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The discovery and application of genome editing introduced a new era of plant breeding by giving researchers efficient tools for the precise engineering of crop genomes1. Here we demonstrate the power of genome editing for engineering broad-spectrum disease resistance in rice (Oryza sativa). We first isolated a lesion mimic mutant (LMM) from a mutagenized rice population. We then demonstrated that a 29-base-pair deletion in a gene we named RESISTANCE TO BLAST1 (RBL1) caused broad-spectrum disease resistance and showed that this mutation caused an approximately 20-fold reduction in yield. RBL1 encodes a cytidine diphosphate diacylglycerol synthase that is required for phospholipid biosynthesis2. Mutation of RBL1 results in reduced levels of phosphatidylinositol and its derivative phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2). In rice, PtdIns(4,5)P2 is enriched in cellular structures that are specifically associated with effector secretion and fungal infection, suggesting that it has a role as a disease-susceptibility factor3. By using targeted genome editing, we obtained an allele of RBL1, named RBL1Δ12, which confers broad-spectrum disease resistance but does not decrease yield in a model rice variety, as assessed in small-scale field trials. Our study has demonstrated the benefits of editing an LMM gene, a strategy relevant to diverse LMM genes and crops.

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.

Plant pathogens cause devastating diseases, leading to serious losses to agriculture. Mechanistic understanding of pathogenesis of plant pathogens lays the foundation for the development of fungicides for disease control. Mitophagy, a specific form of autophagy, is important for fungal virulence. The role of cardiolipin, mitochondrial signature phospholipid, in mitophagy and pathogenesis is largely unknown in plant pathogenic fungi. The functions of enzymes involved in cardiolipin biosynthesis and relevant inhibitors were assessed using a set of assays, including genetic deletion, plant infection, lipidomics, chemical‐protein interaction, chemical inhibition, and field trials. Our results showed that the cardiolipin biosynthesis‐related gene MoGEP4 of the rice blast fungus Magnaporthe oryzae regulates growth, conidiation, cardiolipin biosynthesis, and virulence. Mechanistically, MoGep4 regulated mitophagy and Mps1‐MAPK phosphorylation, which are required for virulence. Chemical alexidine dihydrochloride (AXD) inhibited the enzyme activity of MoGep4, cardiolipin biosynthesis and mitophagy. Importantly, AXD efficiently inhibited the growth of 10 plant pathogens and controlled rice blast and Fusarium head blight in the field. Our study demonstrated that MoGep4 regulates mitophagy, Mps1 phosphorylation and pathogenesis in M. oryzae. In addition, we found that the MoGep4 inhibitor, AXD, displays broad‐spectrum antifungal activity and is a promising candidate for fungicide development. Summary Statement: This study demonstrated that MoGep4 regulates mitophagy, Mps1 activation and pathogenesis in Magnaporthe oryzae. Additionally, we found that the MoGep4 inhibitor, alexidine dihydrochloride, displays broad‐spectrum antifungal activity and is effective in disease control in the field. [ABSTRACT FROM AUTHOR]

One of the bottleneck issues for commercial scale-up of Ti additive manufacturing lies in high cost of raw material, i.e. the spherical Ti powder that is often made by gas atomization. In this study, we address this significant issue by way of powder modification & ball milling processing, which shows that it is possible to produce printable Ti powders based on ultra-low cost, originally unprintable hydrogenation-dehydrogenation (HDH) Ti powder. It is also presented that the as-printed Ti using the modified powder exhibits outstanding mechanical properties, showing a combination of excellent fracture strength (~895 MPa) and high ductility (~19.0% elongation).