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Summary As an obligate parasite, Puccinia striiformis f. sp. tritici (Pst) forms haustoria to obtain nutrients from plant cells for development, and these structures are essential for pathogen survival. To better understand the contribution of haustoria to the interactions with the host plants, we isolated haustoria from susceptible wheat leaves infected with Pst race CYR31 and sequenced their transcriptome as well as those of urediospores and germ tubes, and compared the three transcriptomes. A total of 3524 up‐regulated genes were obtained from haustoria, of which 73 genes were related to thiamine biosynthesis, glycolysis and lipid metabolic processes. Silencing seven of the genes reduced the growth and development of Pst in wheat. More interestingly, 1197 haustorial secreted proteins (HASPs) were detected in haustoria, accounting for 34% of the total proteins, indicating that these HASPs play important roles in haustorium‐mediated pathogenic progression. Furthermore, 69 HASPs were able to suppress Bax‐triggered programmed cell death in tobacco. Additionally, 46 HASPs significantly reduced callose deposition in wheat using the type III secretion system. This study identified a large number of effectors through transcriptome sequencing, and the results revealed components of metabolic pathways that impact the growth and colonization of the pathogen and indicate essential functions of haustoria in the growth and pathogenicity of Pst.

Key messageAnalysis of a wheat multi-founder population identified 14 yellow rust resistance QTL. For three of the four most significant QTL, haplotype analysis indicated resistance alleles were rare in European wheat.Stripe rust, or yellow rust (YR), is a major fungal disease of wheat (Triticum aestivum) caused by Puccinia striiformis Westend f. sp. tritici (Pst). Since 2011, the historically clonal European Pst races have been superseded by the rapid incursion of genetically diverse lineages, reducing the resistance of varieties previously showing durable resistance. Identification of sources of genetic resistance to such races is a high priority for wheat breeding. Here we use a wheat eight-founder multi-parent population genotyped with a 90,000 feature single nucleotide polymorphism array to genetically map YR resistance to such new Pst races. Genetic analysis of five field trials at three UK sites identified 14 quantitative trait loci (QTL) conferring resistance. Of these, four highly significant loci were consistently identified across all test environments, located on chromosomes 1A (QYr.niab-1A.1), 2A (QYr.niab-2A.1), 2B (QYr.niab-2B.1) and 2D (QYr.niab-2D.1), together explaining ~ 50% of the phenotypic variation. Analysis of these four QTL in two-way and three-way combinations showed combinations conferred greater resistance than single QTL, and genetic markers were developed that distinguished resistant and susceptible alleles. Haplotype analysis in a collection of wheat varieties found that the haplotypes associated with YR resistance at three of these four major loci were rare (≤ 7%) in European wheat, highlighting their potential utility for future targeted improvement of disease resistance. Notably, the physical interval for QTL QYr.niab-2B.1 contained five nucleotide-binding leucine-rich repeat candidate genes with integrated BED domains, of which two corresponded to the cloned resistance genes Yr7 and Yr5/YrSp.

Summary Southern corn rust (SCR), caused by Puccinia polysora Underw (P. polysora), is a catastrophic disease affecting maize, leading to significant global yield losses. The disease manifests primarily as pustules on the upper surface of corn leaves, obscuring our understanding of its cellular heterogeneity, the maize's response to its infection and the underlying gene expression regulatory mechanisms. In this study, we dissected the heterogeneity of maize's response to P. polysora infection using single‐cell RNA sequencing. We delineated cell‐type‐specific gene expression alterations in six leaf cell types, creating the inaugural single‐cell atlas of a maize leaf under fungal assault. Crucially, by reconstructing cellular trajectories in susceptible line N110 and resistant line R99 during infection, we identified diverse regulatory programs that fortify R99's resistance across different leaf cell types. This research uncovers an immune‐like state in R99 leaves, characterized by the expression of various fungi‐induced genes in the absence of fungal infection, particularly in guard and epidermal cells. Our findings also highlight the role of the fungi‐induced glycoside hydrolase family 18 chitinase 7 protein (ZmChit7) in conferring resistance to P. polysora. Collectively, our results shed light on the mechanisms of maize resistance to fungal pathogens through comparative single‐cell transcriptomics, offering a valuable resource for pinpointing novel genes that bolster resistance to P. polysora.

