Wheat leaf rust, caused by Puccinia triticina, is a widespread economically important wheat disease. During infection, P. triticina secretes effectors proteins to manipulate host immunity. Here we identified and characterized the P. triticina effector Pt3863, which is highly expressed during the early phase of infection and significantly enhances fungal virulence. We also identified the wheat receptor-like cytoplasmic kinase TaRLCK176 as a target of Pt3863. Functional assays demonstrated that TaRLCK176 positively regulates wheat resistance against leaf rust and is required for chitin-induced reactive oxygen species (ROS) accumulation. Pt3863 subverts this defence through a dual inhibitory mechanism: first, it suppresses TaRLCK176 phosphorylation; second, it promotes TaRLCK176 degradation via the ubiquitin-26S proteasome pathway. Host-induced gene silencing Pt3863 attenuated P. triticina virulence, while its overexpression in transgenic wheat lines increased susceptibility to P. tritici. Conversely, virus-induced gene silencing of TaRLCK176 compromised wheat resistance. Our findings establish TaRLCK176 as a critical immune hub that positively modulates wheat resistance to leaf rust and is specifically targeted by the P. triticina effector Pt3863. Notably, Pt3863 has evolved a sophisticated virulence strategy to simultaneously disrupt both the phosphorylation-mediated activation and proteasomal stability of TaRLCK176, thereby impairing host immune responses. This study elucidates a key molecular mechanism underlying the suppression of wheat immunity by P. triticina and highlights TaRLCK176 as a promising candidate target for the genetic engineering of durable resistance in wheat against leaf rust.

Fusarium crown rot (FCR), caused by Fusarium pseudograminearum, is a soil-borne disease that continuously threatens wheat and barley production worldwide, resulting in substantial yield losses, particularly in semi-arid regions. This review consolidates the latest insights on Fusarium pseudograminearum epidemiology, genetic diversity, host-pathogen interactions, and the mechanisms of resistance. It integrates findings from genomics, transcriptomics, proteomics, and metabolomics. The resistance to FCR is polygenic, it is controlled by multiple quantitative trait loci, which makes breeding for resistance quite challenging. Recent advancements in omics technologies have unraveled key defense genes, signaling pathways, and virulence factors like deoxynivalenol and various effectors. While cultural methods, chemical treatments and biological control agents can help to a certain extent, they only provide partial solutions. Additionally, environmental factors such as drought can aggravate the severity of FCR, underscoring the need for disease management strategies that integrate genetic resistance, agronomic practices, and predictive diagnostics to ensure sustainable management.

