Transcriptome analysis highlights the influence of temperature on hydrolase and traps in nematode-trapping fungi.

Pine wilt disease caused by Bursaphelenchus xylophilus poses a serious threat to the economic and ecological value of forestry. Nematode trapping fungi trap and kill nematodes using specialized trapping devices, which are highly efficient and non-toxic to the environment, and are very promising for use as biological control agents. In this study, we isolated several nematode-trapping fungi from various regions and screened three for their high nematocidal efficiency. However, the effectiveness of these fungi as nematicides is notably influenced by temperature and exhibits different morphologies in response to temperature fluctuations, which are categorized as "NA," "thin," "dense," and "sparse." The trend of trap formation with temperature was consistent with the trend of nematocidal efficiency with temperature. Both of which initially increased and then decreased with increasing temperature. Among them, Arthrobotrys cladodes exhibited the highest level of nematocidal activity and trap formation among the tested species. Transcriptome data were collected from A. cladodes with various trap morphologies. Hydrolase activity was significantly enriched according to GO and KEGG enrichment analyses. Eight genes related to hydrolases were found to be consistent with the trend of trap morphology with temperature. Weighted gene co-expression analysis and the Cytoscape network revealed that these 8 genes are associated with either mitosis or autophagy. This suggests that they contribute to the formation of "dense" structures in nematode-trapping fungi. One of these genes is the serine protein hydrolase gene involved in autophagy. This study reveals a potentially critical role for hydrolases in trap formation and nematocidal efficiency. And presents a model where temperature affects trap formation and nematocidal efficiency by influencing the serine protease prb1 involved in the autophagy process.

Xylanase Supplement Enhances the Growth Performance of Broiler by Modulating Serum Metabolism, Intestinal Health, Short-Chain Fatty Acid Composition, and Microbiota.

This study aimed to investigate the effects of different levels of xylanase supplementation in a wheat-based diet on growth performance, short-chain fatty acids, intestinal health, microbial composition, and serum metabolism. A total of 1200 male chicks were randomly assigned to four wheat-based diet treatments: Group C (adding 0 mg/kg of xylanase), Group L (adding 50 mg/kg of xylanase), Group M (adding 100 mg/kg of xylanase), and Group H (adding 150 mg/kg of xylanase). The experiment lasted for 56 days. The results indicated that Group H broilers experienced a decreased feed-to-gain ratio throughout the study period. Additionally, dietary supplementation with xylanase led to an increase in the physical barrier, as indicated by increased VH and VH/CD in the gut (p < 0.05). Furthermore, levels of D-lactic acid and endotoxin were reduced. Xylanase supplementation also increased the abundance of Muc-2, ZO-1, and Occludin (p < 0.05). Moreover, xylanase supplementation enhanced the activity of sucrase and maltase in the duodenum (p < 0.05), which may be attributable to the upregulation of the abundance of SI and MGA (p < 0.05). Furthermore, xylanase addition promoted propionic acid produced by specific bacteria, such as Phascolarctobacterium, and influenced the microbial composition to some extent, promoting intestinal health. Additionally, 150 mg/kg of xylanase supplementation increased the amino acid, peptide, and carbohydrate content and upregulated the metabolism of amino acids related to histidine, cysteine, methionine, and other pathways (p < 0.05). These findings suggest adequate xylanase supplementation can enhance nutritional digestibility and absorption, improve growth performance, stimulate endogenous enzyme activity, optimize intestinal morphology and barrier function, and positively influence acid-producing bacteria and amino acid metabolic pathways.

Selenomethionine Attenuated H2O2-Induced Oxidative Stress and Apoptosis by Nrf2 in Chicken Liver Cells.

Earlier studies have shown that selenomethionine (SM) supplements in broiler breeders had higher deposition in eggs, further reduced the mortality of chicken embryos, and exerted a stronger antioxidant ability in offspring than sodium selenite (SS). Since previous studies also confirmed that Se deposition in eggs was positively correlated with maternal supplementation, this study aimed to directly investigate the antioxidant activities and underlying mechanisms of SS and SM on the chicken hepatocellular carcinoma cell line (LMH). The cytotoxicity results showed that the safe concentration of SM was up to 1000 ng/mL, while SS was 100 ng/mL. In Se treatments, both SS and SM significantly elevated mRNA stability and the protein synthesis rate of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), two Se-containing antioxidant enzymes. Furthermore, SM exerted protective effects in the H2O2-induced oxidant stress model by reducing free radicals (including ROS, MDA, and NO) and elevating the activities of antioxidative enzymes, which performed better than SS. Furthermore, the results showed that cotreatment with SM significantly induced apoptosis induced by H2O2 on elevating the content of Bcl-2 and decreasing caspase-3. Moreover, investigations of the mechanism revealed that SM might exert antioxidant effects on H2O2-induced LMHs by activating the Nrf2 pathway and enhancing the activities of major antioxidant selenoenzymes downstream. These findings provide evidence for the effectiveness of SM on ameliorating H2O2-induced oxidative impairment and suggest SM has the potential to be used in the prevention or adjuvant treatment of oxidative-related impairment in poultry feeds.

