Stress biology最新文献

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.

Phytophthora pathogens are devastating agricultural threats that cannot synthesize sterols and must scavenge them from host plants. This study exploits their sterol auxotrophy by engineering a dual-function elicitin protein, SOJ5^V84F, for enhanced disease control. The V84F mutation in the sterol-binding pocket of the Phytophthora sojae elicitin SOJ5 abolishes sterol binding but retains interaction with the pathogen's sterol-sensing receptor kinase SSRK1. SOJ5^V84F acts as a dominant-negative inhibitor: it competitively disrupts SSRK1-mediated sterol signaling (calcium influx, MAPK activation) and significantly inhibits P. sojae growth in an SSRK1-dependent manner. Crucially, SOJ5^V84F retains its ability as a microbe-associated molecular pattern to robustly elicit reactive oxygen species burst in soybean, pepper, tomato, and potato plants. Consequently, pre-treatment with SOJ5^V84F provided superior protection compared to wild-type SOJ5 against P. sojae in soybean, and against Phytophthora capsici and Phytophthora infestans in pepper, tomato, and potato under greenhouse conditions. This work demonstrates that engineered SOJ5^V84F combines direct pathogen inhibition with host immune activation, establishing a novel dual-mechanism strategy for protein-based biocontrol against sterol-auxotrophic oomycetes.

Drought, high salinity, and low temperatures impose osmotic stress, hindering water uptake and severely limiting plant growth and crop productivity. Osmotic stress not only perturbs cellular osmotic homeostasis but also disrupts multiple metabolic processes, including reactive oxygen species (ROS) metabolism. However, the transcriptional regulation underlying these redox processes in plants remains poorly understood. Here, we report that rice NAC WITH TRANS-MEMBRANE MOTIF1- LIKE 2 (OsNTL2) is required for tolerance to salt and osmotic stresses. DNA affinity purification-sequencing (DAP-seq) revealed that OsNTL2 directly targets key genes in the ascorbate-glutathione (ASC-GSH) redox cycle, including ascorbate peroxidase 2 (APX2), monodehydroascorbate reductase 1 (MDHAR1), glutathione reductase 2 (GR2), and glutathione peroxidase 5 (GPX5), as well as peroxidase 3/70 (PRX3/70), which function in the hydrogen peroxide catabolic process. Consistently, OsNTL2 activity was associated with enhanced ASC-GSH cycle enzyme activities, elevated ASC and GSH contents, and reduced ROS accumulation, as confirmed by histochemical staining. Furthermore, integrating DAP-seq with transcriptome analysis, we identified 325 direct transcriptional targets of OsNTL2, with a significant enrichment of genes involved in lignin and xylan biosynthesis. Notably, OsNTL2 bound directly to the promoters of, 4-coumarate-CoA ligase 5 (Os4CL5), and cinnamoyl-CoA reductase (OsCCR), activating their transcription. Correspondingly, stress-induced lignin, xylan, and cellulose accumulation was markedly reduced in ntl2 mutants but enhanced in OsNTL2-overexpressing lines. Together, these findings identify OsNTL2 as a key transcriptional regulator that coordinates the ASC-GSH redox cycle and cell wall biosynthesis to confer osmotic stress tolerance in rice.

The occurrence of apple replant disease (ARD) is closely related to the increase of soil pathogenic fungi abundance. However, the relationship between ARD and fungal community structure remains poorly understood. In this study, Illumina high-throughput sequencing was used to investigate the composition, diversity, and function of rhizosphere fungal communities associated with healthy (HRS) and diseased apple trees (DRS). Microbial taxa related to ARD were also identified. The severity of ARD varied among the sampled orchards. We found that Ascomycota was the dominant phylum in the DRS fungal taxa, and the fungal community abundance and Simpson index of DRS were significantly higher than those of HRS. Cluster and FUNGuild database analyses revealed significant differences in the relative abundance and function of fungal taxa between DRS and HRS. Most fungi isolated from DRS were plant pathogens, predominantly from the genus Fusarium (Ascomycota, Nectriaceae), which was also the predominant fungal genus detected in DRS. In contrast, Mortierella was more abundant in HRS. To validate the sequencing results, Fusarium isolates, including F. proliferatum, F. oxysporum, and F. solani, were verified as pathogens and showed high virulence. Structural equation modeling indicated that the occurrence of ARD was directly or indirectly influenced by Fusarium, Mortierella, phloridin, available phosphorus, and soil organic matter. Further research is needed to elucidate how soil parameters affect ARD. Laboratory tests demonstrated that F. proliferatum MR5 can produce pectinase and cellulase and is sensitive to two fungicides: flusilazole and bromothalonil. In conclusion, the deterioration of rhizosphere fungal community structure may be a key biological factor driving ARD, with Fusarium in DRS identified as a major causative agent of ARD in China. The findings of this study provide valuable insights for developing preventive strategies against ARD.