Fusarium crown rot (FCR) ranks among the most devastating fungal disease affecting wheat globally. During a wheat disease survey in 2023 across counties in Li, Qingyuan, Wangdu, Boye, and Gaoyang in Baoding, Hebei Province, China (38°50′N–39°10′N, 115°20′E–115°45′E), FCR was detected with incidence ranged from 30% to 40% in wheat fields. Symptomatically, the disease is characterized by the appearance of brown lesions on the wheat crown, which subsequently extended to two or more stems causing necrosis, leading to the formation of white heads during grain filling. To determine the Fusarium diversity causing FCR in Baoding, pathogen isolation was performed on the collected 150 diseased crown tissues. Small sections of diseased tissue from each plant were first surface-sterilized with 75% ethanol for 10 s, followed by 2% sodium hypochlorite treatment for 3 min, and rinsed three times with sterile distilled water. The sterilized tissues were then transferred onto potato dextrose agar (PDA) plates and incubated at 25°C for 2 days before mycelium tip purification. Totally, 147 isolates were acquired, in which four isolates (2.72%) presented dense, white aerial mycelium, which were clearly distinguishable from F. pseudograminearum. When proceeding with molecular identification, no band of 520 bp specific for F. pseudograminearum was detected by using the Fp1-1/Fp1-2 primer set amplification (Demeke et al. 2005). Amplification and sequencing of ITS4/5 (White et al. 1990) for the four isolates showed that they were classified as F. luffae within the Fusarium incarnatum-equiseti complex. Thus, one isolate (QY3-4) was selected for further identification by morphological and multi-locus amplification. When cultured on PDA plate, the average mycelial growth rate of the isolate QY3-4 was 8.0 mm per day. The macroconidia are slightly curved, with acute apical cells, 3-5 septa, and measure 32.4-68.7 × 4.7-6.9 μm (n=50). Besides ITS4/ITS5, amplification and sequencing were carried out using CAMF/CAMR, EF1F/EF2R, and RPB2F/RPB2R (O’Donnell et al. 2020; O’Donnell et al. 1998; Reeb et al. 2004). The ITS (GenBank accession no. PX879050), CAM, TEF1α, and RPB2 (GenBank accession no. PX907447-PX907449) sequences showed similarities of 99.79%, 99.51%, 99.67%, and 99.64% with the type species of F. luffae (CGMCC3.19497). The phylogenetic tree was constructed based on multilocus concatenated sequences thus identifying QY3-4 as F. luffae. To confirm pathogenicity, PDA plugs colonized with QY3-4 were inoculated into sterile wheat grain medium, and 15 wheat seedlings were inoculated. The control group seedlings were inoculated with sterile wheat grain without QY3-4 inoculum. The pathogenicity experiment was conducted in a greenhouse and repeated three times. The inoculated plants exhibited obvious FCR symptoms after 30 d, while no disease symptoms observed in the control. The pathogen identical with QY3-4 was re-isolated from the symptomatic stems and confirmed by amplification and sequencing of CAM, consistent with Koch’s postulates. F. luffae has been reported to cause soybean wilt (Sharma et al. 2024; Zhao et al. 2022) and wilt disease on strawberry (Zhang et al. 2025). To the best of our knowledge, this is the first report of F. luffae causing crown rot of wheat in China. This finding contributes valuable information for epidemiological studies and management of FCR in the region.

Fusarium head blight (FHB), caused by Fusarium graminearum, poses a significant threat to wheat production in Ethiopia, causing yield losses of up to 30–70

Wheat leaf rust, caused by the fungal pathogen Puccinia triticina Eriks., is a major biotic constraint to global wheat production, leading to yield losses of up to 50 % and compromising food security. This review provides a comprehensive analysis of the epidemiology, genetic resistance mechanisms, and integrated management strategies of wheat leaf rust. The pathogen thrives in warm, humid climates and exhibits a complex life cycle involving both asexual and sexual reproduction, enabling rapid evolution and adaptability. Over 80 leaf rust resistance genes have been identified, yet the pathogen's ability to overcome these genes underscores the necessity for durable resistance strategies such as gene pyramiding and the deployment of adult plant resistance genes like Lr34 and Lr67. Advances in molecular breeding, including marker-assisted selection, genomic selection, and CRISPR/Cas9 gene editing, offer promising avenues for developing resistant wheat cultivars. Additionally, integrated disease management approaches combining resistant varieties, chemical and biological controls, cultural practices, and nanotechnology-based solutions are critical for sustainable wheat production. Strengthening global surveillance, predictive modeling, and international collaborations will be essential to mitigate the escalating threat of wheat leaf rust and ensure global food security in the face of climate change and evolving pathogen populations. This review highlights the importance of leveraging genetic and genomic tools to augment wheat resilience and ensure global food security.