Carboxymethyl konjac glucomannan-chitosan complex nanogels stabilized emulsions incorporated into alginate as microcapsule matrix for intestinal-targeted delivery of probiotics: In vivo and in vitro studies.

In this study, we developed a novel delivery system using carboxymethyl konjac glucomannan-chitosan (CMKGM-CS) nanogels stabilized single and double emulsion incorporated into alginate hydrogel as microcapsule matrix for intestinal-targeted delivery of probiotics. Through in vitro experiments, it was demonstrated that alginate hydrogel provided favorable biocompatible growth conditions for the proliferation of Lactobacillus reuteri (LR). The alginate hydrogel containing single (ASE) or double emulsions (ACG) enhanced the resistance of LR to various adverse environments. Simulated gastrointestinal digestion experiments revealed that the survivability of LR in free, CON, ASE and ACG group decreased by 6.45 log CFU/g, 4.21 log CFU/g, 1.26 log CFU/g and 0.65 log CFU/g, respectively. In vivo studies conducted in mice showed that ACG maintained its integrity during passage through the stomach and released the probiotics in the targeted intestinal area, whereas the pure alginate hydrogels (CON) were prematurely released in the gastrointestinal tract. Moreover, the viable counts of ACG in different intestinal segments (jejunum, ileum, cecum, and colon) were increased by 1.11, 1.42, 1.68, and 1.89 log CFU/g, respectively, after 72 h of oral administration compared to the CON group. This research contributed valuable insights into the development of an effective microbial delivery system with potential applications in the biopharmaceutical and food industries.

SIRT3 attenuates doxorubicin-induced cardiotoxicity by inhibiting NLRP3 inflammasome via autophagy.

Doxorubicin (DOX) is a highly effective and extensively used chemotherapeutic drug but is limited by its cardiotoxicity. In our previous study, we showed that DOX-induced cardiotoxicity (DIC) triggers autophagy and pyroptosis. Sirtuin 3(SIRT3) is an NAD + -dependent deacetylase of the mitochondria that regulates autophagy. However, it is unknown if the protective effects of SIRT3 on DOX-induced cardiotoxicity involve the inhibition of NLRP3 inflammasome activation. In this study, we constructed in vivo and in vitro DIC models to investigate the effects and potential mechanisms of SIRT3 on DIC. We found that the overexpression of SIRT3 remarkably attenuated DIC through inhibition of the NLRP3 inflammasome. Moreover, we found that the overexpression of SIRT3 restored the dynamic balance of autophagosome/autolysosomes by targeting the mTOR/ULK1 signaling pathway. Application of the mTOR agonist MHY1485 further demonstrated that SIRT3 inhibited NLRP3 inflammasome activation by regulating autophagy. Collectively, the results suggest that SIRT3 effectively attenuates the cardiotoxicity of DOX and provides a theoretical foundation for further exploration of DIC.

Antioxidant processes involving epicatechin decreased symptoms of pine wilt disease.

Since the pine wood nematode (PWN, Bursaphelenchus xylophilus) invasion of Northeast China, both symptomatic and asymptomatic PWN carriers have been found. Asymptomatic PWN carriers, which are more dangerous than symptomatic carriers, constitute a source of infection in the following spring. The simultaneous presence of symptomatic and asymptomatic PWN carriers indicates that Pinus koraiensis has different tolerance levels to PWN. In this study, validity of susceptibility testing discovered differential types of P. koraiensis including Latent Reservoirs, Low Susceptibles, High Susceptibles and Bell Ringers. Among those types, the Low Susceptibles and Latent Reservoirs were asymptomatic PWN carriers, and Latent Reservoirs were the most dangerous. Transcriptome and metabolomic data showed that 5 genes (3 ans and 2 anr gene) involved in the epicatechin (EC) synthesis pathway were significantly upregulated, which increased the content of EC antioxidants in Latent Reservoirs. Hydrogen peroxide (H2O2) staining and content determination showed that the hypersensitive response (HR) and H2O2, which functions as a signaling molecule in systemic acquired resistance, decreased in Latent Reservoirs. However, low contents of EC and high contents of H2O2 were found in the High Susceptibles of P. koraiensis. RT-PCR results showed that the expression of ans and anr was upregulated together only in Latent Reservoirs. These results show that the susceptibility of P. koraiensis to PWN differed among different individuals, although no resistant individuals were found. Latent Reservoirs, in which more PWNs resided without visible symptoms via prolonged incubation period, inhibited the symptoms caused by H2O2 because of increased contents of the EC antioxidants.

