Activation Of Stress Response Genes Research Articles

H2A.Z removal mediates the activation of genes accounting for cell elongation under light and temperature stress.

The histone variant H2A.Z is crucial for the expression of genes involved in cell elongation under elevated temperatures and shade. Its removal facilitates the activation of these genes, particularly through the activities of PHYTOCHROME INTERACTING FACTORs (PIFs) and the SWR1-related INOSITOL REQUIRING 80 (INO80) complex. Arabidopsis seedlings exhibit rapid elongation of hypocotyls and cotyledon petioles in response to environmental stresses, namely elevated temperatures and shade. These phenotypic alterations are regulated by various phytohormones, notably auxin. Under these stress conditions, auxin biosynthesis is swiftly induced in the cotyledons and transported to the hypocotyls, where it stimulates cell elongation. The histone variant H2A.Z plays a pivotal role in this regulatory mechanism. H2A.Z affects the transcription of numerous genes, particularly those activated by the mentioned environmental stresses. Recent studies highlighted that the eviction of H2A.Z from gene bodies is crucial for the activation of genes, especially auxin biosynthetic and responsive genes, under conditions of elevated temperature and shade. Additionally, experimental evidence suggests that PHYTOCHROME INTERACTING FACTORs (PIFs) can recruit the SWR1-related INOSITOL REQUIRING 80 (INO80) complex to remove H2A.Z from targeted loci, thereby activating gene transcription in response to these environmental stresses. This review provides a comprehensive overview of the regulatory role of H2A.Z, emphasizing how its eviction from gene loci is instrumental in the activation of stress-responsive genes under elevated temperature and shade conditions.

Unraveling the genomic secrets of Tritonibacter mobilis AK171: a plant growth-promoting bacterium isolated from Avicennia marina

The scarcity of freshwater resources resulting in a significant yield loss presents a pressing challenge in agriculture. To address this issue, utilizing abundantly available saline water could offer a smart solution. In this study, we demonstrate that the genome sequence rhizosphere bacterium Tritonibacter mobilis AK171, a halophilic marine bacterium recognized for its ability to thrive in saline and waterlogged environments, isolated from mangroves, has the remarkable ability to enable plant growth using saline irrigation. AK171 is characterized as rod-shaped cells, displays agile movement in free-living conditions, and adopts a rosette arrangement in static media. Moreover, The qualitative evaluation of PGP traits showed that AK171 could produce siderophores and IAA but could not solubilize phosphate nor produce hydrolytic enzymes it exhibits a remarkable tolerance to high temperatures and salinity. In this study, we conducted a comprehensive genome sequence analysis of T. mobilis AK171 to unravel the genetic mechanisms underlying its plant growth-promoting abilities in such challenging conditions. Our analysis revealed diverse genes and pathways involved in the bacterium’s adaptation to salinity and waterlogging stress. Notably, T. mobilis AK171 exhibited a high level of tolerance to salinity and waterlogging through the activation of stress-responsive genes and the production of specific enzymes and metabolites. Additionally, we identified genes associated with biofilm formation, indicating its potential role in establishing symbiotic relationships with host plants. Furthermore, our analysis unveiled the presence of genes responsible for synthesizing antimicrobial compounds, including tropodithietic acid (TDA), which can effectively control phytopathogens. This genomic insight into T. mobilis AK171 provides valuable information for understanding the molecular basis of plant-microbial interactions in saline and waterlogged environments. It offers potential applications for sustainable agriculture in challenging conditions.

A General Mechanism for the General Stress Response in Bacteria.