Wheat leaf rust, caused by the biotrophic fungal pathogen Puccinia triticina (Pt), continuously threatens global wheat production, causing considerable yield losses necessitating the implementation of effective management approaches. While conventional breeding and chemical control strategies have been used, priming agents and genetic regulators offer sustainable strategies for wheat leaf rust management. Melatonin (N-acetyl-5-methoxytryptamine), a pleiotropic signaling molecule, induces plant innate immunity against abiotic and biotic stresses. This study demonstrates that exogenous melatonin (100 µM) enhances Lr10-mediated resistance to wheat leaf rust by upregulating TaRAR1, salicylic acid downstream genes, antioxidant enzyme genes, MAPK cascade genes, and WRKY transcription factors during Pt infection. RAR1 serves as an initial convergence point in signaling pathways activated by several R genes. Herein, TaRAR1 was strongly upregulated during early stages of infection in incompatible interactions, and this was associated with increased endogenous SA and melatonin levels, correlating with enhanced defense responses. TaRAR1 silencing compromised TcLr10 resistance, reducing SA and melatonin levels, downregulating defense-related genes, and altering reactive oxygen species dynamics by increasing TaCAT expression and reducing hydrogen peroxide accumulation. TaRAR1 silencing also downregulated TaSGT1, and TaHSP90, suggesting its role in stabilizing NLR proteins. In conclusion, melatonin augments wheat resistance to leaf rust by upregulating TaRAR1, SA signaling, and antioxidant defenses, with MAPK cascades and WRKY transcription factors amplifying downstream responses. This study provides novel insights into the integration of phytohormonal and genetic approaches for enhancing wheat resistance to leaf rust, offering strategies for sustainable disease management.

Puccinia triticina (Pt) is an obligate parasitic fungus that absorbs nutrients through haustoria during infection and secretes a repertoire of effector proteins into the host cells to regulate the immune response of the host. Here, we identify an effector protein Pt3372 from the transcriptome data of interaction between the Pt race JHKT and the susceptible wheat cultivar Thatcher. Pt3372 was highly induced at the early stages in TcLr2a and TcLr18 infected by JHKT. The effector inhibited cell death induced by BAX (Bcl2-associated X) and INF1 (Phytophthora infestans INF1) in Nicotiana benthamiana, as well as cell death induced by Pseudomonas syringae pv. tomato DC3000 in wheat. Pt3372 was proved to be localized in the cell membrane and nucleus of N. benthamiana. When transiently expressed in TcLr2a and TcLr18 through the bacterial type III secretion system, Pt3372 inhibited callose deposition and reactive oxygen species accumulation and suppressed the expression of wheat pathogenesis-related genes PR1 and PR2. Silencing Pt3372 by host-induced gene silencing reduced the Pt race JHKT virulence on TcLr2a and TcLr18. While it was enhanced by the overexpression of Pt3372 in transgenic wheat, which had a down-regulated expression of TaPR2 and glutathione reductase TaGR. Moreover, Pt3372 targets the elicitor-responsive protein TaERP3. Altogether, our results demonstrate that the effector Pt3372 suppresses the expression of TaPR1 and TaPR2 and the innate immunity by targeting the TaERP3.

This study identifies and characterizes pathogenic Fusarium species and their trichothecene genotypes in wheat crops grown in seven regions of Hebei Province, China, from 2019 to 2021. Species-specific primers confirmed the morphological identification of 689 Fusarium strains recovered from wheat seedlings with symptomatic crown/sub-crown tissues. The results suggest that Fusarium pseudograminearum was the most detected strain, accounting for 91 % of the identified strains. Other species, including F. graminearum, F. oxysporum, F. proliferatum, F. asiaticum, and F. culmorum, were detected at lower rates, ranging from 0.15 % to 8.56 %. Toxin genotype detection results showed that F. pseudograminearum and F. graminearum were the most common species linked to wheat crown rot, producing high detection rates of trichothecene genotypes. F. pseudograminearum strains had detection rates of 84.50 % for deoxynivalenol (DON) and other mycotoxins, including 3-acetyl-deoxynivalenol (3-AcDON) and 15-acetyl-deoxynivalenol (15-AcDON). On the other hand, strains (F. graminearum) of the 15-AcDON chemotype were detected at 15 L-AcDON, with detection rates of 34.37 %, 21.88 %, 21.88 %, and 18.75 % in Handan, Shijiazhuang, Xingtai, and Baoding, respectively. The study also indicated that F. pseudograminearum and F. graminearum had strong pathogenicity, while F. asiaticum and F. culmorum showed weak pathogenicity to wheat in Hebei Province. This study identifies F. pseudograminearum as the predominant cause of Fusarium crown rot in Hebei Province, with the majority of strains classified as DON genotypes.

