Regulation Of Stress Response Research Articles

Melatonin alleviates LPS-induced depression-like behavior in mice by inhibiting ferroptosis by regulating RNA methylation-mediated SIRT6/Nrf2/HO-1 pathway.

The objective of this study is to investigate the impact of ferroptosis on depression and elucidate the molecular mechanism underlying melatonin's inhibitory effect on ferroptosis in the treatment of depression. In this study, a depression-like behavior model was induced in mice using LPS, and the effect of melatonin on depression-like behavior was evaluated through behavioral experiments (such as forced swimming test (FST) and sucrose preference test (SPT)). Additionally, molecular biological techniques (including real-time fluorescence quantitative PCR, Western blotting, immunoprecipitation) were employed to detect the expression levels and interactions of METTL3, SIRT6 and ferroptosis-related genes in mouse brain tissue. Furthermore, both in vitro and in vivo experiments were conducted to verify the regulatory effect of melatonin on Nrf2/HO-1 pathway and explore its potential molecular mechanism for regulating ferroptosis. Melatonin was found to significantly ameliorate depression-like behavior in mice, as evidenced by reduced immobility time in the forced swimming test and increased sucrose intake in the sucrose preference test. Subsequent investigations revealed that melatonin modulated SIRT6 stability through METTL3-mediated ubiquitination of SIRT6, leading to its degradation. As a deacetylase, SIRT6 plays a pivotal role in cellular metabolism regulation and antioxidative stress response. This study elucidated potential signaling pathways involving Nrf2/HO-1 through which SIRT6 may exert its effects. The findings suggest that melatonin can improve depressive behavior by suppressing ferroptosis and protecting neurons through its antioxidant properties. Additionally, targeting the Nrf2/HO-1 pathway via METTL3 and NEDD4 regulation may be a potential therapeutic approach for depression.

Identification of the Novel Small Compound Stress Response Regulators 1 and 2 That Affect Plant Abiotic Stress Signaling

Identification of the Novel Small Compound Stress Response Regulators 1 and 2 That Affect Plant Abiotic Stress Signaling

Acptp2,3 participates in the regulation of spore production, stress response, and pigments synthesis in Aspergillus cirstatus

Background Aspergillus cristatus was a filamentous fungus that produced sexual spores under hypotonic stress and asexual spores under hypertonic stress. It could be useful for understanding filamentous fungi’s sporulation mechanism. Previously, we conducted functional studies on Achog1, which regulated the hyperosmotic glycerol signaling (HOG) pathway and found that SI65_02513 was significantly downregulated in the transcriptomics data of ΔAchog1 knockout strain. This gene was located at multiple locations in the HOG pathway, indicating that it might play an important role in the HOG pathway of A. cristatus. Furthermore, the function of this gene had not been identified in Aspergillus fungi, necessitating further investigation. This gene’s conserved domain study revealed that it has the same protein tyrosine phosphatases (PTPs) functional domain as Saccharomyces cerevisiae, hence SI65_02513 was named Acptp2,3. Methods The function of this gene was mostly validated using gene knockout and gene complementation approaches. Knockout strains exhibited sexual and asexual development, as well as pigments synthesis. Morphological observations of the knockout strain were carried out under several stress conditions (osmotic stress, oxidative stress, Congo Red, and sodium dodecyl sulfate (SDS). Real-time fluorescence polymerase chain reaction (PCR) identified the expression of genes involved in sporulation, stress response, and pigments synthesis. Results The deletion of Acptp2,3 reduced sexual and asexual spore production by 4.4 and 4.6 times, demonstrating that Acptp2,3 positively regulated the sporulation of A. cristatus. The sensitivity tests to osmotic stress revealed that ΔAcptp2,3 strains did not respond to sorbitol-induced osmotic stress. However, ΔAcptp2.3 strains grew considerably slower than the wild type in high concentration sucrose medium. The ΔAcptp2,3 strains grew slower than the wild type on media containing hydrogen peroxide, Congo red, and SDS. These findings showed that Acptp2,3 favorably controlled osmotic stress, oxidative stress, and cell wall-damaging chemical stress in A. cristatus. Deleting Acptp2,3 resulted in a deeper colony color, demonstrating that Apctp2,3 regulated pigment synthesis in A. cistatus. The expression levels of numerous stress-and pigments-related genes matched the phenotypic data. Conclusion According to our findings, Acptp2,3 played an important role in the regulation of sporulation, stress response, and pigments synthesis in A. cristatus. This was the first study on the function of PTPs in Aspergillus fungi.

