Stress biology最新文献

Cryptocaryon irritans is an obligate parasitic ciliate that significantly endangers marine fish. Hypoxia suppresses the development and hatchability of C. irritans during the tomont stage, which often develops on the seafloor under hypoxic conditions. Despite this knowledge, the underlying adaptation mechanisms of tomonts remain poorly understood. We aimed to determine how hypoxia reprograms tomont metabolism and whether ferroptosis contributes to hypoxia-induced vulnerability. Herein, metabolomic profiling revealed 2,964 differential metabolites under hypoxia. Notably, there were significantly elevated glucose levels, suggesting enhanced glycolytic activity. Enzymatic and qRT-PCR analyses further confirmed hypoxia-induced metabolic reprogramming, including increased hexokinase and pyruvate kinase activities and upregulation of glycolysis-related genes. Hypoxia also induced surface depressions, disrupted cell walls, mitochondrial deformation, reduced mitochondrial membrane potential, disrupted energy homeostasis, and increased NAD⁺/NADH ratio fluctuations and lactate accumulation. To probe ferroptotic susceptibility under hypoxia, hypoxic tomonts were exposed to the ferroptosis inducer erastin, resulting in a hatchability of 13% and promoting reactive oxygen species (ROS) accumulation, lipid peroxidation, and mitochondrial damage. Fluorescence staining revealed strong PI and ROS signals in hypoxic tomonts exposed to the ferroptosis inducer erastin. Notably, mitochondrial dysfunction was accompanied by Ca²⁺ and Fe²⁺ accumulation. Ferroptosis-related genes were upregulated at 24 h post-hypoxia induction. In contrast, gpx4 and mitochondrial electron transport chain components were downregulated at 48 h post-hypoxia induction. These findings demonstrate that hypoxia triggers glycolytic reprogramming and mitochondrial dysfunction in C. irritans, whereas erastin induces ferroptosis under hypoxic stress. This study provides new insights into protozoan hypoxia adaptation and highlights ferroptosis as a potential therapeutic target for controlling parasitic infections in marine aquaculture.

Cold stress is a major environmental challenge limiting the survival and productivity of tropical aquaculture species such as Nile tilapia (Oreochromis niloticus). The brain and gill represent two key organs that orchestrate systemic and environmental responses: the brain serves as the central thermosensory integrator and neuroendocrine control center, while the gill serves as the primary interface for respiration, ion regulation, and immune defense. However, the molecular mechanisms underlying their tissue-specific and potentially coordinated responses to cold remain unclear. Here, we applied integrative ATAC-seq and RNA-seq analyses to systematically investigate chromatin accessibility and gene expression dynamics in tilapia brain and gill tissues under cold stress. We identified thousands of differentially expressed genes and accessible regions, with significant correlations between transcriptional changes. Transcription factor footprinting revealed that Fra1 and Nrf act as key tissue-specific regulators, governing immune, apoptotic, and metabolic reprogramming in the brain and gill, respectively. Notably, the Fra1 module in the brain activated signaling pathways associated with stress response, neurodevelopment, and metabolic regulation which may influence peripheral responses by coordinating systemic physiological adjustments under cold stress, while Nrf-mediated regulation in the gill supported local homeostasis through redox and transport-related mechanisms. These findings highlight the hierarchical and organ-specific transcriptional control underlying cold adaptation in ectotherms. Our study provides the first chromatin accessibility atlas of cold-responsive regulatory networks across central and peripheral organs in fish, offering mechanistic insight and molecular targets for breeding cold-tolerant aquaculture strains.

Starch is a principal storage component in plants, significantly influencing the yield and quality traits of major crops. Climate change, particularly drought and high temperatures, severely affects starch biosynthesis in crops, leading to reduced starch yield and quality. The composition and properties of native starch, such as its low amylose content, substantially affect its nutritional value and industrial applications. To tackle these issues, genes coding for starch synthetic enzymes or those involved in the regulation of starch biosynthesis could be targeted for site-directed mutation to improve starch traits in crops. The application of gene editing technology in crops, notably CRISPR/Cas9, has facilitated the precise manipulation of starch biosynthesis. This review summarizes current knowledge on the biosynthesis and regulation of starch and the influence of climate change on these processes. It highlights advancements in modifying starch biosynthesis in food crops using CRISPR/Cas9. We discuss the strategy of improving starch traits and stress tolerance in response to climate change challenges and propose future directions for research on starch modification in food crops. Developing climate resilient crops capable of stable starch production is crucial for ensuring food security in the face of a changing global climate and an increasing world population.