Wheat rusts caused by biotrophic fungi of the genus Puccinia continuously threaten global wheat production and food security. The rapid evolution of virulent races, and the limitations of chemical fungicides, including environmental contamination, human health concerns, and resistance development, necessitate a shift towards integrated management strategies. This review explores biocontrol agents (BCAs), including fungal (Trichoderma spp., Cladosporium cladosporioides), bacterial (Bacillus subtilis, Pseudomonas spp.), and actinomycetes (Streptomyces spp.), as foundational components of wheat rusts management. We highlight their modes of action such as mycoparasitism, antibiosis, competition, and the induction of systemic resistance. Additionally, we explore how cutting-edge adjunct technologies can enhance the efficacy and sustainability of BCAs. These include nano-formulations, for targeted antimicrobial actions and plant defense potentiation; plant extracts and antimicrobial peptides as natural defense elicitors; and artificial intelligence (AI) tools, for presymptomatic detection, severity quantification, epidemic forecasting, and early warning systems that enable precise application of BCAs and nano-formulations. While BCAs, nanoformulations, plant extracts and AI-driven tools offer powerful, environmentally benign alternatives capable of significantly reducing reliance on synthetic chemicals, chemical fungicides remain an essential component of current wheat rusts management, particularly during severe epidemics or when rapid knockdown of inoculum is required. A truly integrated and sustainable strategy therefore combines these novel approaches with the judicious, resistance-management-oriented use of effective chemical fungicides applied according to economic thresholds and in rotation or mixture to delay resistance development, thereby maximizing durability and minimizing environmental impact. However, the successful translation of this strategy to the field hinges on overcoming key challenges in formulation stability, scalable production, and seamless integration into existing and chemical-based agricultural practices to mitigate the impact of wheat rusts and safeguard global wheat yields and food security.

As an obligate biotrophic fungus, the leaf rust pathogen Puccinia triticina (Pt) secretes a repertoire of effector proteins into host cells for modulating plant immunity and promoting fungal pathogenesis. Here, we identify the Pt31812 effector and characterize its function in pathogenesis and immune-related activity in plants. In the study, Pt31812 was cloned by PCR, and the expression pattern and structure were analyzed by qRT-PCR and online softwares. Subcellular localization of Pt31812 was analyzed using transient expression on Nicotiana Benthamiana. Further functional analysis was conducted using transient expression and host-induced gene silencing (HIGS). The results showed that Pt31812 encodes candidate effector with a predicted signaling peptide (SP) at the N-terminus, and its expression was highly up-regulated during Pt infection of wheat. Subcellular localization analysis revealed that Pt31812 is localized in cytoplasm and nucleus when expressed in N. Benthamiana. Co-expression of Pt31812 and mammalian BAX protein revealed that Pt31812 inhibited BAX-induced cell death in N. Benthamiana, and the fragment of 22-88 aa from the N-terminus of the effector was important for the inhibiting activity. Interestingly, expression of Pt31812 in a panel of wheat differential lines with different Lr resistance genes showed that Pt31812 specifically triggered cell death in a Lr42-harboring wheat line. Furthermore, transient gene silencing of Pt31812 through BSMV-HIGS approach rendered loss of Lr42-mediated resistance against rust race Pt.-THSN and altered the infection type from resistant to susceptible. Our data reveal that Pt31812, as a candidate effector with immune inhibiting activity, acts as an avirulence determinant factor during Pt infection of Lr42-harboring wheat line. These findings highlight immune-related activity of specific Pt effectors and lay the foundation for further investigation into mechanisms of leaf rust fungal pathogenesis and recognition.