LCZ696 protects against doxorubicin-induced cardiotoxicity by inhibiting ferroptosis via AKT/SIRT3/SOD2 signaling pathway activation.

Doxorubicin (DOX) is an effective and widely used anticancer drug but has limited clinical applicability because of its cardiotoxicity. Ferroptosis plays a key role in DOX-induced cardiac damage and cardiomyocyte cell death. The inhibition of ferroptosis reverses DOX-induced cardiotoxicity (DIC). LCZ696, a first-in-class angiotensin receptor neprilysin inhibitor, protects against DIC. However, the mechanism of action of LCZ696, especially its effect on ferroptosis, is incompletely understood. This study investigates the cardioprotective effects of LCZ696 on DIC in vivo and in vitro.Cardiotoxicity was induced in Wistar rats by tail intravenous injection of 2.5 mg/kg DOX once a week for six weeks. Rats and H9c2 cells were treated with or without LCZ696 to determine the cardioprotective role and underlying mechanisms of LCZ696 against DIC. To assess the role of SIRT3 and correlated pathways in ferroptosis, SIRT3 knockout was performed using lentiviral vectors, and AKT was inhibited with LY294002. LCZ696 significantly attenuated DIC by decreasing the concentrations of lipid reactive oxygen species and malondialdehyde and increasing the levels of glutathione peroxidase-4 and reduced glutathione in cells and heart tissues. Moreover, LCZ696 remodeled myocardial structures and improved heart ventricular function in DOX-treated rats. LCZ696 treatment increased SIRT3 expression and deacetylated its target gene SOD2, and these changes were mediated by AKT activation. SIRT3 knockdown and AKT inhibition induced lipid peroxidation and reduced the protective effect of LCZ696 in H9c2 cells. Collectively,LCZ696 prevents DIC by inhibiting ferroptosis via AKT/SIRT3/SOD2 signaling pathway activation. Thus, LZC696 is a potential therapeutic strategy for DIC.

Bacterial Metabolite Reuterin Attenuated LPS-Induced Oxidative Stress and Inflammation Response in HD11 Macrophages.

Reuterin is well-known for its broad-spectrum antimicrobial ability, while the other potential bioactivity is not yet clear. The present study aims to investigate the immunomodulatory activity of reuterin on chicken macrophage HD11 cells for the first time and evaluate whether reuterin is able to regulate the lipopolysaccharide-stimulated inflammatory response. The results showed that the safe medication range of reuterin was less than 250 µM. Reuterin treatment for 6 h decreased the transcriptional of CD86, IL-1ß and iNOS and increased the expression of CD206 in a dose-dependent way, but reuterin treatment for 12 h contrary increased the expression of IL-1ß, IL-6 and IL-10. However, it was noticed that reuterin treatment for 12 h significantly decreased the production of reactive oxygen species (ROS) and suppressed the phagocytosis activity of HD11 macrophages against bacteria. Further, the results showed that preincubation or coincubation with reuterin significantly attenuated the promotive effects of lipopolysaccharide (LPS) on transcription of proinflammatory cytokines (including IL-1ß, IL-6 and TNF-α) and obviously inhibited nitric oxide (NO) production as well as the protein expression of inducible nitric oxide synthase (iNOS). Meanwhile, Mechanism studies implied that reuterin might exert an anti-inflammatory effect on LPS-stimulated cells by downregulating the expression of TLR4/MyD88/TRAF6 and blocking the activation of NF-κB as well as MAPKs signaling pathways. Additionally, it was found that both pretreatment and cotreatment with reuterin remarkably inhibited the oxidative stress induced by LPS stimulation by activating the Nrf2/HO-1 signaling pathway and enhancing the activities of antioxidative enzymes. These findings suggested the immunoregulatory function of reuterin and indicated this bacterial metabolite was able to inhibit the inflammation and oxidative stress of HD11 macrophages once exposed to LPS stimulation.

