Stress biology最新文献

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.

Cellulose is synthesized by cellulose synthases (CESAs) in plasma membrane-localized complexes, which act as a central component of the cell wall and influence plant growth and defense responses. Puccinia striiformis f. sp. tritici (Pst) is an airborne fungus that causes stripe rust to seriously endanger wheat production. In this study, a CESA gene, TaCESA7, was identified to be significantly up-regulated during Pst infection in wheat (Triticum aestivum L.). TaCESA7 was localized on the plasma membrane in dimeric form, and the dimers interact to assemble into CESA complexes. Stable overexpression of TaCESA7 weakened the resistance of wheat to Pst. Knockdown of TaCESA7 by RNA interference (RNAi) and virus-induced gene silencing led to restricted hyphal spread, increased necrotic area, and simultaneously promotes reactive oxygen species (ROS) accumulation and the expression of pathogenesis-related (PR) genes. Transcriptome analysis of TaCESA7-RNAi plants revealed that the up-regulated genes were significantly enriched in the phenylpropanoid biosynthesis and plant-pathogen interaction pathways. Moreover, silencing TaCESA7 promoted the deposition of lignin and the expression of genes related to lignin synthesis. CRISPR-Cas9-mediated inactivation of TaCESA7 in wheat could confer broad-spectrum resistance against Pst without affecting agronomic traits. These findings provide valuable candidate gene resources and guidance for molecular breeding to improve the resistance of wheat to fungal disease.

Receptor-like cytoplasmic kinases (RLCKs) function as a central player in plant receptor kinases-mediated signaling, which regulate various aspects of plant immunity and growth. RLCKs receive signals from pattern recognition receptors (PRRs) to activate pattern-triggered immunity (PTI), including reactive oxygen species (ROS) production, Ca²⁺ influx, mitogen-activated protein kinase (MAPK) cascades, cellulose synthesis, phosphatidic acid (PA) production, hormone synthesis and signaling, and transcriptional remodeling. Besides, RLCK also participate in effector-triggered immunity (ETI) and the interplay between ETI and PTI. Increasing evidences show that much more RLCKs are involved in plant immune responses and form an intertwined signaling network. This review summarizes the recent findings about RLCKs-mediated signaling in plant immune responses and emphasizes signal convergence and divergence involved which provides new insights into the RLCKs signaling network in diverse biological processes.

During interactions, pathogenic fungi are subjected to endoplasmic reticulum (ER) stress from the host plants, resulting in the activation of the unfolded protein response (UPR) pathway. We identified the bZIP transcription factor CfHac1 in C. fructicola, which is a pathogenic organism implicated in a variety of plant diseases, and we found it to be crucial for the ER stress response and pathogenicity. However, the role of CfHac1 in regulating the degradation of ER-associated misfolded proteins remains unclear. In this study, we discovered that the CfHAC1 gene regulates conidial production, appressorium formation, response to ER stress, and pathogenicity through unconventional splicing. Further research revealed that the CfHAC1 gene also affects the ubiquitination of ER-associated misfolded proteins and mediates their degradation. We further identified two ubiquitin ligase genes, CfHRD1 and CfHRD3, that exhibit significant down-regulation in the ΔCfhac1 mutant strain. Subsequent investigations revealed that the CfHAC1 gene affects CfHRD1 and CfHRD3 expression through unconventional splicing, with both genes managing the degradation of ER-associated misfolded proteins via ubiquitination and influencing C. fructicola pathogenicity. Taken together, our results reveal a mechanism by which the transcription factor CfHac1 affects the expression of the ubiquitin ligase genes CfHRD1 and CfHRD3, leading to the ubiquitination and degradation of ER-associated misfolded proteins and pathogenicity. This provides a theoretical basis for the development of novel agents targeting key genes within this pathway.

Trail development is more prevalent as tourism develops globally. The depth effect of trail development on plant diversity and native species' stress response via tuning flavonoids in natural ecosystems remain relatively poorly understood. We investigated the depth effects by comparing plant species diversity and flavonoid contents (of six common native species) in sampling plots plots (Rabbit Mountain Open Space, Boulder County, CO, USA) with varying distances away from trail. We found plant diversity to be lowest in plots immediately proximal to trails and highest in intermediate plots. We also found the concentrations of total flavonoids to vary significantly between plots closer and away from trails. Specifically, we found the concentrations of isoorientin and myricetin higher in plots closer to trails. On the contrary, the concentrations of vitexin and kaempferol were higher in plots away from trails. Quercetin was higher in the intermediate plots. Overall, trail development negatively impacted herbaceous plant diversity, which was evident as depth effects. The plant species responded to environmental stresses imposed by trail development through fine-tuned flavonoid accumulation.