Summary Plants have evolved a sophisticated immunity system for specific detection of pathogens and rapid induction of measured defences. Over‐ or constitutive activation of defences would negatively affect plant growth and development. Hence, the plant immune system is under tight positive and negative regulation. MAP kinase phosphatase1 (MKP1) has been identified as a negative regulator of plant immunity in model plant Arabidopsis. However, the molecular mechanisms by which MKP1 regulates immune signalling in wheat (Triticum aestivum) are poorly understood. In this study, we investigated the role of TaMKP1 in wheat defence against two devastating fungal pathogens and determined its subcellular localization. We demonstrated that knock‐down of TaMKP1 by CRISPR/Cas9 in wheat resulted in enhanced resistance to rust caused by Puccinia striiformis f. sp. tritici (Pst) and powdery mildew caused by Blumeria graminis f. sp. tritici (Bgt), indicating that TaMKP1 negatively regulates disease resistance in wheat. Unexpectedly, while Tamkp1 mutant plants showed increased resistance to the two tested fungal pathogens they also had higher yield compared with wild‐type control plants without infection. Our results suggested that TaMKP1 interacts directly with dephosphorylated and activated TaMPK3/4/6, and TaMPK4 interacts directly with TaPAL. Taken together, we demonstrated TaMKP1 exert negative modulating roles in the activation of TaMPK3/4/6, which are required for MAPK‐mediated defence signalling. This facilitates our understanding of the important roles of MAP kinase phosphatases and MAPK cascades in plant immunity and production, and provides germplasm resources for breeding for high resistance and high yield.

Southern corn rust (SCR) caused by Puccinia polysora Underw. ( P. polysora ) poses a serious threat to global maize ( Zea mays L.) production. This study used six maize inbred lines (DTMA-45, DTMA-50, R99, N110, P767 and 15B020F3) as materials to systematically explore the response mechanism of maize to southern corn rust through phenotype identification, transcriptome sequencing, functional enrichment analysis, gene co-expression network analysis, and quantitative RT-PCR experiments. Phenotypic analysis shows that DTMA-50, R99 and P767 have strong resistance, while DTMA-45, N110 and 15B020F3 are more sensitive. Transcriptome analysis identified a large number of differentially expressed genes (DEGs), whereas gene ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis showed that these genes are involved in multiple biological processes and metabolic pathways such as defense response, cytoskeleton organization, and plant hormone signaling transduction. Weighted gene co-expression network analysis (WGCNA) identified modules and key genes related to resistance, such as cell wall tissue related genes in the coral2 module and some genes in the ABC transporter and plant pathogen interaction pathways up-regulated in the resistant strain. Quantitative real-time PCR showed that ABCG11 ( LOC100281487 ) and CCR1 ( LOC103649447 ) genes are continuously up-regulated in the early stages of infection in the resistant line R99, which may play an important role in resisting fungal invasion. This study reveals the complex molecular mechanisms underlying maize’s response to southern corn rust, offering important theoretical support and potential targets for maize disease resistance breeding.

