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The widely used rice variety Lijiangxintuanheigu (LTH) shows a universal susceptibility to thousands of Magnaporthe oryzae isolates, the causal agent of devastating rice blast, making LTH an ideal line in resistance (R) gene cloning. However, the underlying genetic mechanism of the universal susceptibility has not been fully revealed because of the lack of a high-quality genome. Here, we took a genomic approach together with experimental assays to investigate LTHs universal susceptibility to rice blast. Using Nanopore long reads, we assembled a chromosome-level genome. Millions of genomic variants were detected by comparing LTH with 10 other rice varieties, of which large-effect variants could affect plant immunity. Gene family analyses show that the number of R genes and leucine-rich repeat receptor-like protein kinase (LRR-RLK)-encoding genes decrease significantly in LTH. Rice blast resistance genes called Pi genes are either absent or disrupted by genomic variations. Additionally, residual R genes of LTH are likely under weak pathogen selection pressure, and other plant defense-related genes are weakly induced by rice blast. In contrast, the pattern-triggered immunity (PTI) of LTH is normal, as demonstrated by experimental assays. Therefore, we conclude that weak effector-trigger immunity (ETI)-mediated primarily by Pi genes but not PTI results in the universal susceptibility of LTH to rice blast. The attenuated ETI of LTH may be also associated with reduced numbers of R genes and LRR-RLKs, and minimally functional residual defense-related genes. Finally, we demonstrate the use of the LTH genome by rapid cloning of the Pi gene Piak from a resistant variety.

Summary: Lipids and lipid metabolites have essential roles in plant–pathogen interactions. GDSL‐type lipases are involved in lipid metabolism modulating lipid homeostasis. Some plant GDSLs modulate lipid metabolism altering hormone signal transduction to regulate host‐defence immunity. Here, we functionally characterized a rice lipase, OsGELP77, promoting both immunity and yield. OsGELP77 expression was induced by pathogen infection and jasmonic acid (JA) treatment. Overexpression of OsGELP77 enhanced rice resistance to both bacterial and fungal pathogens, while loss‐of‐function of osgelp77 showed susceptibility. OsGELP77 localizes to endoplasmic reticulum and is a functional lipase hydrolysing universal lipid substrates. Lipidomics analyses demonstrate that OsGELP77 is crucial for lipid metabolism and lipid‐derived JA homeostasis. Genetic analyses confirm that OsGELP77‐modulated resistance depends on JA signal transduction. Moreover, population genetic analyses indicate that OsGELP77 expression level is positively correlated with rice resistance against pathogens. Three haplotypes were classified based on nucleotide polymorphisms in the OsGELP77 promoter where OsGELP77Hap3 is an elite haplotype. Three OsGELP77 haplotypes are differentially distributed in wild and cultivated rice, while OsGELP77Hap3 has been broadly pyramided for hybrid rice development. Furthermore, quantitative trait locus (QTL) mapping and resistance evaluation of the constructed near‐isogenic line validated OsGELP77, a QTL for broad‐spectrum disease resistance. In addition, OsGELP77‐modulated lipid metabolism promotes JA accumulation facilitating grain yield. Notably, the hub defence regulator OsWRKY45 acts upstream of OsGELP77 by initiating the JA‐dependent signalling to trigger immunity. Together, OsGELP77, a QTL contributing to immunity and yield, is a candidate for breeding broad‐spectrum resistant and high‐yielding rice. [ABSTRACT FROM AUTHOR]

Summary: Plants have evolved complex signalling networks to regulate growth and defence responses under an ever‐changing environment. However, the molecular mechanisms underlying the growth‐defence tradeoff are largely unclear. We previously reported that rice CALCIUM‐DEPENDENT PROTEIN KINASE 18 (OsCPK18) and MITOGEN‐ACTIVATED PROTEIN KINASE 5 (OsMPK5) mutually phosphorylate each other and that OsCPK18 phosphorylates and positively regulates OsMPK5 to suppress rice immunity. In this study, we found that OsCPK18 and its paralog OsCPK4 positively regulate plant height and yield‐related traits. Further analysis reveals that OsCPK18 and OsMPK5 synergistically regulate defence‐related genes but differentially regulate development‐related genes. In vitro and in vivo kinase assays demonstrated that OsMPK5 phosphorylates C‐terminal threonine (T505) and serine (S512) residues of OsCPK18 and OsCPK4, respectively. The kinase activity of OsCPK18T505D, in which T505 was replaced by aspartic acid to mimic T505 phosphorylation, displayed less calcium sensitivity than that of wild‐type OsCPK18. Interestingly, editing the MAPK phosphorylation motif in OsCPK18 and its paralog OsCPK4, which deprives OsMPK5‐mediated phosphorylation but retains calcium‐dependent activation of kinase activity, simultaneously increases rice yields and immunity. This editing event also changed the last seven amino acid residues of OsCPK18 and attenuated its binding with OsMPK5. This study presents a new regulatory circuit that fine tunes the growth‐defence tradeoff by modulating OsCPK18/4 activity and suggests that CRISPR/Cas9‐mediated engineering phosphorylation pathways could simultaneously improve crop yield and immunity. [ABSTRACT FROM AUTHOR]

The article explores the impact of knocking out phosphatidate phosphohydrolase (PAH) genes in plants, specifically rice and Arabidopsis. The researchers discovered that this knockout resulted in the accumulation of phosphatidic acid (PA), which in turn enhanced the plants' resistance to various pathogens. The study also revealed that PAHs are present in a wide range of plants and play a role in plant defense. The findings suggest that targeting PAH genes could be a promising approach for developing disease-resistant crops. Additionally, the researchers found that while the knockout of PAH genes improved resistance to pathogens, it also hindered plant growth. They identified changes in gene expression and lipid metabolism associated with the knockout, indicating that manipulating PAH genes could potentially enhance plant resistance without compromising yield. [Extracted from the article]