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Activation of innate immunity by membrane-localized receptors is conserved across eukaryotes. Plant genomes contain hundreds of such receptor-like genes and those encoding proteins with an extracellular leucine-rich repeat (LRR) domain represent the largest family. Here, we develop a high-throughput approach to study LRR receptor-like genes on a genome-wide scale. In total, 257 tobacco rattle virus-based constructs are generated to target 386 of the 403 identified LRR receptor-like genes in Nicotiana benthamiana for silencing. Using this toolkit, we identify the LRR receptor-like protein Response to XEG1 (RXEG1) that specifically recognizes the glycoside hydrolase 12 protein XEG1. RXEG1 associates with XEG1 via the LRR domain in the apoplast and forms a complex with the LRR receptor-like kinases BAK1 and SOBIR1 to transduce the XEG1-induced defense signal. Thus, this genome-wide silencing assay is demonstrated to be an efficient toolkit to pinpoint new immune receptors, which will contribute to developing durable disease resistance. The role of most plant leucine-rich repeat (LRR) receptors in innate immunity is unknown. Here, the authors develop virus-based constructs to silence LRR receptor-like genes in the Nicotiana benthamiana genome and identify Response to XEG1 that specifically recognizes the glycoside hydrolase 12 protein XEG1.

Oomycete pathogens secrete host cell-entering effector proteins to manipulate host immunity during infection. We previously showed that PsAvh52, an early-induced RxLR effector secreted from the soybean root rot pathogen, Phytophthora sojae, could suppress plant immunity. Here, we found that PsAvh52 is required for full virulence on soybean and binds to a novel soybean transacetylase, GmTAP1, in vivo and in vitro. PsAvh52 could cause GmTAP1 to relocate into the nucleus where GmTAP1 could acetylate histones H2A and H3 during early infection, thereby promoting susceptibility to P. sojae. In the absence of PsAvh52, GmTAP1 remained confined to the cytoplasm and did not modify plant susceptibility. These results demonstrate that GmTAP1 is a susceptibility factor that is hijacked by PsAvh52 in order to promote epigenetic modifications that enhance the susceptibility of soybean to P. sojae infection. Just like animals, plants can become infected and diseased. Among the microbes that infect plants, one group tends to stand out. Named Phytophthora after the Greek for ‘the plant destroyer’, these fungus-like microbes cause diseases in many species of plant, including important food crops. These diseases are difficult to control, and as a result Phytophthora diseases cost the farming industry billions of dollars every year. Effective control of Phytophthora diseases is likely to depend on scientists first gaining a better understanding of how these microbes infect plants. Also like animals, plants have an immune system to protect themselves from disease. Yet many disease-causing microbes make so-called effector proteins to overcome their hosts’ defenses. Previously in 2015, researchers reported that one effector made by a species known as Phytophthora sojae could suppress the immune system of soybean plants during the early stages of an infection. But it was not clear how the effector achieved this. Now, Li et al., who include many of the researchers involved in the 2015 study, go on to show that the same effector, known as PsAvh52, helps P. sojae to infect soybean plants by interacting with a previously unknown soybean enzyme. The enzyme is a transacetylase, meaning it belongs to a group of enzymes that transfer a chemical marker called an acetyl group on to other molecules including proteins. Li et al. went on to show that the PsAvh52 effector essentially hijacks the transacetylase enzyme, moving it to a location in the cell nucleus where it could chemically modify the proteins that package the soybean plant’s DNA. These chemical changes activate nearby genes that would have otherwise been switched off, and these incorrectly activated genes make the plant more susceptible to the infection. By deciphering one of the strategies that helps P. sojae to infect soybean plants, Li et al. have uncovered two possible approaches that may help to get this plant disease under control. The findings highlight the effector PsAvh52 as a weapon that could be blocked; they also reveal the transacetylase enzyme as a vulnerable point in the plant that could be protected. The next step will be to explore if there are chemical or genetic means that can achieve either of these two goals.