Lactobacilli Cell-Free Supernatants Modulate Inflammation and Oxidative Stress in Human Microglia via NRF2-SOD1 Signaling

Microglia are macrophage cells residing in the brain, where they exert a key role in neuronal protection. Through the gut–brain axis, metabolites produced by gut commensal microbes can influence brain functions, including microglial activity. The nuclear factor erythroid 2-related factor 2 (NRF2) is a key regulator of the oxidative stress response in microglia, controlling the expression of cytoprotective genes. Lactobacilli-derived cell-free supernatants (CFSs) are postbiotics that have shown antioxidant and immunomodulatory effects in several in vitro and in vivo studies. This study aimed to explore the effects of lactobacilli CFSs on modulating microglial responses against oxidative stress and inflammation. HMC3 microglia were exposed to lipopolysaccaride (LPS), as an inflammatory trigger, before and after administration of CFSs from three human gut probiotic species. The NRF2 nuclear protein activation and the expression of NRF2-controlled antioxidant genes were investigated by immunoassay and quantitative RT-PCR, respectively. Furthermore, the level of pro- and anti-inflammatory cytokines was evaluated by immunoassay. All CFSs induced a significant increase of NRF2 nuclear activity in basal conditions and upon inflammation. The transcription of antioxidant genes, namely heme oxygenase 1, superoxide dismutase (SOD), glutathione-S transferase, glutathione peroxidase, and catalase also increased, especially after inflammatory stimulus. Besides, higher SOD1 activity was detected relative to inflamed microglia. In addition, CFSs pre-treatment of microglia attenuated pro-inflammatory TNF-α levels while increasing anti-inflammatory IL-10 levels. These findings confirmed that gut microorganisms’ metabolites can play a relevant role in adjuvating the microglia cellular response against neuroinflammation and oxidative stress, which are known to cause neurodegenerative diseases.Graphical Gut-brain crosstalk: molecular point of view. Metabolites contained in the supernatant derived from Lactobacilli can cross the gut barrier and reach the central nervous system, where they are taken up by microglial cells. They induce the activation of the NRF2 pathway and the production of inflammatory mediators. This interaction attenuates two important events: oxidation (with high levels of NRF2) and inflammation (with high levels of IL-10 and low levels of TNF-α).

Non-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction.

Lipidated ATG8/LC3 proteins are recruited to single membrane compartments as well as autophagosomes, supporting their functions. Although recent studies have shown that Golgi-LC3 lipidation follows Golgi damage, its molecular mechanism and function under Golgi stress remain unknown. Here, by combining DLK1 overexpression as a new strategy for induction of Golgi-specific LC3 lipidation, and the application of Golgi-damaging reagents, we unravel the mechanism and role of Golgi-LC3 lipidation. Upon DLK1 overexpression, LC3 is lipidated on the Golgi apparatus in an ATG12-ATG5-ATG16L1 complex-dependent manner; a post-Golgi trafficking blockade is the primary cause of this lipidation. During Golgi stress, ATG16L1 is recruited through its interaction with V-ATPase for Golgi-LC3 lipidation. After post-Golgi trafficking inhibition, TFE3, a key regulator of the Golgi stress response, is translocated to the nucleus. Defects in LC3 lipidation disrupt this translocation, leading to an attenuation of the Golgi stress response. Together, our results reveal the mechanism and unexplored function of Golgi-LC3 lipidation in the Golgi stress response.

PSVIII-23 Attenuation of oxidative stress and inflammatory response improves gut integrity in piglets after infection