The General Stress Response promotes survival of bacteria in adverse conditions, but how sensor proteins transduce species-specific signals to initiate the response is not known. The serine/threonine phosphatase RsbU initiates the General Stress Response in B. subtilis upon binding a partner protein (RsbT) that is released from sequestration by environmental stresses. We report that RsbT activates RsbU by inducing otherwise flexible linkers of RsbU to form a short coiled-coil that dimerizes and activates the phosphatase domains. Importantly, we present evidence that related coiled-coil linkers and phosphatase dimers transduce signals from diverse sensor domains to control the General Stress Response and other signaling across bacterial phyla. These results additionally resolve the mystery of how shared sensory domains control serine/threonine phosphatases, diguanylate cyclases and histidine kinases, revealing a common coiled-coil linker transduction mechanism. We propose that this provides bacteria with a modularly exchangeable toolkit for the evolution of diverse signaling pathways.

Activation of stress-response genes by retrograde signaling-mediated destabilization of nuclear importin IMPα-9 and its interactor TPR2

Stress-induced retrograde signal transmission from the plastids to the nucleus has long puzzled plant biologists. To address this, we performed a suppressor screen of the ceh1 mutant, which contains elevated 2-C-methyl-d-erythritol-2,4-cyclopyrophosphate (MEcPP) levels, and identified the gain-of-function mutant impα-9, which shows reversed dwarfism and suppressed expression of stress-response genes in the ceh1 background despite heightened MEcPP. Subsequent genetic and biochemical analyses established that the accumulation of MEcPP initiates an upsurge in Arabidopsis SKP1-like 1 (ASK1) abundance, a pivotal component in the proteasome degradation pathway. This increase in ASK1 prompts the degradation of IMPα-9. Moreover, we uncovered a protein-protein interaction between IMPα-9 and TPR2, a transcriptional co-suppressor and found that a reduction in IMPα-9 levels coincides with a decrease in TPR2 abundance. Significantly, the interaction between IMPα-9 and TPR2 was disrupted in impα-9 mutants, highlighting the critical role of a single amino acid alteration in maintaining their association. Disruption of their interaction results in the reversal of MEcPP-associated phenotypes. Chromatin immunoprecipitation coupled with sequencing analyses revealed that TPR2 binds globally to stress-response genes and suggested that IMPα-9 associates with the chromatin. They function together to suppress the expression of stress-response genes under normal conditions, but this suppression is alleviated in response to stress through the degradation of the suppressing machinery. The biological relevance of our discoveries was validated under high light stress, marked by MEcPP accumulation, elevated ASK1 levels, IMPα-9 degredation, reduced TPR2 abundance, and subsequent activation of a network of stress-response genes. In summary, our study collectively unveils fresh insights into plant adaptive mechanisms, highlighting intricate interactions among retrograde signaling, the proteasome, and nuclear transport machinery.

The SWI/SNF chromatin remodeling complex: a critical regulator of metabolism.

The close relationship between chromatin and metabolism has been well-studied in recent years. Many metabolites have been found to be cofactors used to modify chromatin, and these modifications can in turn affect gene transcription. One chromatin-associated factor responsible for regulating transcription is the SWI/SNF complex, an ATP-dependent chromatin remodeler conserved throughout eukaryotes. SWI/SNF was originally described in yeast as regulating genes involved in carbon source metabolism and mating type switching, and its mammalian counterpart has been extensively studied for its role in diseases such as cancer. The yeast SWI/SNF complex is closely associated with activation of stress response genes, many of which have metabolic functions. It is now recognized that this is a conserved function of the complex, and recent work has shown that mammalian SWI/SNF is also a key regulator of metabolic transcription. Emerging evidence suggests that loss of SWI/SNF introduces vulnerabilities to cells due to this metabolic influence, and that this may present opportunities for treatment of SWI/SNF-deficient cancers.

Epigenetic arsenal for stress mitigation in plants

Plant's ability to perceive, respond to, and ultimately adapt to various stressors is a testament to their remarkable resilience. In response to stresses, plants activate a complex array of molecular and physiological mechanisms. These include the rapid activation of stress-responsive genes, the manufacturing of protective compounds, modulation of cellular processes and alterations in their growth and development patterns to enhance their chances of survival. Epigenetic mechanisms play a pivotal role in shaping the responses of plants to environmental stressors. This review explores the intricate interplay between epigenetic regulation and plant stress mitigation. We delve into the dynamic landscape of epigenetic modifications, highlighting their influence on gene expression and ultimately stress tolerance. This review assembles current research, shedding light on the promising strategies within plants' epigenetic arsenal to thrive amidst adverse conditions.