Protein kinase MoCK2 has been identified as a pivotal regulator in the rice blast fungus Magnaporthe oryzae , orchestrating critical biological processes including hyphal growth, conidiation, and host infection. Building upon our previous investigations into its interplay with cellular energy metabolism and polar regeneration during appressorium formation, this study systematically delineated the MoCK2 regulatory network through integrated proteomic and phosphoproteomic analyses. Three key mechanistic insights emerged from this research. Firstly, while MoCK2 deficiency did not directly impair mitochondrial functionality, it disrupted intracellular vesicular trafficking systems, thereby constraining substrate availability for mitochondrial metabolism and ultimately leading to energy homeostasis defects. Secondly, absence of MoCK2 nucleolar localization in regulatory subunit deletion mutants substantially compromised ribosome biogenesis, creating a bottleneck in protein synthesis capacity that failed to meet cellular demands. Thirdly, phosphoregulation analysis demonstrated MoCK2’s multifaceted role as a signaling node, modulating critical developmental transitions through phosphorylation-dependent control of conidial germination, appressorial morphogenesis, and host penetration apparatus assembly. These findings established MoCK2 as a central coordinator linking organelle dynamics, translational regulation, and infection-related signaling cascades. This study provides a conceptual framework for future investigations into the functional characterization of MoCK2, while also offering methodological references for CK2 research across diverse biological systems.

L-type lectin receptor-like kinases (LecRKs) comprise an important class of membrane-localized receptor-like kinases that are involved in plant adaptation. In this study, we performed an inventory analysis of LecRKs in Glycine max (soybean). In total, 64 GmLecRKs containing the canonical LecRK feature were identified. Phylogenetic analysis revealed that 48 GmLecRKs have close orthologs in Arabidopsis or Solanum lycopersicum, while 16 are likely present only in the leguminous plant species. Transcriptome analyses revealed that expressions of multiple GmLecRK genes are either induced or suppressed during infection by the soybean root rot pathogen Phytophthora sojae. In addition, overexpression of the three LecRKs (Glyma.17G085000, Glyma.05G041300 or Glyma.17G224600) in the soybean hairy roots enhanced resistance to P. sojae. Upon inoculation with Bradyrhizobium diazoefficiens, overexpression of Glyma.17G085000 in the soybean hairy roots does not significantly influence the nodulation, while overexpression of Glyma.05G041300 or Glyma.17G224600 slightly reduced the number and dry weight of nodules. This study highlights the importance of LecRKs in regulating plant–microbe interactions and provides new knowledge on the deployment of LecRKs to increase resistance in soybean.

Background Previous studies have shown that protein kinase MoKin1 played an important role in the growth, conidiation, germination and pathogenicity in rice blast fungus, Magnaporthe oryzae . ΔMokin1 mutant showed significant phenotypic defects and significantly reduced pathogenicity. However, the internal mechanism of how MoKin1 affected the development of physiology and biochemistry remained unclear in M. oryzae . Result This study adopted a multi-omics approach to comprehensively analyze MoKin1 function, and the results showed that MoKin1 affected the cellular response to endoplasmic reticulum stress (ER stress). Proteomic analysis revealed that the downregulated proteins in ΔMokin1 mutant were enriched mainly in the response to ER stress triggered by the unfolded protein. Loss of MoKin1 prevented the ER stress signal from reaching the nucleus. Therefore, the phosphorylation of various proteins regulating the transcription of ER stress-related genes and mRNA translation was significantly downregulated. The insensitivity to ER stress led to metabolic disorders, resulting in a significant shortage of carbohydrates and a low energy supply, which also resulted in severe phenotypic defects in ΔMokin1 mutant. Analysis of MoKin1-interacting proteins indicated that MoKin1 really took participate in the response to ER stress. Conclusion Our results showed the important role of protein kinase MoKin1 in regulating cellular response to ER stress, providing a new research direction to reveal the mechanism of MoKin1 affecting pathogenic formation, and to provide theoretical support for the new biological target sites searching and bio-pesticides developing.

Rice is a crucial food crop worldwide, but its yield and quality are significantly affected by Meloidogyne graminicola is a root knot nematode. No rice variety is entirely immune to this nematode disease in agricultural production. Thus, the fundamental strategy to combat this disease is to utilize rice resistance genes. In this study, we conducted transcriptome and metabolome analyses on two rice varieties, ZH11 and IR64. The results indicated that ZH11 showed stronger resistance than IR64. Transcriptome analysis revealed that the change in gene expression in ZH11 was more substantial than that in IR64 after M. graminicola infection. Moreover, GO and KEGG enrichment analysis of the upregulated genes in ZH11 showed that they were primarily associated with rice cell wall construction, carbohydrate metabolism, and secondary metabolism relating to disease resistance, which effectively enhanced the resistance of ZH11. However, in rice IR64, the number of genes enriched in disease resistance pathways was significantly lower than that in ZH11, which further explained susceptibility to IR64. Metabolome analysis revealed that the metabolites detected in ZH11 were enriched in flavonoid metabolism and the pentose phosphate pathway, compared to IR64, after M. graminicola infection. The comprehensive analysis of transcriptome and metabolome data indicated that flavonoid metabolism plays a crucial role in rice resistance to M. graminicola infection. The content of kaempferin, apigenin, and quercetin in ZH11 significantly increased after M. graminicola infection, and the expression of genes involved in the synthetic pathway of flavonoids also significantly increased in ZH11. Our study provides theoretical guidance for the precise analysis of rice resistance and disease resistance breeding in further research.