Key messageA genome-wide association analysis identified diverse loci for seedling and adult plant resistance to leaf rust and stripe rust. KASP markers were developed and validated for marker-assisted selection.Wheat leaf rust and stripe rust cause significant losses in many wheat producing regions worldwide. The objective of this study was to identify chromosome regions conferring resistance to both leaf rust and stripe rust at the seedling and adult plant stages. A diversity panel of 268 wheat lines, including 207 accessions from different wheat growing regions in China, and 61 accessions from foreign countries, were evaluated for leaf rust response at seedling stage using eight Chinese Puccinia triticina pathotypes, and also tested for leaf rust and stripe rust at adult plant stage in multiple field environments. The panel was genotyped with the Wheat 90 K Illumina iSelect SNP array. Genome-wide association mapping (GWAS) was performed using the mixed linear model (MLM). Twenty-two resistance loci including the known Lr genes, Lr1, Lr26, Lr3ka, LrZH22, and 18 potentially new loci were identified associated with seedling resistance, explaining 4.6 to 25.2% of the phenotypic variance. Twenty-two and 23 adult plant resistance (APR) QTL associated with leaf and stripe rust, respectively, were identified at adult stage, explaining 4.2–11.5% and 4.4–9.7% of the phenotypic variance. Among them, QLr-2BS was the potentially most valuable all-stage resistance gene. Seven and six consistent APR QTL were identified in multiple environments including best linear unbiased prediction (BLUP) data, respectively. Comparison with previously mapped resistance loci indicated that three of the seven leaf rust resistance APR QTL, and two of the six stripe rust resistance APR QTL were new. Four potentially pleiotropic APR QTL, including Lr46/Yr29, QLr-2AL.1/QYr-2AL.1, QLr-2AL.2/QYr-2AL.2, and QLr-5BL/QYr-5BL.1, were identified. Twelve associated SNPs were converted into kompetitive allele-specific PCR (KASP) markers and verified in bi-parental populations. The study reports genetic loci conferring resistance to both diseases, and the closely linked markers should be applicable for marker-assisted wheat breeding.

This review summarises the current advances and future perspectives on high‐temperature resistance in wheat against stripe rust, caused by the airborne fungal pathogen Puccinia striiformis f. sp. tritici (Pst). High‐temperature resistance, comprising high‐temperature adult‐plant (HTAP) and high‐temperature all‐stage (HTAS) resistance, is critical for durable disease control. HTAP resistance occurs in adult plants at relatively high temperatures, whereas HTAS resistance acts across all growth stages at relatively high temperatures. Genetic mapping has identified numerous HTAP‐resistance genes and quantitative trait loci (QTLs) in various chromosomal regions, especially in the B subgenome. Cloned genes, such as Yr18, Yr36 and Yr46, reveal mechanisms involving cell necrosis induction, photosynthesis modulation and nutrient transportation. For HTAS resistance, defence‐related factors such as nucleotide‐binding site‐leucine‐rich repeat proteins, transcription factors and receptor‐like kinases that mediate resistance via plant–pathogen interactions have been identified; however, research on identifying the genes or QTLs that can be used in breeding programmes is limited. To overcome host defence, Pst secretes effectors that suppress high‐temperature resistance by targeting host proteins. Future research should focus on novel gene mining, regulatory network deciphering, effector–host interaction studies and breeding applications via marker‐assisted selection and gene editing. High‐temperature resistance: A gentle might to cradle wheat against stripe rust—it draws heat's strength, spanning growth stages, outpacing pathogen shifts, a shield for fields in a warming world.

As the largest subfamily of small GTPases, the Rab subfamily plays a pivotal role in regulating biotic and abiotic stresses in plants. However, the functions of Rabs in resistance to wheat stripe rust caused by Puccinia striiformis f. sp. tritici (Pst) remain unclear. Here, we identified a Rab subfamily gene, TaRABH1bL, from Xiaoyan 6 (XY6), a wheat cultivar known for non‐race‐specific and durable high‐temperature all‐stage (HTAS) resistance to stripe rust. The expression level of TaRABH1bL was exclusively up‐regulated with Pst inoculation under the relatively high‐temperature treatment, which indicated that TaRABH1bL might concurrently respond to both biotic and abiotic stress signals. The TaRABH1bL gene was primarily expressed in leaves. Barley stripe mosaic virus (BSMV)‐induced TaRABH1bL gene silencing significantly reduced HTAS resistance to Pst, resulting in increased sporulation. Transient expression of TaRABH1bL in Nicotiana benthamiana leaves and wheat protoplasts confirmed its subcellular localisation in both cytoplasm and nuclei. The GTP‐binding state of TaRABH1bL (TaRABH1bLQ69L) exclusively interacted with the transcription factor ethylene‐responsive transcription factor 1‐like (TaERF1L) in nuclei. TaERF1L directly bound to and suppressed the activity of the GCC‐box motif, and this inhibitory effect was enhanced by the exclusive interaction between TaRABH1bLQ69L and TaERF1L. Silencing TaERF1L significantly reduced HTAS resistance. These results suggested that under dual signals of Pst infection and relatively high temperature treatment, TaRABH1bL transferred into its GTP‐binding state and interacted with TaERF1L. Additionally, TaRABH1bLQ69L enhanced the suppression of TaERF1L on its downstream susceptible or temperature‐sensitive genes containing the GCC‐box motif, thereby activating HTAS resistance to Pst in XY6. Under dual treatment of Puccinia striiformis f. sp. tritici (Pst) infection and relatively high temperature treatment, TaRABH1bLQ69L (GTP‐binding state of TaRABH1bL) interacts with TaERF1L. TaRABH1bLQ69L enhances the suppression of TaERF1L on its downstream genes containing the GCC‐box motif, thereby activating high‐temperature all‐stage (HTAS) resistance to Pst.

Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is one of the most destructive wheat diseases. The plant hormone abscisic acid (ABA) plays a key regulatory role in plant response to stress. ABA‐, stress‐, ripening‐induced proteins (ASR) have been shown to be abundantly induced in response to biotic and abiotic stresses to protect plants from damage. However, the function of wheat ASR2‐like protein (TaASR2L) in plants under biotic stress remains unclear. In this study, transient silencing of TaASR2L using a virus‐induced gene silencing system substantially reduced wheat resistance to Pst. TaASR2L interaction with serine/arginine‐rich splicing factor SR30‐like (TaSR30) was validated mainly in the nucleus. Knockdown of TaSR30 expression substantially reduced wheat resistance to Pst. Overexpression of TaASR2L and TaSR30 demonstrated that they can promote the expression of ABA‐ and resistance‐related genes to enhance wheat resistance to Pst. In addition, the expression levels of TaSR30 and TaASR2L were substantially increased by exogenous ABA, and the resistance of wheat to Pst was increased, and the expression of PR genes was induced. Therefore, these results suggest that TaASR2L interacts with TaSR30 by promoting PR genes expression and enhancing wheat resistance to Pst. The interaction of TaASR2L and TaSR30 positively regulates resistance to stripe rust (Puccinia striiformis f. sp. tritici) in wheat.

Sunflower rust, caused by the fungus Puccinia helianthi, poses a significant threat to global sunflower production. However, the fundamental mechanisms of P. helianthi infection and development remain poorly understood. This study aims to elucidate the infection process of P. helianthi in sunflower leaves through histological and cytological observations. P. helianthi is an autoecious fungus that undergoes five spore stages: teliospores, basidiospores, pycniospores, aeciospores, and urediospores. Our findings revealed that basidiospores germinated by producing a germ tube at 24 hours post-inoculation (hpi). This germ tube entered the leaf through the stomata or directly penetrated the epidermal cells without forming an appressorium, resulting in the formation of monokaryotic intercellular hyphae. The hyphae grew along the cell wall, which thickened when the hyphae came in touch with the mesophyll cells. The monokaryotic haustorium formed within the host cells at 48 hpi. Chlorotic dots began to appear on the upper surface of the leaves five to six days after the basidiospores were inoculated. After 14 days post-inoculation (dpi), flask-shaped orange pycnia developed. By approximately 18 d, honeydew started appearing on the pycnia. Aecia began to develop six or seven days after fertilization; they were cylinder-shaped and adorned with coglike ornaments. Aeciospores and urediospores germinated by producing a germ tube at 4 hpi, which subsequently developed a dome-shaped appressorium that penetrated the sunflower leaves through the stomata at 6 hpi. Intercellular hyphae produced septa apically and further differentiated into haustorial mother cells, which invaded the host cell and formed multinucleate haustoria at 24 hpi, with all the cytoplasm from the haustorial mother cells flowing into the haustorium. Aeciospores with warty surfaces invaded the host and produced oval-shaped urediospores at 14 dpi, which exhibited dense, thorny protrusions on their surfaces. By regulating the temperature, the urediospore-infected leaves were induced to produce teliospores after 20 days, which consisted of two cells with smooth surfaces.