Expression analysis of transcription factor (CBF/DREB) gene and biochemical response of Cannabis sativa to cadmium toxicity and foliar application of molybdenum

Plants respond to heavy metals stress by the activation of stress responsive genes to establish biochemical defense mechanisms against the stress. We have investigated the molecular and biochemical response of Cannabis sativa to cadmium (Cd) stress in the presence of molybdenum (Mo) foliar treatments. For this purpose, C. sativa plants were allowed to grow in pots containing Cd polluted soil, for two month duration. Aqueous solutions of ammonium molybdate pentahydrate (0.5, 1.0 and 2.0 ppm) were foliarly sprayed on the plants, at two weeks intervals. Various parameters were inter-correlated i.e., Plant biomass, Cd phyto-accumulation, transcript level/expression of CBF/DREB genes, concentrations of free proline, polyphenolics, and chlorophyll contents. Phenolic compounds were analyzed by High Performance Liquid Chromatography Diode Array Detector (HPLC-DAD) and Cd contents were analyzed by Atomic Absorption Spectrophotometer. Biomass and chlorophyll contents decreased while the concentrations of free proline and polyphenolics increased under Cd stress. Dry biomass of the all the plant parts (roots (1.87 ± 0.22 g), stem (3.28 ± 0.39 g) and leaves (3.54 ± 0.87 g) and free proline in roots (69.00 ± 8.28 µg/g) and leaves (40.56 ± 4.87 µg/g) were most significantly increased with foliar spray of 2.00 ppm Mo. Nineteen (19) different polyphenolic compounds were identified and quantified in leaves and most of them were highly increased in concentration under Cd stress. The highest concentration was noted in Caffeoyl tyramine (1111 µg/g) in plants treated with 2.00 ppm Mo. Transcript level of CBF/DREB genes in control plants were less as compared to Mo treated plants, where a high increase in transcript level of these genes were found. Expression of CBF /DREB genes showed significant positive correlations with Cd accumulation (R2= 0.751) and concentrations of free proline (R2 = 0.62) and polyphenolics (R2 = 0.65) in leaves. The results suggested that Mo increased the expression of CBF/DREB genes and subsequently the concentration of phenolic compounds and free proline to combat plant against the toxicity of high concentration of Cd on plants.

Abstract 2118: Development of RNAscope multiplex-based assay for exploratory pharmacodynamic biomarkers assessment in breast cancer patients from Phase I clinical trial of ORM-5029, a potent GSPT1 degrader

