Molecular plant pathology最新文献

Pathogenic fungi have developed complex and specific infection strategies to invade host tissues successfully. Regulator of G-protein signalling (RGS) proteins exhibit GTPase-accelerating protein activities and play a crucial role in the formation of infection structures in pathogenic fungi. However, specific regulatory mechanisms remain unclear. In the present study, observations of infection structure indicated that the deletion of AaRgs2 resulted in a significant increase in spore germination. Appressorium-like formation rate was compared to that of the wild-type strain on a Gelbond hydrophobic membrane coated with 16-hydroxyhexadecanoic acid or 1,16-hexadecanediol, which are cutin monomers in pear peel. Transcriptome analysis during the appressorium-like formation stage revealed 4124 differentially expressed genes (DEGs) that were annotated in the wild-type strain and the ΔAaRgs2 mutant. KEGG enrichment analysis showed that the cAMP-PKA signalling pathway, MAPK signalling pathway, peroxisome and autophagy pathway were closely associated with appressorium-like formation regulated by AaRgs2. Yeast two-hybrid and bimolecular fluorescence complementation assays demonstrated a specific physical interaction between AaRgs2 and AaGα1, further confirming that AaGα1 interacted with the Pfam domain of adenylate cyclase AC. Our studies provide evidence suggesting that AaRgs2 negatively regulates appressorium-like formation of A. alternata induced by pear cutin monomer via the AaRgs2-AaGα1-AaAC module.

Powdery mildew, caused by Podosphaera aphanis, poses a significant threat to strawberry production, while current chemical controls raise environmental and food safety concerns. In this study, we have identified the key regulatory module, FaMYB63/FvWRKY75-PR10.14, that confers enhanced powdery mildew resistance in transgenic strawberry (Fragaria vesca). FaMYB63, an R2R3-MYB transcription factor, was induced by P. aphanis infection and responsive to the application of defence signalling molecules, including salicylic acid (SA), methyl jasmonate (JA), abscisic acid (ABA), and 1-aminocyclopropane-1-carboxylic acid (ACC). Silencing of FaMYB63 led to reduced SA levels and increased powdery mildew susceptibility, accompanied by suppressed reactive oxygen species (ROS) bursts and down-regulation of PR10.14 expression. Conversely, overexpressing PR10.14 in transgenic lines inhibited P. aphanis spore germination and enhanced ROS accumulation, indicating a dual role in direct pathogen inhibition and hypersensitive response-triggered defence. Yeast one-hybrid, electrophoretic mobility shift assay, β-glucuronidase, and luciferase assays confirmed that FaMYB63 and FvWRKY75 were directly bound to the MYB-binding sites and W-box of the PR10.14 promoter, respectively, and activated its transcription, while WRKY75 negatively regulated the expression of MYB63. PR10.14 exhibited tissue-specific expression, with the highest levels in red-ripening fruits, suggesting a role in developmental-stage-dependent defence. These findings suggest FaMYB63 as an SA-dependent regulator of PR10.14-mediated resistance, bridging hormone signalling and pathogen response. This study provides a molecular target for breeding powdery mildew-resistant strawberry cultivars through genetic engineering approaches, offering an alternative to fungicides for sustainable and environmental disease management in horticultural crops and advances our understanding of MYB- or WRKY-PR10P networks in plant immunity.

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.

RING-type E3 ubiquitin ligases play crucial roles in plant immunity by ubiquitinating their downstream substrates for degradation. We previously revealed, using CRISR/Cas9-mediated knockout mutant lines, that the RING-H2 E3 ubiquitin ligase OsRFPH2-6, transcriptionally regulated by the NAC transcription factor ONAC083, negatively modulates rice blast resistance. In this study, we further confirmed the negative role of OsRFPH2-6 in rice immunity through overexpression lines and investigated its underlying regulatory mechanism. OsRFPH2-6 possesses E3 ubiquitin ligase activity, which depends on each cysteine residue within its RING domain. OsRFPH2-6 interacts with and ubiquitinates OsNF-YA1, a subunit of nuclear factor Y transcription factor, leading to its degradation. Knockout of OsNF-YA1 attenuates rice blast resistance and weakens chitin-induced immune responses. Transcriptome analysis revealed that OsNF-YA1 regulates a set of defence-associated genes. Notably, some negative immune regulators, like ONAC083, MNAC3 and OsSGR, were upregulated, whereas several positive immune regulators, such as genes encoding for phytoalexin biosynthesis and phenylpropanoid pathway enzymes, hydrolytic enzymes and pathogenesis-related proteins, including OsPAL6, OsATL15, OsCPS4, OsWRKY6, OsPR10a, and chi11, were downregulated in osnf-ya1 mutant plants. These findings suggest that OsNF-YA1 positively regulates rice immunity by modulating the transcription of a set of immune-associated genes. This study extends the previously established ONAC083-OsRFPH2-6 regulatory module in rice immunity by integrating OsNF-YA1 as a downstream substrate of OsRFPH2-6, offering possibilities to improve rice disease resistance through targeted genome editing of the ONAC083-OsRFPH2-6-OsNF-YA1 module.

