The additional PRC2 subunit and Sin3 histone deacetylase complex are required for the normal distribution of H3K27me3 occupancy and transcriptional silencing in Magnaporthe oryzae.

Development in higher organisms requires proper gene silencing, partially achieved through trimethylation of lysine 27 on histone H3 (H3K27me3). However, how the normal distribution of this modification is established and maintained and how it affects gene expression remains unclear, especially in fungi. Polycomb repressive complex 2 (PRC2) catalyses H3K27me3 to assemble transcriptionally repressed facultative heterochromatin and is crucial in animals, plants, and fungi. Here, we report on the critical role of an additional PRC2 subunit in the normal distribution of H3K27me3 occupancy and the stable maintenance of gene repression in the rice fungal pathogen Magnaporthe oryzae. P55, identified as an additional PRC2 subunit, is physically associated with core subunits of PRC2 and is required for a complete level of H3K27me3 modification. Loss of P55 caused severe global defects in the normal distribution of H3K27me3 and transcriptional reprogramming on the H3K27me3-occupied genes. Furthermore, we found that the Sin3 histone deacetylase complex was required to sustain H3K27me3 occupancy and stably maintain gene repression by directly interacting with P55. Our results revealed a novel mechanism by which P55 and Sin3 participate in the normal distribution of facultative heterochromatic modifications and the stable maintenance of gene repression in eukaryotes.

Dual impact of ambient humidity on the virulence of Magnaporthe oryzae and basal resistance in rice.

Humidity is a critical environmental factor affecting the epidemic of plant diseases. However, it is still unclear how ambient humidity affects the occurrence of diseases in plants. In this study, we show that high ambient humidity enhanced blast development in rice plants under laboratory conditions. Furthermore, we found that high ambient humidity enhanced the virulence of Magnaporthe oryzae by promoting conidial germination and appressorium formation. In addition, the results of RNA-sequencing analysis and the ethylene content assessment revealed that high ambient humidity suppressed the accumulation of ethylene and the activation of ethylene signaling pathway induced by M. oryzae in rice. Knock out of ethylene signaling genes OsEIL1 and OsEIN2 or exogenous application of 1-methylcyclopropene (ethylene inhibitor) and ethephon (ethylene analogues) eliminated the difference of blast resistance between the 70% and 90% relative humidity conditions, suggesting that the activation of ethylene signaling contributes to humidity-modulated basal resistance against M. oryzae in rice. In conclusion, our results demonstrated that high ambient humidity enhances the virulence of M. oryzae and compromises basal resistance by reducing the activation of ethylene biosynthesis and signaling in rice. Results from this study provide cues for novel strategies to control rice blast under global environmental changes.

MoWhi2 Mediates Mitophagy to Regulate Conidiation and Pathogenesis in Magnaporthe oryzae.

Mitophagy refers to the specific process of degrading mitochondria, which is an important physiological process to maintain the balance of mitochondrial quantity and quality in cells. At present, the mechanisms of mitophagy in pathogenic fungi remain unclear. Magnaporthe oryzae (Syn. Pyricularia oryzae), the causal agent of rice blast disease, is responsible for the most serious disease of rice. In M. oryzae, mitophagy occurs in the foot cells and invasive hyphae to promote conidiation and infection. In this study, fluorescent observations and immunoblot analyses showed that general stress response protein MoWhi2 is required for mitophagy in M. oryzae. In addition, the activation of the autophagy, pexophagy and cytoplasm-to-vacuole targeting (CVT) pathway upon nitrogen starvation was determined using the GFP-MoATG8, GFP-SRL and MoAPE1-GFP strains and the ΔMowhi2 mutant in these backgrounds. The results indicated that MoWhi2 is specifically required for mitophagy in M. oryzae. Further studies showed that mitophagy in the foot cells and invasive hyphae of the ΔMowhi2 was interrupted, leading to reduced conidiation and virulence in the ΔMowhi2 mutant. Taken together, we found that MoWhi2 contributes to conidiation and invasive growth by regulating mitophagy in M. oryzae.

Similarities and Differences of Autophagy in Mammals, Plants, and Microbes.

