Stress biology最新文献

Environmental stress adaptation is crucial for the survival and pathogenicity of plant fungal pathogens. In this study, we identified a transcription factor FgMsn2 in Fusarium graminearum, an ortholog of Msn2 in budding yeast. Structural analysis showed that the C2H2 zinc-finger domain is highly conserved across fungi, while other regions are less conserved, suggesting that FgMsn2 may have species-specific functions. Subsequently, we revealed that FgMsn2 is critical for vegetative growth, and conidiogenesis. Deletion of FgMSN2 severely reduced the deoxynivalenol (DON) production and pathogenicity, while enhancing tolerance to oxidative, osmotic, cell wall and membrane stresses. Furthermore, our RNA-seq analysis revealed that FgMsn2 regulates genes involved in energy metabolism, lipid metabolism and stress responses, emphasizing its role in maintaining metabolic balance and stress adaptability. Notably, FgMsn2 influences mitochondrial morphology, as the Fgmsn2 mutant exhibited disrupted mitochondrial structures and reduced ATP production. The Fgmsn2 mutant also showed increased lipid droplet accumulation, indicating the FgMsn2's role in lipid metabolism. Taken together, the FgMsn2 serves as a key regulator in fungal development, plant infection, stress responses, and metabolism. Our study provides valuable insights into the molecular mechanisms of fungal stress adaptation and pathogenicity, suggesting a potential target for the development of more effective fungicides and disease management strategies.

Cucumber target spot, a major disease that threatens cucumber production, is caused by Corynespora cassiicola. Cyclobutrifluram, a novel succinate dehydrogenase inhibitor (SDHI) developed by Syngenta, has demonstrated strong inhibitory activity against various plant pathogenic fungi and nematodes. However, its antifungal spectrum, resistance risk as well as underlying mechanisms of resistance in C. cassiicola remain poorly understood. In this study, cyclobutrifluram exhibited potent inhibitory activity against anamorphic fungi and selected ascomycetes, with the mean sensitivity of C. cassiicola isolates to the fungicide being 0.98 ± 1.26 μg/mL. Additionally, five laboratory-derived cyclobutrifluram-resistant mutants showed comparable or lower biological fitness than their respective parental isolates. The resistant mutants and field isolates were also found to possess nine distinct point mutations in the CcSdhB, CcSdhC or CcSdhD genes. Finally, cyclobutrifluram exhibited positive cross-resistance with other SDHIs, with the resistance levels varying depending on the specific mutations present. In conclusion, cyclobutrifluram was found to be effective against anamorphic fungi and selected ascomycetes. C. cassiicola's risk of resistance development to cyclobutrifluram was assessed as moderate to high and was primarily associated with mutations in CcSdh genes.

Crown rot (CR), caused by Fusarium pseudograminearum and related species, is a soil-borne disease threatening global wheat (Triticum aestivum) production, with yield losses exceeding 50% under severe infections. The rapid spread of CR in China, driven by straw retention policies and warming climates, highlights the need for interdisciplinary solutions. This review systematically integrates advances in CR research and addresses pathogen biology, host resistance, and sustainable management. Research on pathogen biology has clarified the distribution of major Fusarium species, the infection process, toxin profiles, mating types, and virulence factors. Host resistance to CR is quantitatively controlled, and through quantitative trait locus (QTL) mapping and omics-based approaches, several genes encoding transcription factors, receptor-like kinases and enzymes, signaling pathways and secondary metabolites involved in resistance have been identified. Advances in control strategies, including chemical and biological methods, as well as the application of nanotechnology, have shown promising results. The review also highlights future research directions, such as investigating the molecular mechanisms of pathogen-host interactions, identifying effectors and susceptibility genes for CR in wheat, and integrating multi-omics studies with high-resolution genetic maps to pinpoint CR resistance genes. These efforts are crucial for improving our understanding of the disease and developing effective management strategies.

