Stress-responsive Factor Research Articles

Two new enzymes that liberate undecaprenyl-phosphate to replenish the carrier lipid pool during envelope stress.

The 55-carbon isoprenoid, undecaprenyl-phosphate (UndP), is a universal carrier lipid that ferries most glycans and glycopolymers across the cytoplasmic membrane in bacteria. In addition to peptidoglycan precursors, UndP transports O-antigen, capsule, wall teichoic acids, and sugar modifications. How this shared but limited lipid is distributed among competing pathways is just beginning to be elucidated. We recently reported that in the bacterium Bacillus subtilis, the stress-response sigma factor SigM and its cognate anti-sigma factor complex respond to changes in the free UndP pool. When levels are low, SigM activates genes that increase flux through the essential cell wall synthesis pathway, promote the recycling of the lipid carrier, and liberate the carrier from other polymer pathways. Here, we report that two additional enzymes under SigM control help maintain the free pool of UndP. One, UshA (YqjL), resembles alpha-beta hydrolases and liberates UndP from undecaprenyl-monophosphate-linked sugars. The other, UpsH (YpbG), resembles metallophosphoesterases and releases UndP from undecaprenyl-diphosphate-linked wall teichoic acids polymers but not lipid-linked peptidoglycan precursors. UshA becomes critical for growth when UndP-linked sugars are sequestered, and the carrier lipid pool is depleted. Similarly, UpsH becomes essential for viability when UndPP-linked intermediates accumulate. Mutations in the predicted catalytic residues of both putative hydrolases abrogate their function arguing that they act directly to release UndP. These findings define two new enzymes that liberate the carrier lipid from UndP- and UndPP-linked intermediates and bolster the model that the SigM stress-response pathway maintains the UndP pool and prioritizes its use for peptidoglycan synthesis.IMPORTANCEMotivated by the success of naturally occurring glycopeptide antibiotics like vancomycin, one arm of recent antibiotic discovery efforts has focused on compounds that bind lipid-linked precursors used to build extracytoplasmic polymers. Trapping these precursors depletes the universal carrier lipid undecaprenyl-phosphate, which is required for the synthesis of virtually all surface polymers, including peptidoglycan. Understanding how cells respond to this stress to restore the carrier lipid pool is critical to identifying effective drugs. Here, we report the identification of two new enzymes that are produced in response to the depletion of the carrier lipid pool. These enzymes recover the carrier lipid but cleave distinct lipid-linked precursors to do so.

Multiplexed single-cell imaging reveals diverging subpopulations with distinct senescence phenotypes during long-term senescence induction.

Cellular senescence is a phenotypic state that contributes to the progression of age-related disease through secretion of pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). Understanding the process by which healthy cells become senescent and develop SASP factors is critical for improving the identification of senescent cells and, ultimately, understanding tissue dysfunction. Here, we reveal how the duration of cellular stress modulates the SASP in distinct subpopulations of senescent cells. We used multiplex, single-cell imaging to build a proteomic map of senescence induction in human epithelial cells induced to senescence over the course of 31 days. We map how the expression of SASP proteins increases alongside other known senescence markers such as p53, p21, and p16INK4a. The aggregated population of cells responded to etoposide with an accumulation of stress response factors over the first 11 days, followed by a plateau in most proteins. At the single-cell level, however, we identified two distinct senescence cell populations, one defined primarily by larger nuclear area and the second by higher protein concentrations. Trajectory inference suggested that cells took one of two discrete molecular paths from unperturbed healthy cells, through a common transitional subpopulation, and ending at the discrete terminal senescence phenotypes. Our results underscore the importance of using single-cell proteomics to identify the mechanistic pathways governing the transition from senescence induction to a mature state of senescence characterized by the SASP.

Genome-Wide Identification of CONSTANS-like (COL) Gene Family and the Potential Function of ApCOL08 Under Salt Stress in Andrographis paniculata.