Autophagy, a highly conserved metabolic process in eukaryotes, is a widespread degradation/recycling system. However, there are significant differences (as well as similarities) between autophagy in animals, plants, and microorganisms such as yeast. While the overall process of autophagy is similar between different organisms, the molecular mechanisms and the pathways regulating autophagy are different, which is manifested in the diversity and specificity of the genes involved. In general, the autophagy system is much more complicated in mammals than in yeast. In addition, there are some differences in the types of autophagy present in animals, plants, and microorganisms. For example, there is a unique type of selective autophagy called the cytoplasm-to-vacuole targeting (Cvt) pathway in yeast, and a special kind of autophagy, chloroplast autophagy, exists in plants. In conclusion, although autophagy is highly conserved in eukaryotes, there are still many differences between autophagy of animals, plants, and microorganisms.

Recent Progress in Rice Broad-Spectrum Disease Resistance.

Rice is one of the most important food crops in the world. However, stable rice production is constrained by various diseases, in particular rice blast, sheath blight, bacterial blight, and virus diseases. Breeding and cultivation of resistant rice varieties is the most effective method to control the infection of pathogens. Exploitation and utilization of the genetic determinants of broad-spectrum resistance represent a desired way to improve the resistance of susceptible rice varieties. Recently, researchers have focused on the identification of rice broad-spectrum disease resistance genes, which include R genes, defense-regulator genes, and quantitative trait loci (QTL) against two or more pathogen species or many isolates of the same pathogen species. The cloning of broad-spectrum disease resistance genes and understanding their underlying mechanisms not only provide new genetic resources for breeding broad-spectrum rice varieties, but also promote the development of new disease resistance breeding strategies, such as editing susceptibility and executor R genes. In this review, the most recent advances in the identification of broad-spectrum disease resistance genes in rice and their application in crop improvement through biotechnology approaches during the past 10 years are summarized.

F-box proteins MoFwd1, MoCdc4 and MoFbx15 regulate development and pathogenicity in the rice blast fungus Magnaporthe oryzae.

The Skp1-Cul1-F-box-protein (SCF) ubiquitin ligases are important parts of the ubiquitin system controlling many cellular biological processes in eukaryotes. However, the roles of SCF ubiquitin ligases remain unclear in phytopathogenic Magnaporthe oryzae. Here, we cloned 24 F-box proteins and confirmed that 17 proteins could interact with MoSkp1, showing their potential to participate in SCF complexes. To determine their functions, null mutants of 21 F-box-containing genes were created. Among them, the F-box proteins MoFwd1, MoCdc4 and MoFbx15 were found to be required for growth, development and full virulence. Fluorescent-microscopy observations demonstrated that both MoFbx15 and MoCdc4 were localized to the nucleus, compared with MoFwd1, which was distributed in the cytosol. MoCdc4 and MoFwd1 bound to MoSkp1 via the F-box domain, the deletion of which abrogated their function. Race tube and qRT-PCR assays confirmed that MoFwd1 was involved in circadian rhythm by regulating transcription and protein stability of the core circadian clock regulator MoFRQ. Moreover, MoFWD1 also orchestrates conidial germination by influencing conidial amino acids pools and oxidative stress release. Overall, our results indicate that SCF ubiquitin ligases play indispensable roles in development and pathogenicity in M. oryzae.

Autophagy in plant pathogenic fungi.

Autophagy is a conserved cellular process that degrades cytoplasmic constituents in vacuoles. Plant pathogenic fungi develop special infection structures and/or secrete a range of enzymes to invade their plant hosts. It has been demonstrated that monitoring autophagy processes can be extremely useful in visualizing the sequence of events leading to pathogenicity of plant pathogenic fungi. In this review, we introduce the molecular mechanisms involved in autophagy. In addition, we explore the relationship between autophagy and pathogenicity in plant pathogenic fungi. Finally, we discuss the various experimental strategies available for use in the study of autophagy in plant pathogenic fungi.

VPS9 domain-containing proteins are essential for autophagy and endocytosis in Pyricularia oryzae.

Pyricularia oryzae is the causal pathogen of rice blast disease. Autophagy has been shown to play important roles in P. oryzae development and plant infection. The P. oryzae endosomal system is highly dynamic and has been shown to be associated with conidiogenesis and pathogenicity as well. To date, the crosstalk between autophagy and endocytosis has not been explored in P. oryzae. Here, we identified three P. oryzae VPS9 domain-containing proteins, PoVps9, PoMuk1 and PoVrl1. We found that PoVps9 and PoMuk1 are localized to vesicles and are each co-localized with PoVps21, a recognized marker of early endosomes. Deletion of PoVPS9 resulted in severe defects in endocytosis and autophagosome degradation and impaired the localization of PoVps21 to endosomes. Additionally, deletion of the PoMUK1 gene in the ΔPovps9 mutant background exhibited more severe defects in development, autophagy and endocytosis compared with the ΔPovps9 mutant. Pull-down assay showed that PoVps9 interacts with PoVps21, PoRab11 and PoRab1, which have been verified to participate in endocytosis. Furthermore, yeast two-hybrid and co-immunoprecipitation assays confirmed that PoVps9 directly interacts with the GDP form of PoVps21. Thus, PoVps9 is a key protein involved in autophagy and in endocytosis.