Mechanisms Underlying the Protective Effect of Maternal Zinc (ZnSO4 or Zn-Gly) against Heat Stress-Induced Oxidative Stress in Chicken Embryo.

Environmental factors such as high temperature can cause oxidative stress and negatively affect the physiological status and meat quality of broiler chickens. The study was conducted to evaluate the effects of dietary maternal Zn-Gly or ZnSO4 supplementation on embryo mortality, hepatocellular mitochondrial morphology, liver antioxidant capacity and the expression of related genes involved in liver oxidative mechanisms in heat-stressed broilers. A total of 300 36-week-old Lingnan Yellow broiler breeders were randomly divided into three treatments: (1) control (basal diet, 24 mg zinc/kg); (2) inorganic ZnSO4 group (basal diet +80 mg ZnSO4/kg); (3) organic Zn-Gly group (basal diet +80 mg Zn-Gly/kg). The results show that maternal zinc alleviated heat stress-induced chicken embryo hepatocytes' oxidative stress by decreasing the content of ROS, MDA, PC, 8-OHdG, and levels of HSP70, while enhancing T-SOD, T-AOC, CuZn-SOD, GSH-Px, CTA activities and the content of MT. Maternal zinc alleviated oxidative stress-induced mitochondrial damage in chick embryo hepatocytes by increasing mitochondrial membrane potential and UCP gene expression; and Caspase-3-mediated apoptosis was alleviated by increasing CuZn-SOD and MT gene expression and decreasing Bax gene expression and reducing the activity of caspase 3. Furthermore, maternal zinc treatment significantly increased Nrf2 gene expression. The results above suggest that maternal zinc can activate the Nrf2 signaling pathway in developing chick embryos, enhance its antioxidant function and reduce the apoptosis-effecting enzyme caspase-3 activities, thereby slowing oxidative stress injury and tissue cell apoptosis.

Single-Cell RNA Sequencing Reveals Smooth Muscle Cells Heterogeneity in Experimental Aortic Dissection.

Purpose: This study aims to illustrate the cellular landscape in the aorta of experimental aortic dissection (AD) and elaborate on the smooth muscle cells (SMCs) heterogeneity and functions among various cell types. Methods: Male Apolipoprotein deficient (ApoE-/-) mice at 28 weeks of age were infused with Ang II (2,500 ng/kg/min) to induce AD. Aortas from euthanized mice were harvested after 7 days for 10×Genomics single-cell RNA sequencing (scRNA-seq), followed by the identification of cell types and differentially expressed genes (DEGs). Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was conducted. Results: AD was successfully induced in ApoE-/- mice. scRNA-seq identified 15 cell clusters and nine cell types, including non-immune cells (endothelials, fibroblasts, and SMCs) and immune cells (B cells, natural killer T cell, macrophages, dendritic cells, neutrophils, and mast cells). The relative numbers of SMCs were remarkably changed, and seven core DEGs (ACTA2,IL6,CTGF,BGN,ITGA8,THBS1, and CDH5) were identified in SMCs. Moreover, we found SMCs can differentiate into 8 different subtypes through single-cell trajectory analysis. Conclusion: scRNA-seq technology can successfully identify unique cell composition in experimental AD. To our knowledge, this is the first study that provided the complete cellular landscape in AD tissues from mice, seven core DEGs and eight subtypes of SMCs were identified, and the SMCs have evolution from matrix type to inflammatory type.

Ferroptosis and its role in cardiomyopathy.

Heart disease is the leading cause of death worldwide. Cardiomyopathy is a disease characterized by the heart muscle damage, resulting heart in a structurally and functionally change, as well as heart failure and sudden cardiac death. The key pathogenic factor of cardiomyopathy is the loss of cardiomyocytes, but the related molecular mechanisms remain unclear. Ferroptosis is a newly discovered regulated form of cell death, characterized by iron accumulation and lipid peroxidation during cell death. Recent studies have shown that ferroptosis plays an important regulatory roles in the occurrence and development of many heart diseases such as myocardial ischemia/reperfusion injury, cardiomyopathy and heart failure. However, the systemic association of ferroptosis and cardiomyopathy remains largely unknown and needs to be elucidated. In this review, we provide an overview of the molecular mechanisms of ferroptosis and its role in individual cardiomyopathies, highlight that targeting ferroptosis maybe a potential therapeutic strategy for cardiomyopathy therapy in the future.