Andrographis paniculata is an important medicinal herb known as a "natural antibiotic", which has been used in Southeast Asia for thousands of years. The CONSTANS-like (COL) gene is an important regulatory factor for plant photoperiod flowering and stress response. However, there is currently no detailed research on the COL genes of A. paniculata. In our study, we performed a genome-wide analysis of A. paniculata COL (ApCOL) family members using bioinformatics tools and identified nine ApCOL genes. Based on phylogenetic analysis, ApCOLs were categorized into three groups, with members of the same group having similar structures. Gene duplication events indicated that only one pair of duplicated genes was identified, possibly caused by segmental duplication. In terms of evolutionary relationships, the COL proteins of A. paniculata and Sesamum indicum were closely related, showing that they are highly similar in the phylogenetic tree. In addition, ApCOL genes showed tissue specificity and were specifically highly expressed mainly in leaves and flowers. Based on the cis-regulatory element prediction results, we examined the expression levels of ApCOLs under hormone and salt stress, and ApCOL08 was significantly induced. With subcellular localization results consistent with the prediction, we transformed ApCOL08 into yeast and showed significant resistance to salt stress. Our study suggests that ApCOL genes have important roles in response to abiotic stress and plant development and initially identifies key genes for future molecular regulation studies.

UBIQUITIN-CONJUGATING ENZYME34 mediates pyrophosphatase AVP1 turnover and regulates abiotic stress responses in Arabidopsis.

Understanding the molecular mechanisms of abiotic stress responses in plants is instrumental for the development of climate-resilient crops. Key factors in abiotic stress responses, such as the proton- pumping pyrophosphatase (AVP1), have been identified, but their function and regulation remain elusive. Here, we explored the post-translational regulation of AVP1 by the ubiquitin-conjugating enzyme UBC34 and its relevance in the salt stress and phosphate starvation responses of Arabidopsis (Arabidopsis thaliana). Through in vitro and in vivo assays, we established that UBC34 interacts with and ubiquitylates AVP1. Mutant lines in which UBC34 was downregulated showed higher tolerance to salt and low inorganic phosphate (Pi) stresses, while we observed the opposite for plants overexpressing UBC34. Our results showed that UBC34 co-localizes with AVP1, and AVP1 activity is enhanced in the plasma membrane fractions of ubc34 mutants, indicating that UBC34 mediates the turnover of plasma membrane-localized AVP1. We also observed that UBC34 affects the apoplastic pH, but not the vacuolar pH of root cells. Based on our results, we propose a mechanistic model in which UBC34 mediates AVP1 turnover at the plasma membrane of root epidermal cells. Downregulation of UBC34 under salt and phosphate starvation conditions enhances AVP1 activity, leading to a higher proton gradient available for sodium sequestration and phosphate uptake.

WRKY Transcription Factors Modulate the Flavonoid Pathway of Rhododendron chrysanthum Pall. Under UV-B Stress.

The depletion of the ozone layer has resulted in elevated ultraviolet-B (UV-B) radiation levels, posing a significant risk to terrestrial plant growth. Rhododendron chrysanthum Pall. (R. chrysanthum), adapted to high-altitude and high-irradiation environments, has developed unique adaptive mechanisms. This study exposed R. chrysanthum to UV-B radiation for two days, with an 8 h daily treatment, utilizing metabolomic and transcriptomic analyses to explore the role of WRKY transcription factors in the plant's UV-B stress response and their regulation of flavonoid synthesis. UV-B stress resulted in a significant decrease in rETR and Ik and a significant increase in 1-qP. These chlorophyll fluorescence parameters indicate that UV-B stress impaired photosynthesis in R. chrysanthum. Faced with the detrimental impact of UV-B radiation, R. chrysanthum is capable of mitigating its effects by modulating its flavonoid biosynthetic pathways to adapt positively to the stress. This study revealed changes in the expression of 113 flavonoid-related metabolites and 42 associated genes, with WRKY transcription factors showing significant correlation with these alterations. WRKY transcription factors can influence the expression of key enzyme genes in the flavonoid metabolic pathway, thereby affecting metabolite production. A theoretical reference for investigating plant stress physiology is provided in this work, which also offers insights into the stress responses of alpine plants under adverse conditions.