MoRad6-mediated ubiquitination pathways are essential for development and pathogenicity in Magnaporthe oryzae.

The ubiquitin system modulates protein functions through targeting substrates for ubiquitination. Here, E2 conjugating enzyme MoRad6-related ubiquitination pathways are identified and analyzed in Magnaporthe oryzae, the causal agent of rice blast disease. Disruption of MoRad6 leads to severe defects in growth, sporulation, conidial germination, appressorium formation, and plant infection. To depict the functions of MoRad6, three putative ubiquitin ligases, MoRad18, MoBre1 and MoUbr1, are also characterized. Deletion of MoRad18 causes minor phenotypic changes, while MoBre1 is required for growth, conidiation and pathogenicity in M. oryzae. Defects in ΔMobre1 likely resulted from the reduction in di- and tri-methylation level of Histone 3 lysine 4 (H3K4). Notably, MoUbr1 is crucial for conidial adhesion and germination, possibly by degrading components of cAMP/PKA and mitogen-activated protein kinase (MAPK) Pmk1 signaling pathways via the N-end rule pathway. Germination failure of ΔMoubr1 conidia could be rescued by elevation of cAMP level or enhanced Pmk1 phosphorylation resulting from further deletion of MoIra1, the M. oryzae homolog of yeast Ira1/2. These reveal vital effects of cAMP/PKA and MAPK Pmk1 signaling on conidial germination in M. oryzae. Altogether, our results suggest that MoRad6-mediated ubiquitination pathways are essential for the infection-related development and pathogenicity of M. oryzae.

The small GTPase MoYpt7 is required for membrane fusion in autophagy and pathogenicity of Magnaporthe oryzae.

Rab GTPases are required for vesicle-vacuolar fusion during vacuolar biogenesis in fungi. To date, little is known about the biological functions of the Rab small GTPase components in Magnaporthe oryzae. In this study, we investigated MoYpt7 of M. oryzae, a homologue of the small Ras-like GTPase Ypt7 in Saccharomyces cerevisiae. Cellular localization assays showed that MoYpt7 was predominantly localized to vacuolar membranes. Using a targeted gene disruption strategy, a ΔMoYPT7 mutant was generated that exhibited defects in mycelial growth and production of conidia. The conidia of the ΔMoYPT7 mutant were malformed and defective in the formation of appressoria. Consequently, the ΔMoYPT7 mutant failed to cause disease in rice and barley. Furthermore, the ΔMoYPT7 mutant showed impairment in autophagy, breached cell wall integrity, and higher sensitivity to both calcium and heavy metal stress. Transformants constitutively expressing an active MoYPT7 allele (MoYPT7-CA, Gln67Leu) exhibited distinct phenotypes from the ΔMoYPT7 mutant. Expression of MoYPT7-CA in MoYpt7 reduced pathogenicity and produced more appressoria-forming single-septum conidia. These results indicate that MoYPT7 is required for fungal morphogenesis, vacuole fusion, autophagy, stress resistance and pathogenicity in M. oryzae.

Effectors and environment modulating rice blast disease: from understanding to effective control.

Rice blast is a highly destructive crop disease that requires the interplay of three essential factors: the virulent blast fungus, the susceptible rice plant, and favorable environmental conditions. Although previous studies have focused mainly on the pathogen and rice, recent research has shed light on the molecular mechanisms by which the blast fungus and environmental conditions regulate host resistance and contribute to blast disease outbreaks. This review summarizes significant achievements in understanding the sophisticated modulation of blast resistance by Magnaporthe oryzae effectors and the dual regulatory mechanisms by which environmental conditions influence rice resistance and virulence of the blast fungus. Furthermore, it emphasizes potential strategies for developing blast-resistant rice varieties to effectively control blast disease.

MoAti1 mediates mitophagy by facilitating recruitment of MoAtg8 to promote invasive growth in Magnaporthe oryzae.