Abstract Enterotoxigenic Escherichia coli (ETEC) is a primary cause of post-weaning diarrhea in piglets, leading to serious health issues and economic loss in the swine industry. Increased oxidative stress and inflammation have detrimental effects on gut health. The present study aimed to investigate the regulation of oxidative stress and inflammatory response in a piglet model challenged with ETEC and to evaluate whether the chosen probiotic could improve intestinal function in piglets. A total of 24 weaned piglets susceptible to ETEC F4 infection were randomly divided into four groups: Group 1 (control), Group 2 (E. coli infection), Group 3 (E. coli infection received antibiotic avilamycin), and Group 4 (E. coli infection received B. licheniformis HG76). Group 2, Group 3 and Group 4 were infected with E. coli by an oral gavage of ETEC F4 (5 mL, 1 × 106 CFU/mL). Five days after infection, piglets in all groups were euthanized. The blood and intestine samples (a mid-jejunum segment) were collected, and serum was prepared. ETEC infection significantly increased serum and jejunal malondialdehyde (MDA) concentrations and serum diamine oxidase (DAO) activity (P < 0.05). ETEC infection also significantly decreased tight-junction proteins (ZO1, occludin), superoxide dismutase-1 (SOD), and heme oxygenase-1 (HO-1) expression (P < 0.05). Furthermore, ETEC infection significantly increased the expression of pro-inflammatory cytokines [interlueken (IL) -6, tumor necrosis factor (TNF) -α] in the intestine (P < 0.05). Antibiotic or probiotic supplementation mitigated oxidative stress and inflammation, as evidenced by decreased oxidative stress biomarkers, increased expression of antioxidant enzymes (SOD, HO-1) and downregulated the expression of proinflammatory cytokines (IL-6, TNF-α; P < 0.05). Antibiotic or probiotic supplementation also improved intestinal integrity, as demonstrated by decreased DAO activity and increased tight-junction proteins expression (P < 0.05). These results suggest that attenuation of oxidative stress and inflammatory response can improve piglet gut integrity after ETEC infection.

Multi-Omics Exploration of ABA Involvement in Identifying Unique Molecular Markers for Single and Combined Stresses in tomato plants.

Over the past decade, our research group has found that plant responses to combined abiotic stresses are unique and cannot be inferred from studying plants exposed to individual stresses. Understanding how adaptative plant mechanisms integrate from stress perception to biochemical and physiological adjustments is a major challenge in abiotic stress signaling studies. Considering abscisic acid (ABA) as a key regulator in plant abiotic stress responses, in our study, ABA-deficient plants (flc) exposed to single or combined salinity and heat stresses were evaluated and different -omics analyses were conducted. Significant changes in biomass, photosynthesis, ions, transcripts, and metabolites occurred in mutant plants under single or combined stresses. Exogenous ABA application in flc mutants did not fully recover plant phenotypes or metabolic levels but induced cellular reprogramming with changes in specific markers. Multi-omics analysis aimed to identify ABA-dependent, ABA-independent, or stress-dependent markers in plant responses to single or combined stresses. We demonstrated that studying different -omics as a whole led to the identification of specific markers for each stress condition that were not detectable when each -omic was studied individually. This resource article provides an important and novel reference for scientists working in the field of plant abiotic stress. Future exploration of the transcriptomic, ionomic and metabolomic data presented in this study could lead to the identification of new pathways and genes associated with ABA signaling processes. These findings may be utilized to enhance crop resilience to heat waves, salinity, and their combination, contributing to addressing food security challenges in a climate change scenario.

Inhibiting endothelial cell Mst1 attenuates acute lung injury in mice.

Lung endothelium plays a pivotal role in the orchestration of inflammatory responses to acute pulmonary insults. Mammalian sterile 20-like kinase 1 (Mst1) is a serine/threonine kinase that has been shown to play an important role in the regulation of apoptosis, stress responses, and organ growth. This study investigated the role of Mst1 in lung endothelial activation and acute lung injury (ALI). We found that Mst1 was significantly activated in inflamed lung endothelial cells (ECs) and mouse lung tissues. Overexpression of Mst1 promoted nuclear factor κ-B (NF-κB) activation through promoting JNK and p38 activation in lung ECs. Inhibition of Mst1 by either its dominant negative form (DN-Mst1) or its pharmacological inhibitor markedly attenuated cytokine-induced expression of cytokines, chemokines, and adhesion molecules in lung ECs. Importantly, in a mouse model of lipopolysaccharide-induced (LPS-induced) ALI, both deletion of Mst1 in lung endothelium and treatment of WT mice with a pharmacological Mst1 inhibitor significantly protected mice from LPS-induced ALI. Together, our findings identified Mst1 kinase as a key regulator in controlling lung EC activation and suggest that therapeutic strategies aimed at inhibiting Mst1 activation might be effective in the prevention and treatment of inflammatory lung diseases.