Abstract Breast cancer is the most common invasive cancer in women worldwide and remains a clinical challenge. Addressing the unmet need for better therapeutics, we used our Dual-Precision Targeted Protein Degradation (TPD² TM) approach that merges the power of protein degraders with precision of ADC technology to design ORM-5029. It delivers a highly potent and precise catalytic GSPT1 protein degrader molecule (SMol006) selectively to HER2-expressing tumor cells via conjugation to pertuzumab. GSPT1 is a protein associated with regulation of the translational termination complex, and its loss results in activation of the integrated stress response (ISR) which ultimately leads to apoptosis. Activation of ISR triggers overall reduction of protein synthesis and activation of stress response genes (e.g., ATF3 and DDIT3). ORM-5029 is currently being investigated for safety and tolerability in an open label, multicenter, phase 1, dose escalation and expansion study in patients with HER2-expressing advanced breast tumors (NCT05511844). Here, we evidence that the efficacy of ORM-5029 correlates with pharmacodynamic degradation of GSPT1 and activation of ATP3 and DDIT3 transcripts both in vitro and in tumor xenografts in mice. With the aim of evaluating GSPT1 degradation and consequent activation of ATF3 and DDIT3 in pre- and post-treatment tumor samples from HER2+ breast cancer patients, we are developing an RNAscope multiplex (Leica System) assay panel. This approach combines detection of GSPT1 protein with 20zz ISH probe-mediated detection of ATF3 and DDIT3 mRNA in tumor sections. As a part of method development, we treated BT474 cells with an efficacious concentration of GSPT1 degrader and optimized the immunofluorescence and immunohistochemistry protocol with our in-house generated GSPT1 antibody (MAb001). Data showed that GSPT1- MAb001 could be successfully used for both immunofluorescence and immunohistochemistry assays. The optimized protocol is currently being developed into RNAscope multiplex workflow using BT474 FFPE sections and tissue microarrays. In summary, RNAscope multiplex assay could be used as a method to determine pharmacodynamic response in HER2+ breast cancer patients treated with ORM-5029. Citation Format: Shikha Saini, Yeonjoon Kim, Wesley Wong, Tina Karunaratne, Olaf Christensen, Sujoy Dutta, Palash Bhar, Khuloud Takrouri, Nathan Fishkin, Dong-Ki Choi, Min-Soo Kim, Joanne Lim, Anna Skaletskaya, James Palacino, Peter Park. Development of RNAscope multiplex-based assay for exploratory pharmacodynamic biomarkers assessment in breast cancer patients from Phase I clinical trial of ORM-5029, a potent GSPT1 degrader [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2118.

Seed priming can enhance and retain stress tolerance in ensuing generations by inducing epigenetic changes and trans-generational memory.

The significance of priming in enhancing abiotic stress tolerance is well-established in several important crops. Priming positively impacts plant growth and improves stress tolerance at multiple developmental stages, and seed priming is one of the most used methods. Seed priming influences the pre-germinative metabolism that ensures proper germination, early seedling establishment, enhanced stress tolerance and yield, even under unfavourable environmental conditions. Seed priming involves pre-exposure of seeds to mild stress, and this pre-treatment induces specific changes at the physiological and molecular levels. Interestingly, priming can improve the efficiency of the DNA repair mechanism, along with activation of specific signalling proteins and transcription factors for rapid and efficient stress tolerance. Notably, such acquired stress tolerance may be retained for longer duration, namely, later developmental stages or even subsequent generations. Epigenetic and chromatin-based mechanisms such as DNA methylation, histone modifications, and nucleosome positioning are some of the key molecular changes involved in priming/stress memory. Further, the retention of induced epigenetic changes may influence the priming-induced trans-generational stress memory. This review discusses known and plausible seed priming-induced molecular mechanisms that govern germination and stress memory within and across generations, highlighting their role in regulating the plant response to abiotic stresses. Understanding the molecular mechanism for activation of stress-responsive genes and the epigenetic changes resulting from seed priming will help to improve the resiliency of the crops for enhanced productivity under extreme environments.

Salt- and Osmo-Responsive Sensor Histidine Kinases Activate the Bradyrhizobium diazoefficiens General Stress Response to Initiate Functional Symbiosis.