Negative immune regulator CAD7 is a non-canonical member of the CAD (cinnamyl alcohol dehydrogenase) family in plants. However, little is known on its biochemical functions and underlying mechanisms of immune regulation. Here, we show that Arabidopsis thaliana AtCAD7 harbours substrate-binding residues divergent from lignin-forming CADs (AtCAD4/5), being conserved with bacterial alcohol dehydrogenases EcYahK and EcYjgB. Comparative enzymatic analysis revealed that AtCAD7 exhibits a broad substrate preference for diverse small-molecule aldehydes, including histamine-derived intermediates, being distinct from the canonical lignin-forming AtCAD5. Metabolomic analyses revealed that AtCAD7-overexpression transformants were affected in the biosynthesis and metabolism of amino acids, whereas AtCAD7-silencing lines were activated in the phenylpropanoid pathway and increased in flavonoid accumulation. Histamine was elevated in AtCAD7-overexpression lines and functional validation revealed its promoted effect on plant susceptibility to Phytophthora parasitica. In contrast, phytoalexins scopolin and chlorogenic acid were enriched in AtCAD7-silencing lines, accompanied by upregulated expression of phenylpropanoid pathway-related genes. Functional validation demonstrated that scopolin and chlorogenic acid enhanced plant resistance to P. parasitica. Collectively, our study uncovers that CAD7 functions as a metabolic hub linking small-molecule aldehyde reductase activity to immune suppression, providing a potential novel target for developing crops with enhanced resistance to Phytophthora pathogens.

Mitogen-activated protein kinase kinase kinase (MAPKKK) assumes a pivotal position within the MAPK cascade, converting external stimuli into intracellular responses and mediating plant stress resistance. However, there are limited reports investigating its function in regulating resistance to soybean mosaic virus (SMV). Here, a MAPKKK2-like gene GmMEKK2 (LOC100798607) was identified from an SMV-resistant cultivar, with an amino acid sequence containing the typical conserved G(T/S)Px(W/Y/F)MAPExV domain, showing homology to AtMEKK1, AtMEKK2 (SUMM1) and OsMAPKKK5. Overexpression of GmMEKK2 in soybean reduced SMV accumulation and the disease index, mitigated the yield loss after SMV inoculation and improved yield traits. In contrast, silencing GmMEKK2 via virus-induced gene silencing (VIGS) significantly enhanced SMV susceptibility, with increased disease index and viral content. Transcriptionally, defence responce genes such as PR1s and RPM1s were pre-activated in the overexpression lines before SMV infection, conferring soybean with preventive resistance. While non-transgenic plants showed severe down-regulation of basic metabolic genes and strong induction of genomic repair genes at 14 days post-inoculation (dpi), overexpression lines exhibited minimal changes. Despite lacking kinase activity, GmMEKK2 bound with GmMKK1 and GmMPK4A to block the MKK1/2-MPK4 cascade, thereby indirectly enhancing the salicylic acid-induced defence responses. Additionally, GmMEKK2 overexpression elevated basal reactive oxygen species (ROS) levels to trigger autoimmunity, while maintaining ROS homeostasis via the antioxidant enzyme system in soybean. This study clarifies the function and molecular mechanism of GmMEKK2 in SMV resistance, providing a strategy for improving soybean SMV resistance.

The hypersensitive response (HR) is a powerful plant defence mechanism that restricts pathogen spread through localised cell death. However, constitutive activation of HR can impair growth and development, limiting its utility in crop breeding and protection. In the study, we developed a virus-inducible HR system by coupling an Avirulence/Resistance (Avr/R) gene pair, Avr4/Cf-4 effector-resistance gene pair, with a promoter (Solyc04g076730) specifically activated by geminivirus infection. We demonstrate that co-expression of Avr4 and Cf-4 in Nicotiana benthamiana triggers robust HR and significantly reduces accumulation of multiple geminiviruses, including TYLCV, TYLCCNV, SLCMV and BSCTV. Transcriptomic analysis of virus-infected tomato identified Solyc04g076730 as a virus-responsive promoter with minimal basal activity. Transient assays and stable transformation in both N. benthamiana and tomato revealed that this promoter effectively drives HR only upon viral infection, resulting in reduced viral loads, attenuated symptoms and improved plant vigour. Importantly, transgenic plants expressing the Solyc04g076730::Avr4/Cf-4 construct maintained normal growth under non-infected conditions. Our findings offer a promising strategy for engineering broad-spectrum resistance to viral pathogens in crops.