Growth and differentiation factor 15: An emerging therapeutic target for brain diseases

Growth and differentiation factor 15 (GDF15), a member of the transforming growth factor-βsuperfamily, is considered a stress response factor and has garnered increasing attention in recent years due to its roles in neurological diseases. Although many studies have suggested that GDF15 expression is elevated in patients with neurodegenerative diseases (NDDs), glioma, and ischemic stroke, the effects of increased GDF15 expression and the potential underlying mechanisms remain unclear. Notably, many experimental studies have shown the multidimensional beneficial effects of GDF15 on NDDs, and GDF15 overexpression is able to rescue NDD-associated pathological changes and phenotypes. In glioma, GDF15 exerts opposite effects, it is both protumorigenic and antitumorigenic. The causes of these conflicting findings are not comprehensively clear, but inhibiting GDF15 is helpful for suppressing tumor progression. GDF15 is also regarded as a biomarker of poor clinical outcomes in ischemic stroke patients, and targeting GDF15 may help prevent this disease. Thus, we systematically reviewed the synthesis, transcriptional regulation, and biological functions of GDF15 and its related signaling pathways within the brain. Furthermore, we explored the potential of GDF15 as a therapeutic target and assessed its clinical applicability in interventions for brain diseases. By integrating the latest research findings, this study provides new insights into the future treatment of neurological diseases.

The role of RNA polymerase II transcript elongation factors in plant stress responses.

The elongation phase is a dynamic and highly regulated step of the RNA polymerase II (RNAPII) transcription cycle. A variety of transcript elongation factors (TEFs) comprising regulators of RNAPII activity, histone chaperones and modulators of histone modifications assist transcription through chromatin. Thereby TEFs substantially contribute to establish gene expression patterns during plant growth and development. Beyond that, recent research indicates that TEFs and RNAPII transcriptional elongation also play a key role in plant responses to environmental cues. Thus, certain TEFs (i.e. PAF1C, FACT, TFIIS) were found to mediate by different mechanisms transcriptional reprogramming to establish plant tolerance to abiotic conditions such as heat stress and elevated salt concentrations. At this, TEFs govern RNAPII elongation to generate the transcriptional output adequate for distinct environments. It is to be expected that future research in this developing field will reveal that the function of TEFs is involved in a growing number of plant responses to changing environmental conditions.

Reduction of Chemoresistance by Claudin-14-Targeting Peptide in Human Colorectal Cancer Cells.

The expression of claudins (CLDNs), major components of tight junctions (TJs), is abnormal in various solid tumors. CLDN14 is highly expressed in human colorectal cancer (CRC) tissues and confers chemoresistance. CLDN14 may become a novel therapeutic target for CRC, but CLDN14-targeting drugs have not been developed. Here, we searched for a CLDN14-targeting peptide, which can suppress CLDN14 expression and chemoresistance using human CRC-derived DLD-1 and LoVo cells. Among some short peptides which mimic the second extracellular loop structure of CLDN14, PSGMK most strongly suppressed the protein expression of CLDN14. The mRNA expression of other endogenous TJ components was unchanged by PSGMK. The PSGMK-induced reduction of CLDN14 protein was inhibited by chloroquine, a lysosome inhibitor, and monodansylcadaverine, a clathrin-dependent endocytosis inhibitor, indicating that PSGMK may enhance endocytosis and lysosomal degradation of CLDN14. In a three-dimensional culture model, the oxidative stress was significantly reduced by PSGMK, whereas hypoxia stress was not. Furthermore, the expression levels of nuclear factor erythroid 2-related factor 2, an oxidative stress response factor, and its target genes were decreased by PSGMK. These results suggest that PSGMK relieves stress conditions in spheroids. The cell viability of spheroids was decreased by anticancer drugs such as doxorubicin and oxaliplatin, which was exaggerated by the cotreatment with PSGMK. Our data indicate that CLDN14-targeting peptide, PSGMK has an anti-chemoresistance effect in CRC cells.

Abstract PR002: Hypoxia-induced epigenetic changes coordinate transcription start site selection and translational control through remodeling of 5’UTRs