Phytophthora capsici is frequently found in pepper (Capsicum annuum L.) cultivation, causing severe yield loss and fruit quality deterioration. Light quality is known to influence pepper growth and stress responses, but its role in pepper resistance against P. capsici remains poorly understood. This study displayed that, among pepper plants treated with red, green, and blue light (BL) and infected with P. capsici, those under BL exposure showed the highest disease index accompanied by lower H2O2 and salicylic acid (SA) contents. Correspondingly, the blue light photoreceptor CaCRY2 was induced by both BL exposure and P. capsici infection (PCI). Silencing of CaCRY2 in pepper led to a decrease in disease index and lesion area with higher ROS and SA accumulation, while overexpression of CaCRY2 in tobacco increased disease index. In addition, we also found that CaCRY2 manipulated the resistance of pepper against P. capsici through ROS and SA signaling pathways. These results provide a new perspective on the involvement of blue light exposure in pepper resistance to P. capsici.

The extracellular space (apoplast) of plant tissue represents a critical battleground between plants and attacking microbes. Here we show that a pathogen-secreted apoplastic xyloglucan-specific endoglucanase, PsXEG1, is a focus of this struggle in the Phytophthora sojae–soybean interaction. We show that soybean produces an apoplastic glucanase inhibitor protein, GmGIP1, that binds to PsXEG1 to block its contribution to virulence. P. sojae, however, secretes a paralogous PsXEG1-like protein, PsXLP1, that has lost enzyme activity but binds to GmGIP1 more tightly than does PsXEG1, thus freeing PsXEG1 to support P. sojae infection. The gene pair encoding PsXEG1 and PsXLP1 is conserved in many Phytophthora species, and the P. parasitica orthologs PpXEG1 and PpXLP1 have similar functions. Thus, this apoplastic decoy strategy may be widely used in Phytophthora pathosystems.

Hosts and pathogens are engaged in a continuous evolutionary struggle for physiological dominance. A major site of this struggle is the apoplast. In Phytophthora sojae–soybean interactions, PsXEG1, a pathogen-secreted apoplastic endoglucanase, is a key focal point of this struggle, and the subject of two layers of host defense and pathogen counterdefense. Here, we show that N-glycosylation of PsXEG1 represents an additional layer of this coevolutionary struggle, protecting PsXEG1 against a host apoplastic aspartic protease, GmAP5, that specifically targets PsXEG1. This posttranslational modification also attenuated binding by the previously described host inhibitor, GmGIP1. N-glycosylation of PsXEG1 at N174 and N190 inhibited binding and degradation by GmAP5 and was essential for PsXEG1’s full virulence contribution, except in GmAP5-silenced soybeans. Silencing of GmAP5 reduced soybean resistance against WT P. sojae but not against PsXEG1 deletion strains of P. sojae. The crucial role of N-glycosylation within the three layers of defense and counterdefense centered on PsXEG1 highlight the critical importance of this conserved apoplastic effector and its posttranslationalmodification in Phytophthora-host coevolutionary conflict.

The organs of a plant species vary in cell structure, metabolism and defence responses. However, the mechanisms that enable a single pathogen to colonise different plant organs remain unclear. Here we compared the transcriptome of the oomycete pathogen Phytophthora sojae during infection of roots versus leaves of soybeans. We found differences in the transcript levels of hundreds of pathogenicity‐related genes, particularly genes encoding carbohydrate‐active enzymes, secreted (effector) proteins, oxidoreductase‐related proteins and transporters. To identify the key regulator for root‐specific infection, we knocked out root‐specific transcription factors (TFs) and found the mutants of PsBZPc29, which encodes a member of an oomycete‐specific class of basic leucine zipper (bZIP) TFs, displayed reduced virulence on soybean roots but not on leaves. More than 60% of the root‐specific genes showed reduced expression in the mutants during root infection. The results suggest that transcriptional regulation underlies the organ‐specific infection by P. sojae, and that a bZIP TF plays a key role in root‐specific transcriptional regulation. Phytophthora sojae mobilises specific genes when infecting different plant organs; PsBZPc29, a basic leucine zipper transcription factor, is a key transcriptional regulator for root‐specific genes that are highly expressed during root infection.