Apple replant disease (ARD) poses a serious threat to apple cultivation, primarily caused by the accumulation of Fusarium species. Bacillus species have demonstrated significant potential as microbial agents, with capabilities in promoting plant growth, suppressing soil-borne pathogens, and improving soil quality. Here in this study, strain LRB-5 was isolated from a healthy apple root system and identified as Bacillus vallismortis based on physiological and biochemical characterization and molecular sequencing analysis. It exhibited broad-spectrum antifungal activity against various Fusarium species, including F. oxysporum, F. moniliforme, F. proliferatum, and F. solani, with inhibition rates exceeding 65%. LRB-5 extracellular metabolites significantly inhibited Fusarium mycelial growth and spore germination. Greenhouse experiments demonstrated that LRB-5 reduced ARD disease severity by more than 50%. The volatile organic compounds produced by LRB-5 exhibited both antimicrobial activity and growth-promoting properties. Further assays revealed LRB-5 can secrete various cell wall-degrading enzymes and possesses plant growth-promoting capabilities. Pot experiments showed LRB-5 had excellent colonization ability in the rhizosphere of Malus hupehensis Rehd. seedlings, significantly increasing seedling biomass, soil bacterial and actinomycete populations, and the activity of root protective enzymes. Moreover, LRB-5 significantly enhanced the activity of soil enzymes while reducing the contents of phlorizin, benzoic acid, and p-hydroxybenzoic acid in the rhizosphere soil. Terminal restriction fragment length polymorphism and quantitative real-time PCR analyses revealed that LRB-5 improved bacterial carbon utilization, increased microbial diversity indices, reduced the abundance of Fusarium spp., and altered the structure of soil microbial communities. Collectively, these rusults suggest that LRB-5 effectively alleviated ARD by protecting apple roots from Fusarium infection and phenolic acid toxicity, optimizing soil microbial communities, and promoting plant growth. Future research should explore the combined application of LRB-5 with other control measures, thereby promoting its practical implementation.

Wall-associated receptor kinases (WAKs) and WAK-likes (WAKLs) play pivotal roles in regulating plant immunity, through multiple downstream signaling components. However, knowledge of WAKs/WAKLs in wheat immune responses to rust diseases remain limited. In this study, we identified and characterized a wheat WAKL, TaWAKL8-2B, which is upregulated during wheat resistance to both Puccinia striiformis f. sp. tritici (Pst) and Puccinia triticina (Ptt), indicating its role in wheat resistance to these two rust fungi. Transgenic wheat plants overexpressing TaWAKL8-2B exhibited enhanced resistance to stripe rust and leaf rust, accompanied by increased reactive oxygen species (ROS) production and up-regulated defense-related gene expression. Whereas, knockout TaWAKL8-2B reduced resistance to Pst and Ptt with less ROS accumulation, highlighting its positive role in wheat resistance. RNA-seq analysis revealed that 33 genes encoding ROS-scavenging enzymes were upregulated in TaWAKL8-2B-KO plants, explaining the reduced ROS. KEGG analysis enriched the monoterpenoid pathway, particularly the linalool biosynthesis pathway, with linalool synthases significantly downregulated in TaWAKL8-2B-KO plants. Correspondingly, linalool synthase content and linalool content decreased in knockout plants. Collectively, our findings uncover a novel mechanism by which TaWAKL8-2B positively modulates wheat rust resistance through modulating linalool biosynthesis and peroxidase activity. These results enhance our understanding of TaWAKL8-2B mediated immune signaling and offer a promising gene for improving wheat broad-spectrum resistance to rust diseases.