Wheat leaf rust caused by Puccinia triticina (Pt) is a prevalent disease worldwide, seriously threatening wheat production. Pt acquires nutrients from host cells via haustoria and secretes effector proteins to modify and regulate the expression of host disease resistance genes, thereby facilitating pathogen growth and reproduction. The study of effector proteins is of great significance for clarifying the pathogenic mechanisms of Pt and effective control of leaf rust. Herein, we report a wheat leaf rust candidate effector protein Pt48115 that is highly expressed in the late stages of infection during wheat–Pt interaction. Pt48115 contains a signal peptide with a secretory function and a transit peptide that can translocate Pt48115 to the host chloroplasts. The amino acid sequence polymorphism analysis of Pt48115 in seven different leaf rust races showed that it was highly conserved. Pt48115 inhibited cell death induced by Bcl-2-associated X protein (BAX) from mice or infestans 1 (INF1) from Phytophthora infestans in Nicotiana benthamiana and by DC3000 in wheat, and its 145–175 amino acids of the C-terminal are critical for its function. Furthermore, Pt48115 inhibited callose deposition and reactive oxygen species accumulation in the wheat cultivar Thatcher, demonstrating that it is an effector that enhances Pt virulence by suppressing wheat defense responses. Our findings lay a foundation for future studies on the pathogenesis of Pt during wheat–fungus interaction.

Wheat leaf rust fungus is an obligate parasitic fungus that can absorb nutrients from its host plant through haustoria and secrete effector proteins into host cells. The effector proteins are crucial factors for pathogenesis as well as targets for host disease resistance protein recognition. Exploring the role of effector proteins in the pathogenic process of Puccinia triticina Eriks. (Pt) is of great significance for unraveling its pathogenic mechanisms. We previously found that a cysteine-rich effector protein, Pt1641, is highly expressed during the interaction between wheat and Pt, but its specific role in pathogenesis remains unclear. Therefore, this study employed techniques such as heterologous expression, qRT-PCR analysis, and host-induced gene silencing (HIGS) to investigate the role of Pt1641 in the pathogenic process of Pt. The results indicate that Pt1641 is an effector protein with a secretory function and can inhibit BAX-induced programmed cell death in Nicotiana benthamiana. qRT-PCR analyses showed that expression levels of Pt1641 were different during the interaction between the high-virulence strain THTT and low-virulence strains FGD and Thatcher, respectively. The highest expression level in the low-virulence strain FGD was four times that of the high-virulence strain THTT. The overexpression of Pt1641 in wheat near-isogenic line TcLr1 induced callose deposition and H2O2 production on TcLr1. After silencing Pt1641 in the Pt low-virulence strain FGD on wheat near-isogenic line TcLr1, the pathogenic phenotype of Pt physiological race FGD on TcLr1 changed from “;” to “3”, indicating that Pt1641 plays a non-toxic function in the pathogenicity of FGD to TcLr1. This study helps to reveal the pathogenic mechanism of wheat leaf rust and provides important guidance for the mining and application of Pt avirulent genes.

Chitin/polysaccharide deacetylases belong to the carbohydrate esterases family 4 (CE4 enzymes). They play a crucial role in modifying the physiochemical characteristics of structural polysaccharides and are also involved in a wide range of biological processes such as fungal autolysis, spore formation, cell wall formation and integrity, and germling adhesion. These enzymes are mostly common in fungi, marine bacteria, and a limited number of insects. They facilitate the deacetylation of chitin which is a structural biopolymer that is abundantly found in fungal cell walls and spores and also in the cuticle and peritrophic matrices of insects. The deacetylases exhibit specificity towards a substrate containing a sequence of four GlcNAc units, with one of these units being subjected to deacetylation. Chitin deacetylation results in the formation of chitosan, which is a poor substrate for host plant chitinases, therefore it can suppress the host immune response triggered by fungal pathogens and enhance pathogen virulence and colonization. This review discusses plant pathogenic fungal chitin/polysaccharide deacetylases including their structure, substrate specificity, biological roles and some recently discovered chitin deacetylase inhibitors that can help to mitigate plant fungal diseases. This review provides fundamental knowledge that will undoubtedly lead to the rational design of novel inhibitors that target pathogenic fungal chitin deacetylases, which will also aid in the management of plant diseases, thereby safeguarding global food security.