Abstract Adaptation to hypoxia enhances cancer cell malignancy and negatively impacts patient outcomes. Reprogramming of mRNA translation is an essential component of the hypoxia-adaptive response. During hypoxia, cells undergo a global decrease in protein synthesis. However, translation of subsets of transcripts encoding stress-response, survival and stemness factors is increased. This selective regulation is thought to be governed largely via the interactions between specific mRNA features and remodeling of the translational apparatus. However, our understanding of the mechanisms that govern translational perturbations under hypoxia remains incomplete. Here, we interrogated the effects of hypoxia on global changes in histone methylation and transcription start site (TSS) selection, coupled with monitoring corresponding alterations in total mRNA levels and translation efficiencies on a genome-wide scale in T47D breast cancer cells and H9 human embryonic stem cells. This revealed widespread epigenetic alterations leading to TSS switching and extensive remodeling of 5’UTRs, and allowed us to map the impact of specific 5’UTR features on translation efficiency under hypoxia. Pyruvate Dehydrogenase Kinase 1 (PDK1), a key enzyme in orchestrating metabolic adaption to hypoxia, undergoes TSS switching leading to increased availability of efficiently translated 5’UTR isoforms, and we show that this effect is coordinated at an epigenetic level. Therefore, our findings uncover a mechanism driving translational reprogramming under hypoxia, whereby alterations in translational apparatus are orchestrated with epigenetic perturbations that result in 5’UTR remodeling of the transcriptome. Citation Format: Kathleen Watt, Bianca Dauber, Krzysztof J Szkop, Laura Lee, Predrag Jovanovic, Shan Chen, Laia Masvidal, Kristofersson Tandoc, Ranveer Palia, Ivan Topisirovic, Ola Larsson, Lynne-Marie Postovit. Hypoxia-induced epigenetic changes coordinate transcription start site selection and translational control through remodeling of 5’UTRs [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: RNAs as Drivers, Targets, and Therapeutics in Cancer; 2024 Nov 14-17; Bellevue, Washington. Philadelphia (PA): AACR; Mol Cancer Ther 2024;23(11_Suppl):Abstract nr PR002.

Identification and Characterization of EIN3/EIL Transcription Factor Family Members in Pinus massoniana Lamb.

Transcription factors refer to types of proteins that perform significant functions in the process of gene expression regulation. The ethylene insensitive 3/ethylene insensitive 3-like (EIN3/EIL) family, functioning as significant transcription factors regulating ethylene, plays a critical role in the growth and development of plants and participates in the plant's response to diverse environmental stresses. Pinus massoniana is an excellent native tree with high economic and ecological value. However, the study of EIN3/EIL genes in gymnosperms, for instance, P. massoniana, is still relatively limited. In this research, four putative EIN3/EIL genes were identified in the transcriptome of P. massoniana. Bioinformatics analysis showed that PmEIL genes contain a highly conserved EIN3 domain and other structural features of acidic, proline-rich and glutamine-rich sites. The molecular evolution tree analysis demonstrated that the EIN3/EIL family was partitioned into three categories (A, B, and C), and the number, type, and distribution of conserved motifs grouped in one category were similar. The results of qRT-PCR indicated that the expression levels of PmEIL genes were markedly elevated in needles compared to other tissues. Through the analysis of expression patterns of the PmEIL genes under various stress treatments, it was found that the PmEIL genes could participate in plant hormone stimulation induction, osmosis, drought and other response processes. In addition, PmEIL is a nuclear localization protein. PmEIL1, PmEIL3, and PmEIL4 are transcriptional activators, while PmEIL2 is a transcriptional suppressor. This research provides a basis for further elucidating the function of EIN3/EIL transcription factors in growth, development and stress response of P. massoniana.

Multiplexed single-cell imaging reveals diverging subpopulations with distinct senescence phenotypes during long-term senescence induction.

Cellular senescence is a phenotypic state that contributes to the progression of age-related disease through secretion of pro-inflammatory factors known as the senescence associated secretory phenotype (SASP). Understanding the process by which healthy cells become senescent and develop SASP factors is critical for improving the identification of senescent cells and, ultimately, understanding tissue dysfunction. Here, we reveal how the duration of cellular stress modulates the SASP in distinct subpopulations of senescent cells. We used multiplex, single-cell imaging to build a proteomic map of senescence induction in human epithelial cells induced to senescence over the course of 31 days. We map how the expression of SASP proteins increases alongside other known senescence markers such as p53, p21, and p16INK4a. The aggregated population of cells responded to etoposide with an accumulation of stress response factors over the first 11 days, followed by a plateau in most proteins. At the single-cell level, however, we identified two distinct senescence cell populations, one defined primarily by larger nuclear area and the second by higher protein concentrations. Trajectory inference suggested that cells took one of two discrete molecular paths from unperturbed healthy cells, through a common transitional subpopulation, and ending at the discrete terminal senescence phenotypes. Our results underscore the importance of using single-cell proteomics to identify the mechanistic pathways governing the transition from senescence induction to a mature state of senescence characterized by the SASP.

Listeriosis: Characteristics, Occurrence in Domestic Animals, Public Health Significance, Surveillance and Control.