Mitophagy is a selective autophagy for the degradation of damaged or excessive mitochondria to maintain intracellular homeostasis. In Magnaporthe oryzae, a filamentous ascomycetous fungus that causes rice blast, the most devastating disease of rice, mitophagy occurs in the invasive hyphae to promote infection. To date, only a few proteins are known to participate in mitophagy and the mechanisms of mitophagy are largely unknown in pathogenic fungi. Here, by a yeast two-hybrid screen with the core autophagy-related protein MoAtg8 as a bait, we obtained a MoAtg8 interactor MoAti1 (MoAtg8-interacting protein 1). Fluorescent observations and protease digestion analyses revealed that MoAti1 is primarily localized to the peripheral mitochondrial outer membrane and is responsible for recruiting MoAtg8 to mitochondria under mitophagy induction conditions. MoAti1 is specifically required for mitophagy, but not for macroautophagy and pexophagy. Infection assays suggested that MoAti1 is required for mitophagy in invasive hyphae during pathogenesis. Notably, no homologues of MoAti1 were found in rice and human protein databases, indicating that MoAti1 may be used as a potential target to control rice blast. By the host-induced gene silencing (HIGS) strategy, transgenic rice plants targeted to silencing MoATI1 showed enhanced resistance against M. oryzae with unchanged agronomic traits. Our results suggest that MoATI1 is required for mitophagy and pathogenicity in M. oryzae and can be used as a target for reducing rice blast.

Two H3K36 methyltransferases differentially associate with transcriptional activity and enrichment of facultative heterochromatin in rice blast fungus.

Di- and tri-methylation of lysine 36 on histone H3 (H3K36me2/3) is catalysed by histone methyltransferase Set2, which plays an essential role in transcriptional regulation. Although there is a single H3K36 methyltransferase in yeast and higher eukaryotes, two H3K36 methyltransferases, Ash1 and Set2, were present in many filamentous fungi. However, their roles in H3K36 methylation and transcriptional regulation remained unclear. Combined with methods of RNA-seq and ChIP-seq, we revealed that both Ash1 and Set2 are redundantly required for the full H3K36me2/3 activity in Magnaporthe oryzae, which causes the devastating worldwide rice blast disease. Ash1 and Set2 distinguish genomic H3K36me2/3-marked regions and are differentially associated with repressed and activated transcription, respectively. Furthermore, Ash1-catalysed H3K36me2 was co-localized with H3K27me3 at the chromatin, and Ash1 was required for the enrichment and transcriptional silencing of H3K27me3-occupied genes. With the different roles of Ash1 and Set2, in H3K36me2/3 enrichment and transcriptional regulation on the stress-responsive genes, they differentially respond to various stresses in M. oryzae. Overall, we reveal a novel mechanism by which two H3K36 methyltransferases catalyze H3K36me2/3 that differentially associate with transcriptional activities and contribute to enrichment of facultative heterochromatin in eukaryotes. Supplementary Information: The online version contains supplementary material available at 10.1007/s42994-023-00127-3.

Antifungal mechanisms of silver nanoparticles on mycotoxin producing rice false smut fungus.

Ustilaginoidea virens, which causes rice false smut disease, is a destructive filamentous fungal pathogen, attracting more attention to search for effective fungicides against U. virens. Here, the results showed that the inhibition of 2 nm AgNPs on U. virens growth and virulence displayed concentration-dependent manner. Abnormalities of fungal morphology were observed upon exposure to AgNPs. RNA-sequencing (RNA-seq) analysis revealed that AgNPs treatment up-regulated 1185 genes and down-regulated 937 genes, which significantly overlapped with the methyltransferase UvKmt6-regulated genes. Furthermore, we found that AgNPs reduced the UvKmt6-mediated H3K27me3 modification, resulting in the up-regulation of ustilaginoidin biosynthetic genes The decrease of H3K27me3 level was associated with the inhibition of mycelial growth by AgNPs treatment. These results suggested that AgNPs are an effective nano-fungicide for the control of rice false smut disease, but when using AgNPs, it needs to be combined with mycotoxin-reducing fungicides to reduce the risk of toxin pollution.

Sucrose non-fermenting protein kinase gene UvSnf1 is required for virulence in Ustilaginoidea virens.