Heat stress (HS) disrupts intestinal homeostasis and hepatic lipid metabolism in poultry, yet effective interventions remain limited. We investigate the protective effects of dietary glycerol monolaurate (GML) supplementation in laying hens under HS conditions. In a 10-week trial, 504 Hy-Line Brown hens were assigned to four groups (control and GML at 65, 195, and 325 mg/kg) with six replicates per group. Hens receiving 325 mg/kg GML exhibited significantly higher egg production and egg weight (P < 0.05), alongside improved egg quality metrics, including increased shell strength and Haugh units by week 8 (P < 0.05). Histological analysis revealed that GML (325 mg/kg) improved duodenal and ileal villus height and duodenal villus-to-crypt ratios while reducing duodenal crypt depth (P < 0.05), thereby restoring gut barrier integrity. These findings were supported by reduced plasma D-lactate (D-LA) levels and upregulated expression of tight-junction proteins ZO-1 and Occludin in the ileum and jejunum (P < 0.05). In the liver, GML supplementation alleviated HS-induced steatosis, reducing lipid droplet accumulation (P < 0.05), plasma low-density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels, and hepatic triglyceride content, while elevating high density lipoprotein cholesterol (HDL-C). Integrated plasma metabolomics and hepatic transcriptomics identified 36 differential metabolites (enriched in sphingolipid metabolism) and 1,176 differentially expressed genes (enriched in PPAR signaling and Fatty acid degradation), with ACSL1 as a central regulatory gene. Key genes (ACSL1, CPT1 A) and metabolites correlated positively with production performance and gut-liver health, while SCD and Probucol showed negative associations. These findings indicate that GML supplementation enhances intestinal barrier function, promotes hepatic fatty acid β-oxidation, and reinforces sphingolipid metabolism, thereby mitigating HS-induced oxidative stress and lipid dysregulation. Our results identify 325 mg/kg GML as the optimal dosage, proposing a practical strategy to enhance poultry resilience during heat stress.

Fusarium head blight (FHB, also known as wheat scab or ear blight), caused primarily by the Fusarium graminearum, is a worldwide disease of wheat (Triticum aestivum L.). Studying the pathogen expansion patterns and molecular mechanisms of disease resistance in resistant wheat varieties is crucial for advancing wheat disease management strategies. Here, we found a significant difference between two wheat cultivars with different resistances, and it was revealed that they exhibited divergent pathogen infestation process. The susceptible cultivar showed extensive pathogen in the spike rachis, while resistant varieties only had limited pathogen spread and colonization. Meanwhile, wheat resistance to FHB was positively correlated with transcriptional reprogramming in the early stages, with higher expression of genes responding to plant defense related genes and phenylpropanoid pathway genes in the early stages of disease resistant variety. Weighted gene co-expression network analysis (WGCNA) of differential expression genes (DEGs) analysis led to the construction of a network modules associated with resistance genes, and an important role of heavy metal-associated (HMA) domain protein in plant defense was identified in the tan module. RNA-induced gene silencing preliminarily identified two key genes that resistance to FHB in wheat: a cytochrome P450 (CYP) gene involved in the flavonoid biosynthesis within the phenylpropanoid pathway and HMA gene. This study provides an in-depth analysis of the infection mechanisms of wheat by F. graminearum and elucidates the key molecular mechanisms involved, while being useful for advancing the breeding of wheat varieties resistant to FHB.