Listeriosis is a dangerous zoonosis caused by bacteria of the genus Listeria, with Listeria monocytogenes (LM) being the most pathogenic species. Listeria monocytogenes has been detected in various animal species and in humans, and its ability to evolve from an environmental saprophyte to a powerful intracellular pathogen is driven by the invasion mechanisms and virulence factors that enable cell invasion, replication and cell-to-cell spread. Key regulatory systems, including positive regulatory factor A (PrfA) and the stress-responsive sigma factor σB, control the expression of virulence genes and facilitate invasion of host cells. Listeriosis poses a significant threat to cattle, sheep and goat herds, leading to abortions, septicemia and meningoencephalitis, and ruminants are important reservoirs for Listeria, facilitating transmission to humans. Other Listeria species such as Listeria ivanovii and Listeria innocua can also cause disease in ruminants. Resilience of LM in food processing environments makes it an important foodborne pathogen that is frequently transmitted through contaminated meat and dairy products, with contamination often occurring along the food production chain. In humans, listeriosis primarily affects immunocompromised individuals, pregnant women and the elderly and leads to severe conditions, such as meningitis, septicemia and spontaneous abortion. Possible treatment requires antibiotics that penetrate the blood-brain barrier. Despite the relatively low antimicrobial resistance, multidrug-resistant LM strains have been detected in animals, food and the environment. Controlling and monitoring the disease at the herd level, along with adopting a One Health approach, are crucial to protect human and animal health and to minimize the potential negative impacts on the environment.

Hypoxia-reoxygenation Extends the Lifespan of Caenorhabditis elegans via SKN-1- and DAF-16A-Dependent Stress Hormesis.

To study the role of hypoxia-reoxygenation and anoxia-starvation on the lifespan of C. elegans and elucidate the mechanism at molecular levels. Increasing evidence indicates that reactive oxygen species (ROS) act as signaling molecules that promote health. Hormesis occurs when a moderate stress level induces a beneficial adaptive response, protecting organisms against subsequent exposure to severe stress. Caenorhabditis elegans is a widely used model organism to study aging and displays a broad hormetic ability to couple with stress. To date, only few methods are available to induce stress hormesis in C. elegans. The objectives of this study were to explore the effects of hypoxia-reoxygenation and anoxia-starvation on the lifespan of C. elegans, exploring the involvement of ROS and oxidative stress-related pathways, and examining the hormetic property of H/R. The C. elegans were cultured in hypoxic conditions (1% O2) with OP50 bacteria for 24 h followed by reoxygenation (20% O2) (H/R) or in anoxic conditions (0% O2; 100% N2) without OP50 bacteria for 24 h followed by reoxygenation (20% O2) and food supplementation (A/S). Survivals were plotted and estimated for probability with Kaplan-Meier analysis. The H/R extended the lifespan of C. elegans, and H/R-pretreated worms showed improved resistance toward A/S compared to naïve worms. The C. elegans SKN-1 and DAF-16 are important oxidative stress response factors homologous to mammalian Nrf2 and FOXO3, respectively. Mutations in SKN-1 and DAF-16 blocked H/R-induced life extension. Next, H/R treatment in C. elegans activated both SKN-1 and DAF-16, as indicated by the upregulation of putative target genes of SKN-1 (gcs-1 and gss-1) and DAF-16 (sod-3). Moreover, pre-treatment with antioxidants (N-acetylcysteine, chlorogenic acid, and sulforaphane) reduced ROS levels and diminished the lifespan extension effect of H/R, indicating their dependency on ROS. These results provide evidence that H/R is beneficial for lifespan and stress resistance by activating the adaptive cellular response pathway (SKN-1 and DAF-16A) toward oxidative stress.

SpbZIP60 confers cadmium tolerance by strengthening the root cell wall compartmentalization in Sedum plumbizincicola