The general stress response (GSR) enables bacteria to sense and overcome a variety of environmental stresses. In alphaproteobacteria, stress-perceiving histidine kinases of the HWE and HisKA_2 families trigger a signaling cascade that leads to phosphorylation of the response regulator PhyR and, consequently, to activation of the GSR σ factor σEcfG. In the nitrogen-fixing bacterium Bradyrhizobium diazoefficiens, PhyR and σEcfG are crucial for tolerance against a variety of stresses under free-living conditions and also for efficient infection of its symbiotic host soybean. However, the molecular players involved in stress perception and activation of the GSR remained largely unknown. In this work, we first showed that a mutant variant of PhyR where the conserved phosphorylatable aspartate residue D194 was replaced by alanine (PhyRD194A) failed to complement the ΔphyR mutant in symbiosis, confirming that PhyR acts as a response regulator. To identify the PhyR-activating kinases in the nitrogen-fixing symbiont, we constructed in-frame deletion mutants lacking single, distinct combinations, or all of the 11 predicted HWE and HisKA_2 kinases, which we named HRXXN histidine kinases HhkA through HhkK. Phenotypic analysis of the mutants and complemented derivatives identified two functionally redundant kinases, HhkA and HhkE, that are required for nodulation competitiveness and during initiation of symbiosis. Using σEcfG-activity reporter strains, we further showed that both HhkA and HhkE activate the GSR in free-living cells exposed to salt and hyperosmotic stress. In conclusion, our data suggest that HhkA and HhkE trigger GSR activation in response to osmotically stressful conditions which B. diazoefficiens encounters during soybean host infection.[Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

CAMP Is a Promising Regulatory Molecule for Plant Adaptation to Heat Stress.

With gradual warming or increased frequency and magnitude of high temperature, heat stress adversely affects plant growth and eventually reduces plant productivity and quality. Plants have evolved complex mechanisms to sense and respond to heat stress which are crucial to avoiding cell damage and maintaining cellular homeostasis. Recently, 33″,55″-cyclic adenosine monophosphate (cAMP) has been proved to be an important signaling molecule participating in plant adaptation to heat stress by affecting multi-level regulatory networks. Significant progress has been made on many fronts of cAMP research, particularly in understanding the downstream signaling events that culminate in the activation of stress-responsive genes, mRNA translation initiation, vesicle trafficking, the ubiquitin-proteasome system, autophagy, HSPs-assisted protein processing, and cellular ion homeostasis to prevent heat-related damage and to preserve cellular and metabolic functions. In this present review, we summarize recent works on the genetic and molecular mechanisms of cAMP in plant response to heat stress which could be useful in finding thermotolerant key genes to develop heat stress-resistant varieties and that have the potential for utilizing cAMP as a chemical regulator to improve plant thermotolerance. New directions for future studies on cAMP are discussed.

Cyclin C-Cdk8 Kinase Phosphorylation of Rim15 Prevents the Aberrant Activation of Stress Response Genes.

Cells facing adverse environmental cues respond by inducing signal transduction pathways resulting in transcriptional reprograming. In the budding yeast Saccharomyces cerevisiae, nutrient deprivation stimulates stress response gene (SRG) transcription critical for entry into either quiescence or gametogenesis depending on the cell type. The induction of a subset of SRGs require nuclear translocation of the conserved serine-threonine kinase Rim15. However, Rim15 is also present in unstressed nuclei suggesting that additional activities are required to constrain its activity in the absence of stress. Here we show that Rim15 is directly phosphorylated by cyclin C-Cdk8, the conserved kinase module of the Mediator complex. Several results indicate that Cdk8-dependent phosphorylation prevents Rim15 activation in unstressed cells. First, Cdk8 does not control Rim15 subcellular localization and rim15∆ is epistatic to cdk8∆ with respect to SRG transcription and the execution of starvation programs required for viability. Next, Cdk8 phosphorylates a residue in the conserved PAS domain in vitro. This modification appears important as introducing a phosphomimetic at Cdk8 target residues reduces Rim15 activity. Moreover, the Rim15 phosphomimetic only compromises cell viability in stresses that induce cyclin C destruction as well as entrance into meiosis. Taken together, these findings suggest a model in which Cdk8 phosphorylation contributes to Rim15 repression whilst it cycles through the nucleus. Cyclin C destruction in response to stress inactivates Cdk8 which in turn stimulates Rim15 to maximize SRG transcription and cell survival.

The functional differences between paralogous regulators define the control of the general stress response in Sphingopyxis granuli TFA.