Effectors are considered to be virulence factors secreted by pathogens, which play an important role during host-pathogen interactions. In this study, the candidate effector Pt9226 was cloned from genomic DNA of Puccinia triticina (Pt) pathotype THTT, and there were six exons and five introns in the 877 bp sequence, with the corresponding open reading frame of 447 bp in length, encoding a protein of 148 amino acids. There was only one polymorphic locus of I142V among the six Pt pathotypes analyzed. Bioinformatics analysis showed that Pt9226 had 96.46% homology with the hypothetical putative protein PTTG_26361 (OAV96349.1) in the Pt pathotype BBBD. RT-qPCR analyses showed that the expression of Pt9226 was induced after Pt inoculation, with a peak at 36 hpi, which was 20 times higher than the initial expression at 0 hpi, and another high expression was observed at 96 hpi. No secretory function was detected for the Pt9226-predicted signal peptide. The subcellular localization of Pt9226Δsp-GFP was found to be multiple, localized in the tobacco leaves. Pt9226 could inhibit programmed cell death (PCD) induced by BAX/INF1 in tobacco as well as DC3000-induced PCD in wheat. The transient expression of Pt9226 in 26 wheat near-isogenic lines (NILs) by a bacterial type III secretion system of Pseudomonas fluorescens EtHAn suppressed callose accumulation triggered by Ethan in wheat near-isogenic lines TcLr15, TcLr25, and TcLr30, and it also suppressed the ROS accumulation in TcLr15. RT-qPCR analysis showed that the expression of genes coded for pathogenesis-related protein TaPR1, TaPR2, and thaumatin-like protein TaTLP1, were suppressed, while the expression of PtEF-1α was induced, with 1.6 times at 72 h post inoculation, and TaSOD was induced only at 24 and 48 h compared with the control, when the Pt pathotype THTT was inoculated on a transient expression of Pt9226 in wheat TcLr15. Combining all above, Pt9226 acts as a virulence effector in the interaction between the Pt pathotype THTT and wheat.

Thaumatin-like proteins (TLPs) in plants play a crucial role in combating stress, and they have been proven to possess antifungal properties. However, the role of TLPs in pathogens has not been reported. We identified a effector protein, Pt9029, which contained a Thaumatin domain in Puccinia triticina (Pt), possessing a chloroplast transit peptide and localized in the chloroplasts. Silencing Pt9029 in the Pt physiological race THTT resulted in a notable reduction in virulence and stunted growth and development of Pt hypha in near-isogenic wheat line TcLr2b. Overexpression of Pt9029 in wheat exerted a suppressive effect on H2O2 production, consequently impeding the wheat's disease resistance mechanisms. The TLP domain of Pt9029 targets the Rubisco activase (TaRCA) in chloroplasts. This interaction effectively inhibited the function of TaRCA, subsequently leading to a decrease in Rubisco enzyme activity. Therefore, this indicates that TLPs in Pt can inhibit host defense mechanisms during the pathogenic process of Pt. Moreover, TaRCA silencing resulted in reduced resistance of TcLr2b against Pt race THTT. This clearly demonstrated that TaRCA positively regulates wheat resistance to leaf rust. These findings reveal a novel strategy exploited by Pt to manipulate wheat rust resistance and promote pathogenicity.