Cadmium (Cd) is a prominent heavy metal pollutant that inhibits plant growth and poses risks to human health. Sedum plumbizincicola, as a Cd/Zn/Pb hyperaccumulator species, exhibits robust resistance to heavy metals and effective enrichment capacities. In our previous study, overexpressing SpbZIP60 in Arabidopsis enhanced Cd tolerance; however, the underlying the molecular mechanism remains to be elucidated. Here, we identified SpbZIP60 as a representative Cd stress response factor with nuclear localization and transcriptional activation activity. SpbZIP60 underwent conservative splicing in response to endoplasmic reticulum (ER) stress, while its response to Cd stress is independent of the ER stress-mediated unfolded protein response pathway. Overexpression of SpbZIP60 in S. alfredii increased the Cd tolerance and antioxidant activity. Furthermore, SpbZIP60 increased the content of cell wall components and thickened cell wall under Cd stress. Transcriptome analysis indicated a significant enrichment of differentially expressed genes within the phenylpropanoid metabolism pathway. Besides, the binding of SpbZIP60 to the promoter region of SpBglu resulted in the activation of gene expression, thereby enhancing the process of lignin deposition. Collectively, our results elucidated a molecular regulatory model in which SpbZIP60 increased the thickness of the root cell wall to impede Cd entry into the cell, consequently improving Cd tolerance.

APOBEC3C-mediated NF-κB activation enhances clear cell renal cell carcinoma progression.

Renowned as the predominant form of kidney cancer, clear cell renal cell carcinoma (ccRCC) exhibits susceptibility to immunotherapies due to its specific expression profile as well as notable immune cell infiltration. Despite this, effectively treating metastatic ccRCC remains a significant challenge, necessitating a more profound comprehension of the underlying molecular mechanisms governing its progression. Here, we unveil that the enhanced expression of the RNA-binding protein DNA dC → dU-editing enzyme APOBEC-3C (APOBEC3C; also known as A3C) in ccRCC tissue and ccRCC-derived cell lines serves as a catalyst for tumor growth by amplifying nuclear factor-kappa B (NF-κB) activity. By employing RNA-sequencing and cell-based assays in ccRCC-derived cell lines, we determined that A3C is a stress-responsive factor and crucial for cell survival. Furthermore, we identified that A3C binds and potentially stabilizes messenger RNAs (mRNAs) encoding positive regulators of the NF-κB pathway. Upon A3C depletion, essential subunits of the NF-κB family are abnormally restrained in the cytoplasm, leading to deregulation of NF-κB target genes. Our study illuminates the pivotal role of A3C in promoting ccRCC tumor development, positioning it as a prospective target for future therapeutic strategies.

NF-Y acts as a molecular platform to guide the binding of the ER stress response factor to the ER-stress elements ERSE and ERSE II. A case of molecular 'asymmetric symmetry'

NF-Y acts as a molecular platform to guide the binding of the ER stress response factor to the ER-stress elements ERSE and ERSE II. A case of molecular 'asymmetric symmetry'

Expression and Functional Identification of SPL6/7/9 Genes under Drought Stress in Sugarbeet Seedlings.

Sugar beet is a significant sugar crop in China, primarily cultivated in arid regions of the north. However, drought often affects sugar beet cultivation, leading to reduced yield and quality. Therefore, understanding the impact of drought on sugar beets and studying their drought tolerance is crucial. Previous research has examined the role of SPL (SQUAMOSA promoter-binding protein-like) transcription factors in plant stress response; however, the precise contribution of SPLs to the drought stress response in sugar beets has yet to be elucidated. In this study, we identified and examined the BvSPL6, BvSPL7, and BvSPL9 genes in sugar beets, investigating their performance during the seedling stage under drought stress. We explored their drought resistance characteristics using bioinformatics, quantitative analysis, physiological experiments, and molecular biology experiments. Drought stress and rehydration treatments were applied to sugar beet seedlings, and the expression levels of BvSPL6, BvSPL7, and BvSPL9 genes in leaves were quantitatively analyzed at 11 different time points to evaluate sugar beets' response and tolerance to drought stress. Results indicated that the expression level of the BvSPL6/9 genes in leaves was upregulated during the mid-stage of drought stress and downregulated during the early and late stages. Additionally, the expression level of the BvSPL7 gene gradually increased with the duration of drought stress. Through analyzing changes in physiological indicators during different time periods of drought stress and rehydration treatment, we speculated that the regulation of BvSPL6/7/9 genes is associated with sugar beet drought resistance and their participation in drought stress response. Furthermore, we cloned the CDS sequences of BvSPL6, BvSPL7, and BvSPL9 genes from sugar beets and conducted sequence alignment with the database to validate the results. Subsequently, we constructed overexpression vectors, named 35S::BvSPL6, 35S::BvSPL7, and 35S::BvSPL9, and introduced them into sugar beets using Agrobacterium-mediated methods. Real-time fluorescence quantitative analysis revealed that the expression levels of BvSPL6/7/9 genes in transgenic sugar beets increased by 40% to 80%. The drought resistance of transgenic sugar beets was significantly enhanced compared with the control group.