As the global warming intensifies, along with increased planting density and straw retention practices, stalk rot (SR) has become one of major diseases that negatively impacts crop yield and quality. The distribution of SR pathogens, encompassing both fungal and bacterial agents, is significantly influenced by climate and agricultural factors. Although significant researches have been conducted on identifying fungal SR in different crop plants, there remains a lack of comprehensive reviews focused on the genetic and molecular mechanisms that contribute to crop resistance against fungal and bacterial SR. This review provides a comprehensive comparison of the pathogenic mechanisms associated with fungal and bacterial SR. It emphasized recently cloned genes and molecular regulations linked to resistance against SR, highlighted the pivotal role of several smart strategies in advancing gene discovery and functional research. Furthermore, it summarized the potential molecular regulatory pathways involved in SR resistance. Ultimately, the article presents insights into several critical areas that warrant further investigation in the study of SR-resistant mechanisms and crop breeding.

Areca palm velarivirus 1 (APV1) is the causative agent of yellow leaf disease (YLD), leading to severe yield losses in areca palms. However, how APV1 counteracts host immunity remains largely underexplored, and the underlying mechanisms are still poorly understood. RNA silencing is an evolutionarily conserved antiviral defense mechanism in eukaryotes. In this study, we identify the APV1-encoded capsid protein (CP) as a viral suppressor of RNA silencing (VSR) that inhibits both local and systemic silencing triggered by single-stranded RNA (ssRNA). Mechanistically, CP interacts with host Suppressor of Gene Silencing 3 (AcSGS3), a key component of the RNA silencing pathway, and promotes its degradation via autophagy. Additionally, CP disrupts the SGS3-AcRDR6 (RNA-dependent RNA polymerase 6) interaction, impairing the RNAi signaling cascade. Our findings reveal a novel dual mechanism to counteract host RNA silencing in which APV1 CP disrupts the SGS3-AcRDR6 complex and exploits the autophagic pathway to degrade AcSGS3, thereby undermining host antiviral defenses.

Zinc (Zn) deficiency in soil can directly result in Zn deficiency in crops, subsequently causing Zn deficiency in humans. Currently, the physiological adaptation mechanisms by which plants respond to Zn deficiency have been fairly well characterized. However, the regulatory mechanisms governing Zn transport in plants remain poorly understood. In this study, we found that CBL1/4/5/8/9-CIPK3/9/23/26 complexes interact with the Zn transporter ZIP2 and phosphorylate its Ser190 residue. Biochemical analyses and complementation experiments in yeast and plants demonstrated that the Ser190 site is essential for the transport activity of ZIP2, and that the Zn transporter ZIP2 is involved in the transport of Zn between the columnar sheath cells in the roots. Notably, the hybrid complementation lines carrying CBL-CIPK-mediated phosphorylation sites of ZIP2 and ZIP12 exhibited enhanced tolerance to Zn deficiency. Overall, these findings suggest that CBL-CIPK-ZIP2/ZIP12 phosphorylation network coordinates Zn allocation in Arabidopsis, providing a potential target for improving Zn deficiency and developing Zn-enriched crop varieties.

The endangered cold-water fish Brachymystax tsinlingensis (B. tsinlingensis) serves as a critical sentinel species for aquatic ecosystem responses to climate change. This study investigates heat stress impacts on behavior, physiology, and molecular homeostasis in B. tsinlingensis, and evaluates neuroprotective effects of anti-stress additives (vitamin C, gamma-aminobutyric acid, trehalose). Behavioral analysis showed a significant increase in center-zone entries under heat stress. Physiological assays showed a reduction in superoxide dismutase (SOD) and catalase (CAT) activities, alongside an upregulation of heat shock protein 70 (Hsp70), glucose-regulated protein 78 (GRP78), and caspase expression under heat stress, with a return to baseline levels following a 12 h recovery. For assays in the brain, histopathological examination identified vacuolation in cerebral tissue after heat stress. Quantitative proteomics analysis identified 831 differentially expressed proteins (DEPs) out of 8,955 proteins during the temperature change process. Pathway analysis revealed that the 'DNA replication' and 'Citrate cycle' pathways were inhibited by heat stress but reactivated during recovery, whereas the 'ECM-receptor interaction' and 'Cell adhesion molecules' pathways exhibited opposite trends. Intervention with additives showed that trehalose enhanced SOD, glutathione peroxidase (GPX), and CAT activities, as well as gene expression related to cell adhesion and barrier function. Gamma-aminobutyric acid maximally suppressed stress-related genes (Hsp70, long-chain-fatty-acid-CoA ligase, and arachidonate lipoxygenase), while vitamin C exhibited general but less targeted effects. As the first proteomic study on B. tsinlingensis, this work reveals that blood-brain barrier reconstruction and energy reallocation are key neural survival strategies under temperature change stress. Furthermore, trehalose demonstrates high potential as an anti-heat stress additive by enhancing both antioxidant defenses and blood-brain barrier integrity. These findings advance our understanding of heat adaptation mechanisms in cold-water fish species and provide scientific foundations for conserving B. tsinlingensis.