Summary Sphingopyxis granuli TFA is a contaminant degrading alphaproteobacterium that responds to adverse conditions by inducing the general stress response (GSR), an adaptive response that controls the transcription of a variety of genes to overcome adverse conditions. The core GSR regulators (the response regulator PhyR, the anti‐σ factor NepR and the σ factor EcfG) are duplicated in TFA, being PhyR1 and PhyR2, NepR1 and NepR2 and EcfG1 and EcfG2. Based on multiple genetic, phenotypical and biochemical evidences including in vitro transcription assays, we have assigned distinct functional features to each paralogue and assessed their contribution to the GSR regulation, dictating its timing and the intensity. We show that different stress signals are differentially integrated into the GSR by PhyR1 and PhyR2, therefore producing different levels of GSR activation. We demonstrate in vitro that both NepR1 and NepR2 bind EcfG1 and EcfG2, although NepR1 produces a more stable interaction than NepR2. Conversely, NepR2 interacts with phosphorylated PhyR1 and PhyR2 more efficiently than NepR1. We propose an integrative model where NepR2 would play a dual negative role: it would directly inhibit the σ factors upon activation of the GSR and it would modulate the GSR activity indirectly by titrating the PhyR regulators.

NuA4 and H2A.Z control environmental responses and autotrophic growth in Arabidopsis

Nucleosomal acetyltransferase of H4 (NuA4) is an essential transcriptional coactivator in eukaryotes, but remains poorly characterized in plants. Here, we describe Arabidopsis homologs of the NuA4 scaffold proteins Enhancer of Polycomb-Like 1 (AtEPL1) and Esa1-Associated Factor 1 (AtEAF1). Loss of AtEAF1 results in inhibition of growth and chloroplast development. These effects are stronger in the Atepl1 mutant and are further enhanced by loss of Golden2-Like (GLK) transcription factors, suggesting that NuA4 activates nuclear plastid genes alongside GLK. We demonstrate that AtEPL1 is necessary for nucleosomal acetylation of histones H4 and H2A.Z by NuA4 in vitro. These chromatin marks are diminished genome-wide in Atepl1, while another active chromatin mark, H3K9 acetylation (H3K9ac), is locally enhanced. Expression of many chloroplast-related genes depends on NuA4, as they are downregulated with loss of H4ac and H2A.Zac. Finally, we demonstrate that NuA4 promotes H2A.Z deposition and by doing so prevents spurious activation of stress response genes.

MDrop-Seq: Massively Parallel Single-Cell RNA-Seq of Saccharomyces cerevisiae and Candida albicans.

Advances in high-throughput single-cell RNA sequencing (scRNA-seq) have been limited by technical challenges such as tough cell walls and low RNA quantity that prevent transcriptomic profiling of microbial species at throughput. We present microbial Drop-seq or mDrop-seq, a high-throughput scRNA-seq technique that is demonstrated on two yeast species, Saccharomyces cerevisiae, a popular model organism, and Candida albicans, a common opportunistic pathogen. We benchmarked mDrop-seq for sensitivity and specificity and used it to profile 35,109 S. cerevisiae cells to detect variation in mRNA levels between them. As a proof of concept, we quantified expression differences in heat shock S. cerevisiae using mDrop-seq. We detected differential activation of stress response genes within a seemingly homogenous population of S. cerevisiae under heat shock. We also applied mDrop-seq to C. albicans cells, a polymorphic and clinically relevant species of yeast with a thicker cell wall compared to S. cerevisiae. Single-cell transcriptomes in 39,705 C. albicans cells were characterized using mDrop-seq under different conditions, including exposure to fluconazole, a common anti-fungal drug. We noted differential regulation in stress response and drug target pathways between C. albicans cells, changes in cell cycle patterns and marked increases in histone activity when treated with fluconazole. We demonstrate mDrop-seq to be an affordable and scalable technique that can quantify the variability in gene expression in different yeast species. We hope that mDrop-seq will lead to a better understanding of genetic variation in pathogens in response to stimuli and find immediate applications in investigating drug resistance, infection outcome and developing new drugs and treatment strategies.