Fungal plant pathogens use proteinaceous effectors as well as newly identified secondary metabolites (SMs) and small non-coding RNA (sRNA) effectors to manipulate the host plant’s defense system via diverse plant cell compartments, distinct organelles, and many host genes. However, most molecular studies of plant–fungal interactions have focused on secreted effector proteins without exploring the possibly equivalent functions performed by fungal (SMs) and sRNAs, which are collectively known as “non-proteinaceous effectors”. Fungal SMs have been shown to be generated throughout the plant colonization process, particularly in the early biotrophic stages of infection. The fungal repertoire of non-proteinaceous effectors has been broadened by the discovery of fungal sRNAs that specifically target plant genes involved in resistance and defense responses. Many RNAs, particularly sRNAs involved in gene silencing, have been shown to transmit bidirectionally between fungal pathogens and their hosts. However, there are no clear functional approaches to study the role of these SM and sRNA effectors. Undoubtedly, fungal SM and sRNA effectors are now a treasured land to seek. Therefore, understanding the role of fungal SM and sRNA effectors may provide insights into the infection process and identification of the interacting host genes that are targeted by these effectors. This review discusses the role of fungal SMs and sRNAs during plant-fungal interactions. It will also focus on the translocation of sRNA effectors across kingdoms, the application of cross-kingdom RNA interference in managing plant diseases and the tools that can be used to predict and study these non-proteinaceous effectors.

[目的]研究小麦品种衡观35 抗茎基腐病EMS突变及其鉴定.[方法]利用不同浓度的甲基磺酸乙酯(EMS),对小麦品种衡观35 进行诱变,以未经诱变的衡观35 为感病对照,以石优 17 为中度抗病对照.人工接种假禾谷镰刀菌,对诱变材料进行抗性鉴定,经温室加代获得抗茎基腐病M3 代材料.[结果]适于衡观35 突变的EMS浓度为0.4%,并且从106 株M3衡观35 材料中获得 7 株期表现免疫的突变株,突变体材料苗期和成株期整体病情指数比感病对照分别降低34.93%和34.62%.[结论]EMS突变小麦衡观35,适宜的突变浓度为0.4%,共从供试突变品种M3代中筛选获得了7 份免疫的抗小麦茎基腐病的资源.

植物病理学是河北农业大学动植物检疫专业的专业核心课.在系统传授植物病理学基本知识、原理和方法的同时深入挖掘切合专业内容的思政元素,在课程教学中具有重要作用.将思政元素与植物病理学专业知识有机融合,有助于引导学生树立正确的理想信念、有效提高学生学习植物病理学的兴趣.通过提高专业课教师的课程思政素养、深入挖掘思政元素并构建精品案例库、将思政元素与课程教学有机融合等途径,能够推动植物病理学课程思政向纵深方向发展.

Wheat leaf rust, caused by the obligate biotrophic fungus Puccinia triticina Eriks. (Pt), is one of the most common wheat foliar diseases that continuously threatens global wheat production. Currently, the approaches used to mitigate pathogen infestation include the application of fungicides and the deployment of resistance genes or cultivars. However, the continuous deployment of selected resistant varieties causes host selection pressures that drive Pt evolution and promote the incessant emergence of new virulent races, resulting in the demise of wheat-resistant cultivars after several years of planting. Intriguingly, diploid wheat accessions were found to confer haustorium formation-based resistance to leaf rust, which involves prehaustorial and posthaustorial resistance mechanisms. The prehaustorial resistance in the interaction between einkorn and wheat leaf rust is not influenced by specific races of the pathogen. The induced defense mechanism, known as systemic acquired resistance, also confers durable resistance against a wide array of pathogens. This review summarizes the host range, pathogenic profile, and evolutionary basis of Pt; the molecular basis underlying wheat–Pt interactions; the cloning and characterization of wheat leaf rust resistance genes; prehaustorial and posthaustorial resistance; systemic acquired resistance; and the role of reactive oxygen species. The interplay between climatic factors, genetic features, planting dates, and disease dynamics in imparting resistance is also discussed.