Rice false smut caused by Ustilaginoidea virens is becoming one of the most devastating diseases in rice production areas in the world. Revealing U. virens potential pathogenic mechanisms provides ideas for formulating more effective prevention and control strategies. Sucrose non-fermenting 1 (Snf1) protein kinase plays a critical role in activating transcription and suppressing gene expression, as well as in cellular response to various stresses, such as nutrient limitation. In our study, we identified the Snf1 homolog UvSnf1 and analyzed its biological functions in U. virens. The expression level of UvSnf1 was dramatically up-regulated during invasion, indicating that UvSnf1 may participate in infection. Phenotypic analyses of UvSnf1 deletion mutants revealed that UvSnf1 is necessary for hyphae growth, spore production, and virulence in U. virens. Moreover, UvSnf1 promotes U. virens to use unfavorable carbon sources when the sucrose is insufficient. In addition, deletion of UvSnf1 down-regulates the expression of the cell wall-degrading enzymes (CWDEs) genes under sucrose limitation conditions in U. virens. Further analyses showed that CWDEs (UvCut1 and UvXyp1) are not only involved in growth, spore production, and virulence but are also required for the utilization of carbon sources. In conclusion, this study demonstrates that UvSnf1 plays vital roles in virulence and carbon source utilization in U. virens, and one of the possible mechanisms is playing a role in regulating the expression of CWDE genes.

The application of zinc oxide nanoparticles: An effective strategy to protect rice from rice blast and abiotic stresses.

The causal agent of blast disease, the filamentous fungus Magnaporthe oryzae, leads to tremendous damage on rice production worldwide. Zinc oxide nanoparticles (ZnO NPs) have multi-functions in plant growth and antimicrobial activity. However, the effects of ZnO NPs on M. oryzae and disease resistance in rice are still unclear. Here, we showed that ZnO NPs have direct antifungal activity against M. oryzae by inhibiting its conidiation and appressorium formation. In addition, ZnO NPs significantly inhibit blast development and enhance basal resistance in rice by inducing ROS accumulation and expression of defense-related genes OsNAC4, OsPR10, OsKSL4, and OsPR1b. Furthermore, we showed that ZnO NPs treatment reduces ABA level in plant, leading to increased ROS accumulation and enhanced resistance against M. oryzae. Importantly, ZnO NPs treatment improves the tolerance of rice seedlings to osmotic and heat stresses.In conclusion, not only being an effective aid in fighting against blast disease, ZnO NPs also provides a novel strategy to enhance the tolerance of rice seedlings to abiotic stress.

The E3 ubiquitin ligase OsRGLG5 targeted by the Magnaporthe oryzae effector AvrPi9 confers basal resistance against rice blast.

Rice blast, caused by Magnaporthe oryzae, is one of the most devastating diseases of rice. During infection, M. oryzae secretes effectors to facilitate blast development. Among these effectors, the avirulence factor AvrPi9 is recognized by Pi9, a broad-spectrum blast resistance protein that triggers Pi9-mediated resistance in rice. However, little is known about the interaction between AvrPi9 and Pi9 and how AvrPi9 exerts virulence to promote infection. In this study, we found that ectopic expression of AvrPi9 in the Pi9-lacking cultivar TP309 suppressed basal resistance against M. oryzae. Furthermore, we identified an AvrPi9-interacting protein in rice, which we named OsRGLG5, encoding a functional RING-type E3 ubiquitin ligase. During infection, AvrPi9 was ubiquitinated and degraded by OsRGLG5. Meanwhile, AvrPi9 affected the stability of OsRGLG5. Infection assays revealed that OsRGLG5 is a positive regulator of basal resistance against M. oryzae, but it is not essential for Pi9-mediated blast resistance in rice. In conclusion, our results revealed that OsRGLG5 is targeted by the M. oryzae effector AvrPi9 and positively regulates basal resistance against rice blast.

Transcriptional Regulation of Autophagy-Related Genes by Sin3 Negatively Modulates Autophagy in Magnaporthe oryzae.