Carboxymethyl konjac glucomannan-chitosan complex nanogels stabilized double emulsions incorporated into alginate hydrogel beads for the encapsulation, protection and delivery of probiotics.

In this study, we developed (W1/O/W2) double emulsions encapsulated by calcium-alginate hydrogel beads system (ACGs) for intestinal-targeted delivery of probiotics (Lactobacillus reuteri). Firstly, the carboxymethyl konjac glucomannan-chitosan (CMKGM-CS) nanogels were successfully fabricated by EDC/NHS initiated crosslinking, as concluded from the TEM images, FTIR spectra, XRD, etc. Then, double emulsions were prepared and encapsulated with various concentrations of alginate to form ACGs hydrogel beads. In vitro probiotic release experiments showed the lyophilized ACG-2 and ACG-3 hydrogel beads had a sustained release in simulated intestinal fluid (SIF), the viability of cells exceeded 107 CFU/mL at 6 h. The lyophilized ACG-3 hydrogel beads exhibited the viable release amount of 8.4 × 107 CFU/mL after storage for 90 d at 4 °C. Besides, the alginate concentration in the ACGs hydrogel beads influences the swelling behavior and structure of hydrogel beads by affecting the hydrogen bonds between alginate and CMKGM-CS, thereby mediating the release of probiotics.

Experimental Voltammetry Analyzed Using Artificial Intelligence: Thermodynamics and Kinetics of the Dissociation of Acetic Acid in Aqueous Solution.

Artificial intelligence (AI) is used to quantitatively analyze the voltammetry of the reduction of acetic acid in aqueous solution generating thermodynamic and kinetic data. Specifically, the variation of the steady-state current for the reduction of protons at a platinum microelectrode as a function of the bulk concentration of acetic acid is recorded and analyzed giving data in close agreement with independent measurements, provided the AI is trained with accurate and precise knowledge of diffusion coefficients of acetic acid, acetate ions, and H+.

Voltammetry in sheep's blood: Membrane-free amperometric measurement of O2 concentration.

An amperometric method was applied for the electroanalytical measurement of oxygen content in sheep's blood. This method was based on a bare platinum microdisc electrode coupled with the use of chronoamperometry. A linear relationship between the chronoamperometric current and the oxygen concentration was observed in both saline solution and sheep's blood. The developed method was able to measure the oxygen percentage with an error of ca. 1.3% in sheep's blood. In addition, this article presents the first study on direct voltammetry in sheep's blood and a dissociative CE process was proposed to explain the electrochemical behaviour of oxygen reduction in blood on a platinum electrode in which the 'free' oxygen was first dissociated from oxyhaemoglobin prior to electron transfer with the magnitude of the observed current controlled by the diffusion of oxyhaemoglobin to the electrode where for sufficiently large electrodes (greater than ca. 1 µm in radius) the dissociation proceeds to completion on the voltammetric timescale allowing quantitative measurements.

Transcriptomic and Coexpression Network Analyses Revealed Pine Chalcone Synthase Genes Associated with Pine Wood Nematode Infection.

Pine wood nematode (PWN) causes serious diseases in conifers, especially pine species. To investigate the transcriptomic profiles of genes involved in pine-PWN interactions, two different pine species, namely, Pinus thunbergii and P. massoniana, were selected for this study. Weighted gene coexpression network analysis (WGCNA) was used to determine the relationship between changes in gene expression and the PWN population after PWN infection. PWN infection negatively affects the expression of most genes in pine trees, including plant defense-related genes such as genes related to plant hormone signal transduction, plant-pathogen interactions, and the MAPK signaling pathway in plants. However, the expression of chalcone synthase genes and their related genes were proportional to the changes in nematode populations, and chalcone synthase genes were dominant within the coexpression module enriched by genes highly correlated with the nematode population. Many genes that were closely related to chalcone synthase genes in the module were related to flavonoid biosynthesis, flavone and flavonol biosynthesis, and phenylpropanoid biosynthesis. Pine trees could actively adjust their defense strategies in response to changes in the number of invasive PWNs, but the sustained expression of chalcone synthase genes should play an important role in the inhibition of PWN infection.

Do carbon nanotubes catalyse bromine/bromide redox chemistry?

The redox chemistries of both the bromide oxidation and bromine reduction reactions are studied at single multi-walled carbon nanotubes (MWCNTs) as a function of their electrical potential allowing inference of the electron transfer kinetics of the Br2/Br- redox couple, widely used in batteries. The nanotubes are shown to be mildly catalytic compared to a glassy carbon surface but much less as inferred from conventional voltammetry on porous ensembles of MWCNTs where the mixed transport regime masks the true catalytic response.