Inducible expression of (pp)pGpp synthetases in Staphylococcus aureus is associated with activation of stress response genes.

The stringent response is characterized by the synthesis of the messenger molecules pppGpp, ppGpp or pGpp (here collectively designated (pp)pGpp). The phenotypic consequences resulting from (pp)pGpp accumulation vary among species and can be mediated by different underlying mechanisms. Most genome-wide analyses have been performed under stress conditions, which often mask the immediate effects of (pp)pGpp-mediated regulatory circuits. In Staphylococcus aureus, (pp)pGpp can be synthesized via the RelA-SpoT-homolog, RelSau upon amino acid limitation or via one of the two small (pp)pGpp synthetases RelP or RelQ upon cell wall stress. We used RNA-Seq to compare the global effects in response to induction of the synthetase of rel-Syn (coding for the enzymatic region of RelSau) or relQ without the need to apply additional stress conditions. Induction of rel-Syn resulted in changes in the nucleotide pool similar to induction of the stringent response via the tRNA synthetase inhibitor mupirocin: a reduction in the GTP pool, an increase in the ATP pool and synthesis of pppGpp, ppGpp and pGpp. Induction of all three enzymes resulted in similar changes in the transcriptome. However, RelQ was less active than Rel-Syn and RelP, indicating strong restriction of its (pp)pGpp-synthesis activity in vivo. (pp)pGpp induction resulted in the downregulation of many genes involved in protein and RNA/DNA metabolism. Many of the (pp)pGpp upregulated genes are part of the GTP sensitive CodY regulon and thus likely regulated through lowering of the GTP pool. New CodY independent transcriptional changes were detected including genes involved in the SOS response, iron storage (e.g. ftnA, dps), oxidative stress response (e.g., perR, katA, sodA) and the psmα1–4 and psmß1-2 operons coding for cytotoxic, phenol soluble modulins (PSMs). Analyses of the ftnA, dps and psm genes in different regulatory mutants revealed that their (pp)pGpp-dependent regulation can occur independent of the regulators PerR, Fur, SarA or CodY. Moreover, psm expression is uncoupled from expression of the quorum sensing system Agr, the main known psm activator. The expression of central genes of the oxidative stress response protects the bacteria from anticipated ROS stress derived from PSMs or exogenous sources. Thus, we identified a new link between the stringent response and oxidative stress in S. aureus that is likely crucial for survival upon phagocytosis.

Cellular effects of PM2.5 from Suzhou, China: relationship to chemical composition and endotoxin content.

Exposure to PM2.5 can cause adverse health outcomes. In this study, we analyzed PM2.5 samples collected from suburban and urban sites, including a traffic tunnel in Suzhou, China, for their physicochemical properties, endotoxin contents, and effects on HepG2 and A549 cells in vitro. The greatest cellular responses, including oxidative stress, cytotoxicity, genotoxicity, inflammatory, and transcriptional activation of stress-responsive genes (i.e., HSPA1A, GADD45α), were observed in cells treated with traffic tunnel PM2.5. Cytokine expression was also measured and closely correlated with endotoxin content, while other toxic effects were largely related to PM2.5-bound metals and polycyclic aromatic hydrocarbons (PAHs). These findings suggested that chemical and biological composition of PM2.5, including adsorbed trace metals, PAHs, and endotoxin, may contribute significantly to their toxicity. In addition to commonly used in vitro toxicity tests, HSPA1A and GADD45α promoter-driven luciferase reporter cells may provide a potential new tool for rapid screening and quantification of PM2.5 toxicity.

The Role of Major Transcription Factors in Solanaceous Food Crops under Different Stress Conditions: Current and Future Perspectives.