Quercus infectoria Gall Ethanolic Extract Accelerates Wound Healing through Attenuating Inflammation and Oxidative Injuries in Skin Fibroblasts

Quercus infectoria Olivier (Fagaceae) nutgall, a traditional Asian medicine, is renowned for its efficacy in treating wounds and skin disorders. Although the gall extract has shown promising results in accelerating wound healing in diabetic animal models, its mechanisms, particularly the effects on redox balance, remain poorly understood. This study aims to investigate the effects and mechanisms of Q. infectoria gall ethanolic extract (QIG) on wound healing in fibroblasts, with a specific emphasis on its modulation of oxidative stress. Hydrogen peroxide (H2O2)-treated L929 cells were used as an in vitro model of oxidation-damaged fibroblasts. QIG exhibited potent antioxidant activity with 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS), and ferric reducing antioxidant power (FRAP) assay values of 305.43 ± 7.48, 508.94 ± 15.12, and 442.08 ± 9.41 µM Trolox equivalents (TE)/µg, respectively. Elevated H2O2 levels significantly reduced L929 cell viability, with a 50% lethal concentration of 1.03 mM. QIG mitigated H2O2-induced cytotoxicity in a dose-dependent manner, showing protective effects in pre-, post-, and co-treatment scenarios. QIG significantly reduced H2O2-induced intracellular reactive oxygen species production and inflammation-related gene expression (p < 0.05). Additionally, at 25 µg/mL, QIG remarkably improved wound closure in H2O2-treated L929 cells by approximately 9.4 times compared with the H2O2 treatment alone (p < 0.05). These findings suggest QIG has potential therapeutic applications in wound healing, mediated through the regulation of oxidative stress and inflammatory response.

Research progress on plant stress-associated protein (SAP) family: Master regulators to deal with environmental stresses.

Every year, unfavorable environmental factors significantly affect crop productivity and threaten food security. Plants are sessile; they cannot move to escape unfavorable environmental conditions, and therefore, they activate a variety of defense pathways. Among them are processes regulated by stress-associated proteins (SAPs). SAPs have a specific zinc finger domain (A20) at the N-terminus and either AN1 or C2H2 at the C-terminus. SAP proteins are involved in many biological processes and in response to various abiotic or biotic constraints. Most SAPs play a role in conferring transgenic stress resistance and are stress-inducible. The emerging field of SAPs in abiotic or biotic stress response regulation has attracted the attention of researchers. Although SAPs interact with various proteins to perform their functions, the exact mechanisms of these interactions remain incompletely understood. This review aims to provide a comprehensive understanding of SAPs, covering their diversity, structure, expression, and subcellular localization. SAPs play a pivotal role in enabling crosstalk between abiotic and biotic stress signaling pathways, making them essential for developing stress-tolerant crops without yield penalties. Collectively, understanding the complex regulation of SAPs in stress responses can contribute to enhancing tolerance against various environmental stresses through several techniques such as transgenesis, classical breeding, or gene editing.

LncRNAs Are Key Regulators of Transcription Factor-Mediated Endothelial Stress Responses.

The functional role of long noncoding RNAs in the endothelium is highly diverse. Among their many functions, regulation of transcription factor activity and abundance is one of the most relevant. This review summarizes the recent progress in the research on the lncRNA-transcription factor axes and their implications for the vascular endothelium under physiological and pathological conditions. The focus is on transcription factors critical for the endothelial response to external stressors, such as hypoxia, inflammation, and shear stress, and their lncRNA interactors. These regulatory interactions will be exemplified by a selected number of lncRNAs that have been identified in the endothelium under physiological and pathological conditions that are influencing the activity or protein stability of important transcription factors. Thus, lncRNAs can add a layer of cell type-specific function to transcription factors. Understanding the interaction of lncRNAs with transcription factors will contribute to elucidating cardiovascular disease pathologies and the development of novel therapeutic approaches.

UPRER-immunity axis acts as physiological food evaluation system that promotes aversion behavior in sensing low-quality food.