Given that lactoferrin (LF) exerts an excellent protection of intestinal homeostasis, the underlying mechanisms, especially epigenetic regulations, are still unknown. This study aimed to investigate the effects of dietary LF epigenetically modulates the oxidative genes by histone modifications to ameliorate ileum inflammation of mice exposed to DON contaminated diet. As expected, we found in the morphology analysis that DON exposure increased ileum crypt depth (CD) and villus width (VW) but reduced villus height (VH) and VH: CD ratio compared to those of the vehicle group. Consistently, the elevated ROS and MDA, along with the decreased ATP, SOD, CAT, GSH, and complex I, III, V were observed in the DON-exposed mice ileum. In contrast, LF markedly ameliorated the impairments of morphological and biochemical indexes. Next, we conducted transcriptome analysis to explore the changed signaling pathways using the ileum RNA of the mice treated with DON or LF. Firstly, the cell cycle pathway genes were significantly downregulated in the DON-exposed mice, and LF improved the cell cycle profile. Again, gene ontology analysis showed that inflammation and oxidative stress were significantly activated by DON exposure, and these were recovered when the DON-exposed mice were supplemented with an LF diet. Consistent with these findings, the signaling pathways of the reduced oxidative phosphorylation and elevated TNFα were also observed to be ameliorated by LF treatment. Importantly, histone modifications, including acetylation, methylation, and lactylation were suggested to be the vital players involved in the DON or LF treatment, in which LF significantly increased the loss of histone modifications on these genes. With a bioinformatics analysis and validation by qRT-PCR, the nuclear receptor NR5A2 was selected as a key master in the ileum of mice stimulated by DON. LF performed the benefit function on the NR5A2-mediated oxidative stress genes Ncoa4 and Prdx3 in the DON-exposed mice. Moreover, a ChIP-qPCR was used to verify that histone marks involving H3K9ac, H3K18ac, H3k27ac, H3K4me1, H3K9la, and H3K18la facilitated the epigenetic regulation of NR5A2-modulated actions. We conclude that dietary LF effectively ameliorated ileum lesions induced by DON in mice by modulating oxidative genes Ncoa4 and Prdx3 through histone modifications.

Heat stress (HS) is a major environmental stress that inhibits plant growth and development. Plants have evolved various mechanisms to cope with heat stress, a key one being the HSF-HSP (Heat stress transcription factor-Heat shock protein) signaling pathway. HSFs can be divided into three classes: A, B, and C. In this study, we report the identification and functional characterization of a specific B2 member LdHSFB2a in Lilium davidii var. unicolor. RT-qPCR (Real-time Quantitative Polymerase Chain Reaction) analyses indicated that LdHSFB2a was highly expressed in HS-exposed leaves. LdHSFB2a was localized in the nucleus, consistent with the characterization of transcription factors. In contrast to other HSFBs, LdHSFB2a did not contain the typical B3 repression domain but exhibited transcriptional repression activity in yeast and plant cells. Transient overexpression and virus-induced gene silencing (VIGS) of LdHSFB2a in lily petals suggested that LdHSFB2a functions positively in lily thermotolerance. Consistent with the implication of LdHSFB2a function in thermotolerance, further analysis revealed that the expression levels of HSFA1, HSFA2, and MBF1c were increased as LdHSFB2a was overexpressed but reduced as LdHSFB2a was silenced. Furthermore, LdHSFB2a bound to the promoters of HSFA3 A, WRKY33, CAT2, and GLOS1. And LdHSFB2a overexpression and silencing enhanced and reduced their expressions, respectively. Therefore, we speculated that LdHSFB2a may be a coactivator that interacts with transcriptional activators to promote thermotolerance in lily by enhancing the expression of heat-responsive genes such as HSFA3 A, WRKY33, CAT2, and GLOS1.

Soil salinization and alkalization have become an increasingly severe global issues, significantly limiting both the yield and quality of apples (Malus × domestica). M9-T337 is a widely used apple dwarfing rootstock; however, it is sensitive to saline-alkali stress. Therefore, developing saline-alkali tolerant apple rootstocks is essential. In this study, we utilized RNAi (RNA interference) technology to knock down GH3 genes in the M9-T337 background, aiming to engineer a dwarfing and stress-tolerant apple rootstock. We found that MdGH3 RNAi plants exhibited superior morphology compared to M9-T337 under saline-alkali stress conditions, characterized by more robust root systems, increased plant height, a lower Na⁺/K⁺ ratio, and enhanced photosynthetic and antioxidant capacities. Moreover, when MdGH3 RNAi plants were used as rootstocks, the GL-3/MdGH3 RNAi plants also displayed greater plant height, root vitality, photosynthetic ability, and antioxidant capacity compared to GL-3 grafted onto M9-T337 rootstock. Taken together, our study constructed a saline-alkali-tolerant apple rootstock by knocking down MdGH3 genes.