The transition from seed to seedling represents a critical developmental phase that determines seedling survival, crop establishment, and yield potential. This intricate developmental process encompasses multiple stages: seed germination beneath the soil surface, the upward growth of etiolated seedlings through the soil environment to reach the soil surface, and subsequent greening to support photoautotrophic growth. The key environmental factors influencing the transition of buried seed to seedling establishment are light, mechanical resistance imposed by soil cover, and the intricate interplay between these factors. Recent studies have significantly enhanced our comprehension of the dynamic and complex nature of this transition: as a seedling pushes upward through the soil, light exposure steadily increases while mechanical resistance gradually decreases. In response, seedlings must orchestrate the initiation of light-regulated developmental processes with adjustments to mechanical stress. This review summarizes the molecular mechanism through which light and mechanical stress interact to facilitate and optimize the transition from seed to seedling in Arabidopsis, with a particular emphasis on deep sowing conditions in rice and maize. Insights into these molecular mechanisms can advance our understanding of the seed-to-seedling biology and contribute to the genetic improvement of crops.

Repeated occurrences of extreme weather events, such as low temperatures, due to global warming present a serious risk to the safety of wheat production. Quantitative assessment of frost damage can facilitate the analysis of key genetic factors related to wheat tolerance to abiotic stress. We collected 491 wheat accessions and selected four image-based descriptors (BLUE band, RED band, NDVI, and GNDVI) to quantitatively assess their frost damage. Image descriptors can complement the visual estimation of frost damage. Combined with genome-wide association study (GWAS), a total of 107 quantitative trait loci (QTL) (r² ranging from 0.75% to 9.48%) were identified, including the well-known frost-resistant locus Frost Resistance (FR)-A1/ Vernalization (VRN)-A1. Additionally, through quantitative gene expression data and mutation experience verification experiments, we identified two other frost tolerance candidate genes TraesCS2A03G1077800 and TraesCS5B03G1008500. Furthermore, when combined with genomic selection (GS), image-based descriptors can predict frost damage with high accuracy (r ≤ 0.84). In conclusion, our research confirms the accuracy of image-based high-throughput acquisition of frost damage, thereby supplementing the exploration of the genetic structure of frost tolerance in wheat within complex field environments.

Ferroptosis has been increasingly implicated in adipose and muscle dysfunction, systemic metabolic disturbances, and several diseases in livestock, which necessitates effective and side-effect-free inhibition strategies. Phloretin, a dihydrochalcone with excellent antioxidant and anti-inflammatory properties, may have the potential to restrain cell ferroptosis. Herein, phloretin was verified to significantly inhibit (1S,3R)-RSL3-induced ferroptosis by reducing intracellular MDA, Fe²⁺, and ROS levels and restoring cell total antioxidant capacity in bovine and mouse preadipocytes or myoblasts. It also alleviated oxidative stress (OS), a vital inducer of ferroptosis, by restoring antioxidant enzyme activity in the above cells and obese mice. In vivo, phloretin gavage significantly reversed the trend where high-fat diet (HFD)-induced OS promoted the expression of ferroptosis-promoting genes and proteins (e.g., ACSL4 and PTGS2) while inhibiting the expression of ferroptosis-negative regulators (e.g., Fth1 and Gpx4). Unlike most flavonoids that exert anti-inflammatory or antioxidant activities by altering the gut microbiota composition, metagenomic sequencing analysis of cecal contents from phloretin-gavaged and HFD mice revealed that phloretin exerts its antioxidative and ferroptosis-inhibitory effects independent of modulating gut microbiota diversity. Further transcriptomic analyses of mouse adipose tissues revealed that phloretin alleviated ferroptosis in adipocytes by modulating the transcription of genes enriched in AMPK and PPAR signaling pathways, such as Camkk2. Hence, based on multi-omics analysis combined with in vivo and in vitro verification, phloretin effectively alleviated the OS to further inhibit ferroptosis of adipose or muscle cells through the AMPK-PPAR pathway, which can provide new research ideas for ameliorating adipose or myocyte dysfunction induced by ferroptosis in animals.