To survive in challenging environments, animals must develop a system to assess food quality and adjust their feeding behavior accordingly. However, the mechanisms that regulate this chronic physiological food evaluation system, which monitors specific nutrients from ingested food and influences food-response behavior, are still not fully understood. Here, we established a low-quality food evaluation assay system and found that heat-killed E. coli (HK-E. coli), a low-sugar food, triggers cellular UPRER and immune response. This encourages animals to avoid low-quality food. The physiological system for evaluating low-quality food depends on the UPRER (IRE-1/XBP-1) - Innate immunity (PMK-1/p38 MAPK) axis, particularly its neuronal function, which subsequently regulates feeding behaviors. Moreover, animals can adapt to a low-quality food environment through sugar supplementation, which inhibits the UPRER -PMK-1 regulated stress response by increasing vitamin C biosynthesis. This study reveals the role of the cellular stress response pathway as physiological food evaluation system for assessing nutritional deficiencies in food, thereby enhancing survival in natural environments.

Overexpression of two DELLA subfamily genes MiSLR1 and MiSLR2 from mango promotes early flowering and enhances abiotic stress tolerance in Arabidopsis

Gibberellic acids (GAs) are a group of endogenous phytohormones that play important roles in plant growth and development. SLENDER RICE (SLR) serves as a vital component of the DELLA gene family, which plays an irreplaceable role in regulating plant flowering and height, as well as stress responses. SLR gene has not been reported in mango, and its function is unknown. In present study, two DELLA subfamily genes MiSLR1 and MiSLR2 were identified from mango. MiSLR1 and MiSLR2 were highly expressed in the stems of the juvenile stage, but were expressed at a low level in flower buds and flowers. Gibberellin treatment could up-regulate the expression of MiSLR1 and MiSLR2 genes, but gibberellin biosynthesis inhibitor prohexadione-calcium (Pro-Ca) and paclobutrazol (PAC) treatments significantly down-regulated the expression of MiSLR1, while MiSLR2 was up-regulated. The expression levels of MiSLR1 and MiSLR2 were up-regulated under both salt and drought treatments. Overexpression of MiSLR1 and MiSLR2 genes significantly resulted early flowering in transgenic Arabidopsis and significantly up-regulated the expression levels of endogenous flower-related genes, such as SUPPRESSOR OF CONSTANS1 (SOC1), APETALA1 (AP1), and FRUITFULL (FUL). Interestingly, MiSLR1 significantly reduced the height of transgenic plants, while MiSLR2 gene increased. Overexpression of MiSLR1 and MiSLR2 increased seed germination rate, root length and survival rate of transgenic plants under salt and drought stress. Physiological and biochemical detection showed that the contents of proline (Pro) and superoxide dismutase (SOD) were significantly increased, while the contents of malondialdehyde (MDA) and H2O2 were significantly decreased. Additionally, protein interaction analysis revealed that MiSLR1 and MiSLR2 interacted with several flowering-related and GA-related proteins. The interaction between MiSLR with MiGF14 and MiSOC1 proteins was found for the first time. Taken together, the data showed that MiSLR1 and MiSLR2 in transgenic Arabidopsis both regulated the flowering time and plant height, while also acting as positive regulators of abiotic stress responses.

Transcriptomic landscape of quiescent and proliferating human corneal stromal fibroblasts

This study analyzed the transcriptional changes in primary human corneal stromal fibroblasts (hCSFs) grown under quiescent (serum-free) and proliferating (serum-supplemented) culture conditions to identify genes, pathways, and protein‒protein interaction networks influencing corneal repair and regeneration. Primary hCSFs were isolated from donor human corneas and maintained in serum-free or serum-laden conditions. RNA was extracted from confluent cultures using Qiagen kit and subjected to RNA sequencing (RNAseq) analysis. Differential gene expression (DGE) and pathway enrichment analyses were conducted using DESeq2 and Gene Set Enrichment Analysis (GSEA), respectively. Protein‒protein interaction (PPI) networks were created exploiting the STRING database and analyzed with Cytoscape and the cytoHubba plugin. RNA-seq revealed 5,181 genes that were significantly differentially expressed/changed among the 18,812 annotated genes (p value ˂0.05). A cutoff value of a log2-fold change of ±1.5 or greater was used to identify 674 significantly upregulated and 771 downregulated genes between quiescent and proliferating hCSFs. Pathway enrichment analysis revealed significant changes in genes linked to cell cycle regulation, inflammatory, and oxidative stress response pathways, such as E2F Targets, G2M Checkpoint, and MYC Targets, TNFA signaling via NF-kB, and oxidative phosphorylation. Protein-protein interaction network analysis highlighted critical hub genes. The FGF22, CD34, ASPN, DPT, LUM, FGF10, PDGFRB, ECM2, DCN, VEGFD, OMD, OGN, ANGPT1, CDH5, and PRELP were upregulated, whereas genes linked to cell cycle regulation and mitotic progression, such as BUB1, TTK, KIF23, KIF11, BUB1B, DLGAP5, NUSAP1, CCNA2, CCNB1, BIRC5, CDK1, KIF20A, AURKB, KIF2C, and CDCA8, were downregulated. The RNA sequences and gene count files have been submitted to the Gene Expression Omnibus (accession # GSE260476). Our study provides a comprehensive information on the transcriptional and molecular changes in hCSFs under quiescent and proliferative conditions and highlights key pathways and hub genes.