Autophagy is a conserved degradation and recycling pathway in eukaryotes and is important for their normal growth and development. An appropriate status of autophagy is crucial for organisms which is tightly regulated both temporally and continuously. Transcriptional regulation of autophagy-related genes (ATGs) is an important layer in autophagy regulation. However, the transcriptional regulators and their mechanisms are still unclear, especially in fungal pathogens. Here, we identified Sin3, a component of the histone deacetylase complex, as a transcriptional repressor of ATGs and negative regulator of autophagy induction in the rice fungal pathogen Magnaporthe oryzae. A loss of SIN3 resulted in upregulated expression of ATGs and promoted autophagy with an increased number of autophagosomes under normal growth conditions. Furthermore, we found that Sin3 negatively regulated the transcription of ATG1, ATG13, and ATG17 through direct occupancy and changed levels of histone acetylation. Under nutrient-deficient conditions, the transcription of SIN3 was downregulated, and the reduced occupancy of Sin3 from those ATGs resulted in histone hyperacetylation and activated their transcription and in turn promoted autophagy. Thus, our study uncovers a new mechanism of Sin3 in modulating autophagy through transcriptional regulation. IMPORTANCE Autophagy is an evolutionarily conserved metabolic process and is required for the growth and pathogenicity of phytopathogenic fungi. The transcriptional regulators and precise mechanisms of regulating autophagy, as well as whether the induction or repression of ATGs is associated with autophagy level, are still poorly understood in M. oryzae. In this study, we revealed that Sin3 acts as a transcriptional repressor of ATGs to negatively regulate autophagy level in M. oryzae. Under the nutrient-rich conditions, Sin3 inhibits autophagy with a basal level through directly repressing the transcription of ATG1-ATG13-ATG17. Upon nutrient-deficient treatment, the transcriptional level of SIN3 would decrease and dissociation of Sin3 from those ATGs associates with histone hyperacetylation and activates their transcriptional expression and in turn contributes to autophagy induction. Our findings are important as we uncover a new mechanism of Sin3 for the first time to negatively modulate autophagy at the transcriptional level in M. oryzae.

UvKmt2-Mediated H3K4 Trimethylation Is Required for Pathogenicity and Stress Response in Ustilaginoidea virens.

Epigenetic modification is important for cellular functions. Trimethylation of histone H3 lysine 4 (H3K4me3), which associates with transcriptional activation, is one of the important epigenetic modifications. In this study, the biological functions of UvKmt2-mediated H3K4me3 modification were characterized in Ustilaginoidea virens, which is the causal agent of the false smut disease, one of the most destructive diseases in rice. Phenotypic analyses of the ΔUvkmt2 mutant revealed that UvKMT2 is necessary for growth, conidiation, secondary spore formation, and virulence in U. virens. Immunoblotting and chromatin immunoprecipitation assay followed by sequencing (ChIP-seq) showed that UvKMT2 is required for the establishment of H3K4me3, which covers 1729 genes of the genome in U. virens. Further RNA-seq analysis demonstrated that UvKmt2-mediated H3K4me3 acts as an important role in transcriptional activation. In particular, H3K4me3 modification involves in the transcriptional regulation of conidiation-related and pathogenic genes, including two important mitogen-activated protein kinases UvHOG1 and UvPMK1. The down-regulation of UvHOG1 and UvPMK1 genes may be one of the main reasons for the reduced pathogenicity and stresses adaptability of the ∆Uvkmt2 mutant. Overall, H3K4me3, established by histone methyltransferase UvKMT2, contributes to fungal development, secondary spore formation, virulence, and various stress responses through transcriptional regulation in U. virens.

Warm temperature compromises JA-regulated basal resistance to enhance Magnaporthe oryzae infection in rice.

Changes in global temperatures profoundly affect the occurrence of plant diseases. It is well known that rice blast can easily become epidemic in relatively warm weather. However, the molecular mechanism remains unclear. In this study, we show that enhanced blast development at a warm temperature (22°C) compared with the normal growth temperature (28°C) is rice plant-determined. Comparative transcriptome analysis revealed that jasmonic acid (JA) biosynthesis and signaling genes in rice could be effectively induced by Magnaporthe oryzae at 28°C but not at 22°C. Phenotypic analyses of the osaoc1 and osmyc2 mutants, OsCOI1 RNAi lines, and OsMYC2-OE plants further demonstrated that compromised M. oryzae-induced JA biosynthesis and signaling lead to enhanced blast susceptibility at the warm temperature. Consistent with these results, we found that exogenous application of methyl jasmonate served as an effective strategy for improving blast resistance under the warm environmental conditions. Furthermore, decreased activation of JA signaling resulted in the downregulated expression of some key basal resistance genes at 22°C when compared with 28°C. Among these affected genes, OsCEBiP (chitin elicitor-binding protein precursor) was found to be directly regulated by OsMYB22 and its interacting protein OsMYC2, a key component of JA signaling, and this contributed to temperature-modulated blast resistance. Taken together, these results suggest that warm temperature compromises basal resistance in rice and enhances M. oryzae infection by reducing JA biosynthesis and signaling, providing potential new strategies for managing rice blast disease under warm climate conditions.