in cucumber (Cucumis sativus L.). Phloem protein 2 (PP2) is conserved as a phloem lectin in plants, and few studies have been conducted on the regulatory mechanism of PP2. Based on our previous study of CsPP2-A1 in cucumber, to further investigate the biological function of CsPP2-A1, we compared the changes of selectivity, non-selectivity, colonization, reproductions of aphids, and the phenotype in wild type (WT), CsPP2-A1 overexpressing (CsPP2-A1-OE), and CsPP2-A1 interfering (CsPP2-A1-RNAi) cucumber plants after inoculation with aphids. We found that CsPP2-A1-OE cucumber plants generated resistance to aphids. The aphid colonization rate and number of reproductions of CsPP2-A1-OE cucumber plants were significantly lower than that of WT and CsPP2-A1-RNAi cucumber plants. Through Pearson's correlation and principal component analysis (PCA), it was found that CsPP2-A1 played a crucial role in the balance of reactive oxygen species (ROS) in plants. Overexpression of the CsPP2-A1 resulted in increased levels of antioxidant enzyme, eliminating ROS and preventing the damage by ROS in cucumber. Furthermore, nutritional imbalance for aphids and content of secondary metabolites were increased in overexpressed CsPP2-A1 cucumber plants, and thus preventing aphid attack. These together may improve cucumber resistance against aphids and the mechanism of CsPP2-A1 defense against aphids was preliminarily explored.

Improvement of leaf K+ retention is a shared mechanism behind CeO2 and Mn3O4 nanoparticles improved rapeseed salt tolerance

Salinity is a global issue limiting efficient agricultural production. Nanobiotechnology has been emerged as an effective approach to improve plant salt tolerance. However, little known is about the shared mechanisms between different nanomaterials-enabled plant salt tolerance. In this study, we found that both PNC [polyacrylic acid coated nanoceria (CeO2 nanoparticles)] and PMO (polyacrylic acid coated Mn3O4 nanoparticles) nanozymes improved rapeseed salt tolerance. PNC and PMO treated rapeseed plants showed significantly fresh weight, dry weight, higher chlorophyll content, Fv/Fm, and carbon assimilation rate than control plants under salt stress. Results from confocal imaging with reactive oxygen species (ROS) fluorescent dye and histochemical staining experiments showed that the ROS over-accumulation level in PNC and PMO treated rapeseed was significantly lower than control plants under salt stress. Confocal imaging results with K+ fluorescent dye showed that significantly higher cytosolic and vacuolar K+ signals were observed in PNC and PMO treated rapeseed than control plants under salt stress. This is further confirmed by leaf K+ content data. Furthermore, we found that PNC and PMO treated rapeseed showed significantly lower cytosolic Na+ signals than control plants under salt stress. While, compared with significantly higher vacuolar Na+ signals in PNC treated plants, PMO treated rapeseed showed significantly lower vacuolar Na+ signals than control plants under salt stress. These results are further supported by qPCR results of genes of Na+ and K+ transport. Overall, our results suggest that besides maintaining ROS homeostasis, improvement of leaf K+ retention could be a shared mechanism in nano-improved plant salt tolerance.

ROS generated from biotic stress: Effects on plants and alleviation by endophytic microbes.

Aerobic living is thought to generate reactive oxygen species (ROS), which are an inevitable chemical component. They are produced exclusively in cellular compartments in aerobic metabolism involving significant energy transfer and are regarded as by-products. ROS have a significant role in plant response to pathogenic stress, but the pattern varies between necrotrophs and biotrophs. A fine-tuned systemic induction system is involved in ROS-mediated disease development in plants. In regulated concentrations, ROS act as a signaling molecule and activate different pathways to suppress the pathogens. However, an excess of these ROS is deleterious to the plant system. Along with altering cell structure, ROS cause a variety of physiological reactions in plants that lower plant yield. ROS also degrade proteins, enzymes, nucleic acids, and other substances. Plants have their own mechanisms to overcome excess ROS and maintain homeostasis. Microbes, especially endophytes, have been reported to maintain ROS homeostasis in both biotic and abiotic stresses by multiple mechanisms. Endophytes themselves produce antioxidant compounds and also induce host plant machinery to supplement ROS scavenging. The structured reviews on how endophytes play a role in ROS homeostasis under biotic stress were very meager, so an attempt was made to compile the recent developments in ROS homeostasis using endophytes. This review deals with ROS production, mechanisms involved in ROS signaling, host plant mechanisms in alleviating oxidative stress,and the roles of endophytes in maintaining ROS homeostasis under biotic stress.

NUPR1 contributes to radiation resistance by maintaining ROS homeostasis via AhR/CYP signal axis in hepatocellular carcinoma

BackgroundRadiotherapy (RT) is one of the major therapeutic approaches to hepatocellular carcinoma (HCC). Ionizing radiation (IR) inducing the generation of reactive oxygen species (ROS) leads to a promising antitumor effect. However, the dysregulation of the redox system often causes radioresistance and impairs the efficacy of RT. Increasing evidence indicates that nuclear protein 1 (NUPR1) plays a critical role in redox reactions. In this study, we aim to explore the role of NUPR1 in maintaining ROS homeostasis and radioresistance in HCC.MethodsThe radioresistant role of NUPR1 was determined by colony formation assay, comet assay in vitro, and xenograft tumor models in vivo. Probes for ROS, apoptosis assay, and lipid peroxidation assay were used to investigate the functional effect of NUPR1 on ROS homeostasis and oxidative stress. RNA sequencing and co-immunoprecipitation assay were performed to clarify the mechanism of NUPR1 inhibiting the AhR/CYP signal axis. Finally, we analyzed clinical specimens to assess the predictive value of NUPR1 and AhR in the radiotherapeutic efficacy of HCC.ResultsWe demonstrated that NUPR1 was upregulated in HCC tissues and verified that NUPR1 increased the radioresistance of HCC in vitro and in vivo. NUPR1 alleviated the generation of ROS and suppressed oxidative stress, including apoptosis and lipid peroxidation by downregulating cytochrome P450 (CYP) upon IR. ROS scavenger N-acetyl-L-cysteine (NAC) and CYP inhibitor alizarin restored the viability of NUPR1-knockdown cells during IR. Mechanistically, the interaction between NUPR1 and aryl hydrocarbon receptor (AhR) promoted the degradation and decreased nuclear translation of AhR via the autophagy-lysosome pathway, followed by being incapable of CYP’s transcription. Furthermore, genetically and pharmacologically activating AhR abrogated the radioresistant role of NUPR1. Clinical data suggested that NUPR1 and AhR could serve as novel biomarkers for predicting the radiation response of HCC.ConclusionsOur findings revealed the role of NUPR1 in regulating ROS homeostasis and oxidative stress via the AhR/CYP signal axis upon IR. Strategies targeting the NUPR1/AhR/CYP pathway may have important clinical applications for improving the radiotherapeutic efficacy of HCC.