Unraveling the Role of MYB Transcription Factors in Abiotic Stress Responses: An Integrative Approach in Eugenia uniflora L.

Unraveling the Role of MYB Transcription Factors in Abiotic Stress Responses: An Integrative Approach in Eugenia uniflora L.

Study on the applicability of the Brief Job Stress Questionnaire based on classical test theory and item response theory

Objective: To evaluate the quality and item characteristics of the Brief Job Stress Questionnaire (BJSQ) among employees in manufacturing and service industries. Methods: From December 2021 to December 2022, a total of 2077 employees from 4 manufacturing and service enterprises in Beijing were selected by the method of combining purpose sampling and convenience sampling. The Chinese version of BJSQ was used to carry out a survey on occupational stress from 57 items in 4 dimensions including job stress factors, stress response, social support factors and satisfaction. Classical test theory (CTT) was used to analyze the validity and reliability of the questionnaire. The Semejima hierarchical response model in item response theory (IRT) was used to analyze the differentiation a, difficulty coefficient b and information content of each item. Results: Among the 2077 subjects, the age M (Q(1), Q(3)) was 33 (28, 37) years old, and the working age M (Q(1), Q(3)) was 4 (2, 8) years. There were 723 (34.8%) people in manufacturing industry and 1354 (65.2%) people in service industry. Eleven common factors were extracted by exploratory factor analysis, with a cumulative variance contribution rate of 62.823%, the variance of the common factors of each entry ranging from 0.451 to 0.865, and the range of factor loading values from 0.413 to 0.825, with 5 items having cross-loadings. The results of the validation factor analysis showed that the model fit indexes of root means square error of approximation was 0.055, comparative fit index was 0.950, Tucker Lewis index was 0.948, and standardized root mean square was 0.066. Content validity results showed that the total scores of the Chinese version of the BJSQ were positively correlated with the scores of the 4 dimensions (r(s)=0.487-0.936, P<0.05) . The results of the reliability analysis showed that the Cronbach's alpha coefficient for the total questionnaire was 0.945, and the Cronbach's alpha coefficients of job stress factors, stress response and social support factors were 0.775, 0.957, and 0.830, respectively. The Spearman-Brown coefficient for the total questionnaire was 0.866, and for the 3 dimensions, it was 0.572, 0.882 and 0.772. The results of IRT analysis showed that only 1 of the 57 items had a differentiation a-value<0.30, the difficulty coefficient b-value of each item ranged from -12.02 to 11.09, of which 8 items had a difficulty coefficient that was too high, 3 items had a difficulty coefficient that was too low, and 3 items did not meet the requirements, and the average amount of information in each item ranged from 0.022 to 2.566, and there were 47 items with average amount of information>0.088 (5/57) . Conclusion: The Chinese version of BJSQ has good reliability and validity in the typical occupational groups of manufacturing and service industries in China, and most of the items have good performance, but some items still need to be further improved and optimized or deleted.

Chronic Stress-Induced Neuroinflammation: Relevance of Rodent Models to Human Disease.

The brain is the central organ of adaptation to stress because it perceives and determines threats that induce behavioral, physiological, and molecular responses. In humans, chronic stress manifests as an enduring consistent feeling of pressure and being overwhelmed for an extended duration. This can result in a persistent proinflammatory response in the peripheral and central nervous system (CNS), resulting in cellular, physiological, and behavioral effects. Compounding stressors may increase the risk of chronic-stress-induced inflammation, which can yield serious health consequences, including mental health disorders. This review summarizes the current knowledge surrounding the neuroinflammatory response in rodent models of chronic stress-a relationship that is continually being defined. Many studies investigating the effects of chronic stress on neuroinflammation in rodent models have identified significant changes in inflammatory modulators, including nuclear factor-κB (NF-κB) and toll-like receptors (TLRs), and cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6. This suggests that these are key inflammatory factors in the chronic stress response, which may contribute to the establishment of anxiety and depression-like symptoms. The behavioral and neurological effects of modulating inflammatory factors through gene knockdown (KD) and knockout (KO), and conventional and alternative medicine approaches, are discussed.