RpoS sigma factor mediates adaptation and virulence in Vibrio mimicus

The alternative sigma factor RpoS functions as a regulator of stress and virulence response in numerous bacterial species. Vibrio mimicus is a critical opportunistic pathogen causing huge losses to aquaculture. However, the exact role of RpoS in V. mimicus remains unclear. In this study, rpoS deletion mutant of V. mimicus was constructed through allelic exchange and the phenotypic and transcriptional changes were investigated to determine the function of RpoS. The abilities of growth, motility, biofilm production, hemolytic activity and pathogenicity were significantly impaired in ΔrpoS strain. Stationary-phase cells of ΔrpoS strain showed lower tolerance to H2O2, heat, ethanol, and starvation stress than the wild-type strain. Transcriptome analyses revealed the involvement of rpoS in various cellular processes, notably bacterial-type flagellum synthesis and assembly, membrane synthesis and assembly and response to various stimuli. Phenotypic and RNA-seq analysis revealed that RpoS is required for biofilm formation, stress resistance, and pathogenicity in V. mimicus. Furthermore, β-galactosidase activity showed that rpoS is essential for optimal transcription of the flgK, fliA, cheA, mcpH mRNA. These results offer significant insight into the function and regulatory network of rpoS/RpoS, thereby improving our understanding and facilitating selection of molecular targets for future prevention strategies against V. mimicus.

Enhancement of immunity and disease resistance in Litopenaeus vannamei through injection of tyramine formulated with polyethylene glycol

This study investigates the prolonged effect of immune disease resistance in Litopenaeus vannamei through the administration of tyramine (TA) formulated with polyethylene glycol (PEG). Facing the challenges of intensive farming, environmental stress, and global climate changes, innovative approaches to improve shrimp health are essential. The research focuses on the role of biogenic amines in stress response and immune regulation, demonstrating that TA, especially when combined with PEG, significantly prolongs immunity and resistance against Vibrio alginolyticus. The experimental design included administering TA, PEG, and TA-PEG, followed by evaluations of immunity, lactate and glucose levels, and immune-related gene expressions. Results showed notable prolonged effects in total hemocyte count, phenoloxidase activity, and phagocytic activity in the TA-PEG group, indicating enhanced immune activation period. Additionally, the expression of prophenoloxidase system-related genes was significantly upregulated in the TA-PEG group. Furthermore, the TA-PEG group exhibited a significantly higher survival rate in a susceptibility test against V. alginolyticus. The results of this study confirm that the combined use of PEG can effectively extend the immunostimulatory duration of TA.

Transcriptomic Analysis of Antimony Response in Tall Fescue (Festuca arundinacea)

Antimony (Sb) is a toxic trace element for plants and animals. With the development of industrial applications and mining, Sb pollution is becoming more serious. Phytoremediation is regarded as an eco-friendly technique to reduce the threat of Sb to the environment and human health, and tall fescue that is highly adaptable to heavy metal stress can be a candidate species for Sb-contaminated soil phytoremediation. However, the mechanism of the Sb stress response in tall fescue is not clear. Therefore, transcriptomic analysis was used in this study to reveal the molecular mechanisms of Sb stress response regulation in tall fescue. The results suggested that the roots and leaves of tall fescue responded to Sb stress in different ways. In roots, the lignin and flavonoids might reduce the toxicity of Sb by anti-oxidation and Sb chelation. At the same time, the DEGs in leaves were mainly enriched in the pathways of glutathione metabolism, β-alanine metabolism, and glycine, serine, and threonine metabolism. Additionally, genes related to the pathways, such as 4CL, GST, AGXT2, and ALDH7A1, especially cytochrome P450 family genes (e.g., CYP73A, CYP75A, and CYP98A), might play key roles in the regulation of the Sb stress response in tall fescue. These findings provided a theoretical reference for the efficient use of tall fescue to control Sb-contaminated soil in the future.