Amperometric Environmental Phosphate Sensors.

We report a novel amperometric sensor for aqueous phosphate ions in freshwater systems based on the reductive square wave voltammetry of molybdate(VI) anions immobilized within a chitosan matrix deposited on a glassy carbon electrode. A sensitivity of 4.4 ± 0.1 µA/µM was realized together with a LOD of 0.15 µM. The sensor was insensitive to chloride and nitrate ions below a threshold concentration of 1.0 mM. Analytical measurements were successfully made in authentic samples of tap and pond water.

Trehalose in pine wood nematode participates in DJ3 formation and confers resistance to low-temperature stress.

BACKGROUND: Recently, pine wood nematode (PWN, Bursaphelenchus xylophilus) has been found in the extreme cold area of northeast China. The third-stage dispersal juvenile (DJ3) of PWN, which is a long-lived stress-resistant stage, plays an important role in the process of PWN spreading to low-temperature areas, as this stage can survive under unfavorable conditions. RESULTS: Weighted correlation network analysis (WGCNA) was used to analyze the expression patterns of 15,889 genes included in 21 RNA-Seq results of PWN at DJ3 and the other 6 different stages, and a total of 12 coexpression modules were obtained. Among them, the magenta module has the highest correlation with DJ3, which included a total of 652 genes. KEGG enrichment analysis showed that most of the genes in the magenta module were involved in metabolic processes, which were related to autophagy and longevity regulation. These pathways included starch and sucrose metabolism, which contains trehalose metabolism. To explore the function of trehalose in DJ3 formation and survival under - 20 °C, a trehalose-6-phosphate synthase encoding gene (Bx-tps), a trehalose-6-phosphate phosphatase encoding gene (Bx-tpp) and 7 trehalase encoding genes (Bx-tres) were identified and investigated. The expression of these 9 genes was related to the formation of DJ3. A treatment under - 20 °C induced the accumulation of trehalose. The survival rate of DJ3 at -20 °C reduced after silencing of any of these trehalose metabolism genes. Further analysis suggested that two trehalose synthesis genes were highly correlated with DJ3 and might be involved in autophagy by regulating with energy conversion related genes. CONCLUSIONS: The above results indicated that trehalose metabolism promotes DJ3 formation and helps DJ3 survive at -20 °C. Although trehalose accumulation is favorable for DJ3 to cope with low-temperature stress, multiple trehalose metabolism genes need to work together. There may be a multi-path regulated physiological process involving trehalose synthesis genes under low-temperature stress resistance. This physiological process may regulate the formation and maintenance of DJ3 through autophagy and energy conversion.

Integrating Transcriptome and Coexpression Network Analyses to Characterize Salicylic Acid- and Jasmonic Acid-Related Genes in Tolerant Poplars Infected with Rust.

Melampsora larici-populina causes serious poplar foliar diseases called rust worldwide. Salicylic acid (SA) and jasmonic acid (JA) are important phytohormones that are related to plant defence responses. To investigate the transcriptome profiles of SA- and JA-related genes involved in poplar rust interaction, two tolerant poplars and one intolerant poplar were selected for this study. Weighted gene coexpression network analysis (WGCNA) was applied to characterize the changes in the transcriptome profiles and contents of SA and JA after infection with the virulent E4 race of M. larici-populina. In response to infection with the E4 race of M. larici-populina, tolerant symptoms were correlated with the expression of genes related to SA and JA biosynthesis, the levels of SA and JA, and the expression of defence-related genes downstream of SA and JA. Tolerant poplars could promptly regulate the occurrence of defence responses by activating or inhibiting SA or JA pathways in a timely manner, including regulating the expression of genes related to programmed cell death, such as Kunitz-type trypsin inhibitor (KTI), to limit the growth of E4 and protect themselves. WGCNA suggested that KTI might be regulated by a Cytochrome P450 family (CYP) gene. Some CYPs should play an important role in both JA- and SA-related pathways. In contrast, in intolerant poplar, the inhibition of SA-related defence signalling through increasing JA levels in the early stage led to continued inhibition of a large number of plant-pathogen interaction-related and signalling-related genes, including NBS-LRRs, EDS1, NDR1, WRKYs, and PRs. Therefore, timely activation or inhibition of the SA or JA pathways is the key difference between tolerant and intolerant poplars.