Plant growth, development, and productivity are adversely affected by environmental stresses such as drought (osmotic stress), soil salinity, cold, oxidative stress, irradiation, and diverse diseases. These impacts are of increasing concern in light of climate change. Noticeably, plants have developed their adaptive mechanism to respond to environmental stresses by transcriptional activation of stress-responsive genes. Among the known transcription factors, DoF, WRKY, MYB, NAC, bZIP, ERF, ARF and HSF are those widely associated with abiotic and biotic stress response in plants. Genome-wide identification and characterization analyses of these transcription factors have been almost completed in major solanaceous food crops, emphasizing these transcription factor families which have much potential for the improvement of yield, stress tolerance, reducing marginal land and increase the water use efficiency of solanaceous crops in arid and semi-arid areas where plant demand more water. Most importantly, transcription factors are proteins that play a key role in improving crop yield under water-deficient areas and a place where the severity of pathogen is very high to withstand the ongoing climate change. Therefore, this review highlights the role of major transcription factors in solanaceous crops, current and future perspectives in improving the crop traits towards abiotic and biotic stress tolerance and beyond. We have tried to accentuate the importance of using genome editing molecular technologies like CRISPR/Cas9, Virus-induced gene silencing and some other methods to improve the plant potential in giving yield under unfavorable environmental conditions.

The role of transposable elements in the ecological morphogenesis under the influence of stress

In natural selection, insertional mutagenesis is an important source of genome variability. Transposons are sensors of environmental stress effects, which contribute to adaptation and speciation. These effects are due to changes in the mechanisms of morphogenesis, since transposons contain regulatory sequences that have cis and trans effects on specific protein-coding genes. In variability of genomes, the horizontal transfer of transposons plays an important role, because it contributes to changing the composition of transposons and the acquisition of new properties. Transposons are capable of site-specific transpositions, which lead to the activation of stress response genes. Transposons are sources of non-coding RNA, transcription factors binding sites and protein-coding genes due to domestication, exonization, and duplication. These genes contain nucleotide sequences that interact with non-coding RNAs processed from transposons transcripts, and therefore they are under the control of epigenetic regulatory networks involving transposons. Therefore, inherited features of the location and composition of transposons, along with a change in the phenotype, play an important role in the characteristics of responding to a variety of environmental stressors. This is the basis for the selection and survival of organisms with a specific composition and arrangement of transposons that contribute to adaptation under certain environmental conditions. In evolution, the capability to transpose into specific genome sites, regulate gene expression, and interact with transcription factors, along with the ability to respond to stressors, is the basis for rapid variability and speciation by altering the regulation of ontogenesis. The review presents evidence of tissue-specific and stage-specific features of transposon activation and their role in the regulation of cell differentiation to confirm their role in ecological morphogenesis.

The inconspicuous gatekeeper: endophytic Serendipita vermifera acts as extended plant protection barrier in the rhizosphere.

In nature, beneficial and pathogenic fungi often simultaneously colonise plants. Despite substantial efforts to understand the composition of natural plant-microbe communities, the mechanisms driving such multipartite interactions remain largely unknown. Here we address how the interaction between the beneficial root endophyte Serendipita vermifera and the pathogen Bipolaris sorokiniana affects fungal behaviour and determines barley host responses using a gnotobiotic soil-based split-root system. Fungal confrontation in soil resulted in induction of B.sorokiniana genes involved in secondary metabolism and a significant repression of genes encoding putative effectors. In S.vermifera, genes encoding hydrolytic enzymes were strongly induced. This antagonistic response was not activated during the tripartite interaction in barley roots. Instead, we observed a specific induction of S.vermifera genes involved in detoxification and redox homeostasis. Pathogen infection but not endophyte colonisation resulted in substantial host transcriptional reprogramming and activation of defence. In the presence of S.vermifera, pathogen infection and disease symptoms were significantly reduced despite no marked alterations of the plant transcriptional response. The activation of stress response genes and concomitant repression of putative effector gene expression in B.sorokiniana during confrontation with the endophyte suggest a reduction of the pathogen's virulence potential before host plant infection.