Recessive resistance, achieved through mutations in host susceptibility genes, offers an effective way for controlling plant viruses. One well-studied gene family involved in such resistance is the eukaryotic translation initiation factor 4E (eIF4E) gene family, which includes eIF4E, eIFiso4E and the atypical novel cap-binding protein (nCBP). Although gene pyramiding of the eIF4E family may provide a promising strategy for broadening virus resistance, it has so far been applied only to a limited set of gene combinations and target viruses. To deepen our understanding of the practicality of eIF4E family gene pyramiding, we analysed a comprehensive set of eIF4E family knockout mutants and six phylogenetically diverse viruses. Double-gene mutant lines ncbp eif4e1 and ncbp eifiso4e exhibited resistance to five and three viruses, respectively, due to both additive resistance pyramiding and the emergence of novel resistance resulting from combined mutations. Notably, the observed resistance spectrum included the Comovirus, Tymovirus, Betacarmovirus and Tobamovirus genera, which were not previously linked to the eIF4E family. These results reveal a broader involvement of the eIF4E family in viral susceptibility, which may have previously been overlooked due to functional redundancy among the family members. On the other hand, plant growth assessment revealed a more severe penalty in the ncbp eif4e1 mutant than in the ncbp eifiso4e mutant, underscoring the need to select compatible gene combinations for resistance pyramiding. Collectively, this study highlights both the advantages and potential drawbacks of eIF4E family gene pyramiding and provides insights for the future development of crop varieties with broad-spectrum virus resistance.

Sugarcane smut, caused by the fungus Sporisorium scitamineum, is a devastating disease that threatens sugar production, leading to significant yield losses. The pathogen disrupts sugarcane growth by forming whip-like structures filled with teliospores, which are disseminated through wind and rain. The control efforts are further complicated by its broad host adaptability, genetic diversity and ability to suppress host defences. Current management relies on resistant cultivars, agronomic practices, chemical and biological control measures, as well as emerging smart monitoring systems. Nevertheless, pathogen evolution and climate change pose ongoing challenges. This review synthesises recent advances in the biology, pathogenesis, host resistance mechanisms and integrated management strategies for sugarcane smut, with a particular focus on multi-omics approaches that provide new insights into pathogen-host interactions. However, translating these insights into durable resistance and sustainable control strategies remains a key challenge for future research.

Taxonomy: Domain Eukaryota, Kingdom Fungi, Phylum Basidiomycota, Class Ustilaginomycetes, Order Ustilaginales, Family Ustilaginaceae, Genus Sporisorium.

Biology: Sporisorium scitamineum is a biotrophic fungus with a complex sexual-asexual life cycle. Diploid teliospores germinate into haploid sporidia under favourable conditions. Compatible sporidia, regulated by tightly linked a and b mating-type loci, mate to form dikaryotic hyphae, which invade sugarcane meristematic tissues via appressoria and cell wall degradation. The hyphae proliferate systemically in meristems and vascular tissues, divert host nutrients and finally induce whip-like sori with new teliospores.

Host range: Primarily infects sugarcane; exhibits geographic genetic differentiation with adapted populations in Southeast Asia, South America and China. This regional adaptation is driven by long-term host-pathogen co-evolution and environmental factors.

Disease symptoms: Characterised by whip-like sori at stalk apices, chlorotic and elongated leaves, increased tillering, thinner stalks and overall stunted growth, these symptoms collectively lead to reduced sugarcane yield and quality.

Disease control: Managed through resistant varieties, hot water treatment of seed cane, crop rotation, fungicides, biocontrol agents and smart systems using remote sensing and AI-based forecasting.

Phytophthora infestans, the causal agent of potato late blight, employs divergent RxLR effectors to undermine host immunity. One such effector, PiAvr3b, is known to activate resistance in plants carrying the R3b gene; however, its virulence mechanism in susceptible hosts remains unclear. Here, we demonstrate that PiAvr3b is delivered from haustoria through a brefeldin A (BFA)-insensitive pathway, bypassing the traditional endoplasmic reticulum-Golgi trafficking process. Through yeast two-hybrid screening and functional validation, we identified potato NADP-malic enzyme 3 (StME3) and its Nicotiana benthamiana ortholog NbME3 as the direct host target of PiAvr3b. StME3/NbME3 acts as a susceptibility factor; its overexpression enhanced pathogen colonisation, while silencing it confered resistance. PiAvr3b stabilises StME3 independently of the 26S proteasome and autophagy pathways, thereby extending the half-life of this metabolic enzyme. Importantly, although PiAvr3b retained immune-suppressive activity in NbME3-silenced plants, it failed to promote infection of P. infestans, revealing that ME3 stabilisation is indispensable for PiAvr3b's virulence function. Binding to PiAvr3b did not alter the enzyme activity of StME3. Our findings uncover a strategy by which an oomycete effector determines a key metabolic enzyme turnover without disturbing enzymatic activity to reprogramme host susceptibility and establish disease.