Proteomic analysis of MsFtsH8 overexpression reveals enhanced salt stress response in alfalfa through PSII stability and antioxidant capacity improvement

The FtsH (Filamentous temperature sensitive H) proteases, known for their crucial roles in protein quality control and maintaining the integrity of photosynthetic machinery, have emerged as key regulators of stress responses in plants. Our previous study revealed the overexpression of MsFtsH8, an FtsH gene from alfalfa (Medicago sativa L.), confers salt stress tolerance to the plant. By comparing the proteomic profiles of MsFtsH8-overexpressing alfalfa and wild type under salt stress conditions, we elucidate the molecular pathways underlying MsFtsH8-mediated salt stress resilience. We identified 730 differentially expressed proteins (DEPs) in MsFtsH8-overexpressing alfalfa under salt stress, compared to 498 DEPs in wild type alfalfa under the same growth condition. Our results reveal significant alterations in the expression of proteins involved in the photosynthetic system, consistent with the chloroplast subcellular localization of MsFtsH8. Specifically, MsFtsH8 overexpression stabilizes key components of Photosystem II (PSII) and enhances electron transport processes, leading to increased photosynthetic efficiency and oxidative photodamage repair capacity under salt stress. Moreover, MsFtsH8-overexpressing alfalfa exhibits elevated levels of antioxidative enzymes, further mitigating oxidative damage induced by high salinity. These findings deepen our understanding of the regulatory role of MsFtsH8 in salt stress response and highlight its potential for improving crop resilience under adverse environmental conditions.

The stress response regulator HSF1 modulates natural killer cell anti-tumour immunity.

Diverse cellular insults converge on activation of the heat shock factor 1 (HSF1), which regulates the proteotoxic stress response to maintain protein homoeostasis. HSF1 regulates numerous gene programmes beyond the proteotoxic stress response in a cell-type- and context-specific manner to promote malignancy. However, the role(s) of HSF1 in immune populations of the tumour microenvironment remain elusive. Here, we leverage an in vivo model of HSF1 activation and single-cell transcriptomic tumour profiling to show that augmented HSF1 activity in natural killer (NK) cells impairs cytotoxicity, cytokine production and subsequent anti-tumour immunity. Mechanistically, HSF1 directly binds and regulates the expression of key mediators of NK cell effector function. This work demonstrates that HSF1 regulates the immune response under the stress conditions of the tumour microenvironment. These findings have important implications for enhancing the efficacy of adoptive NK cell therapies and for designing combinatorial strategies including modulators of NK cell-mediated tumour killing.

Abscisic acid-induced H2O2 production positively regulates the activity of SAPK8/9/10 through oxidation of the type one protein phosphatase OsPP47.

Subclass III sucrose nonfermenting1-related protein kinase 2s (SnRK2s) are positive regulators of abscisic acid (ABA) signaling and abiotic stress responses. However, the underlying activation mechanisms of osmotic stress/ABA-activated protein kinase 8/9/10 (SAPK8/9/10) of rice (Oryza sativa) subclass III SnRK2s in ABA signaling remain to be elucidated. In this study, we employed biochemical, molecular biology, cell biology, and genetic approaches to identify the molecular mechanism by which OsPP47, a type one protein phosphatase in rice, regulates SAPK8/9/10 activity in ABA signaling. We found that OsPP47 not only physically interacted with SAPK8/9/10 but also interacted with ABA receptors PYLs. OsPP47 negatively regulated ABA sensitivity in seed germination and root growth. In the absence of ABA, OsPP47 directly inactivated SAPK8/9/10 by dephosphorylation. In the presence of ABA, ABA-bound OsPYL2 formed complexes with OsPP47 and inhibited its phosphatase activity, partially releasing the inhibition of SAPK8/9/10. SAPK8/9/10-mediated H2O2 production inhibited OsPP47 activity by oxidizing Cys-116 and Cys-256 to form OsPP47 oligomers, resulting in not only preventing the OsPP47-SAPK8/9/10 interaction but also blocking the inhibition of SAPK8/9/10 activity by OsPP47. Our results reveal novel pathways for the inhibition of SAPK8/9/10 in the basal state and for the activation of SAPK8/9/10 induced by ABA in rice.