Summary: Rice sheath blight (RSB) is an economically significant disease affecting rice yield worldwide. Genetic resistance to RSB is associated with multiple minor genes, with each providing a minor phenotypic effect, but the underlying dominant resistance genes remain unknown. A genome‐wide association study (GWAS) of 259 diverse rice varieties, with genotypes based on a single nucleotide polymorphism (SNP) and haplotype, was conducted to assess their sheath blight reactions at three developmental stages (seedlings, tillering and booting). A total of 653 genes were correlated with sheath blight resistance, of which the disease resistance protein RPM1 (OsRSR1) and protein kinase domain‐containing protein (OsRLCK5) were validated by overexpression and knockdown assays. We further found that the coiled‐coil (CC) domain of OsRSR1 (OsRSR1‐CC) and full‐length OsRLCK5 interacted with serine hydroxymethyltransferase 1 (OsSHM1) and glutaredoxin (OsGRX20), respectively. It was found that OsSHM1, which has a role in the reactive oxygen species (ROS) burst, and OsGRX20 enhanced the antioxidation ability of plants. A regulation model of the new RSB resistance though the glutathione (GSH)‐ascorbic acid (AsA) antioxidant system was therefore revealed. These results enhance our understanding of RSB resistance mechanisms and provide better gene resources for the breeding of disease resistance in rice.

Rhizoctonia solani AG1 IA is a necrotrophic fungus that causes rice sheath blight, one of the most significant rice diseases in the world. However, little is known about the pathogenic mechanisms and functions of effectors in R. solani AG1 IA. We performed functional studies on effectors in R. solani AG1 IA and found that, of 11 putative effectors tested, only RsIA_NP8 caused necrosis in the leaves of Nicotiana benthamiana. The predicted signal peptide of this protein was required to induce cell death, whereas predicted N-glycosylation sites were not required. RsIA_NP8 was upregulated during early infection, and the encoded protein was secreted. Furthermore, the ability of RsIA_NP8 to trigger cell death in N. benthamiana depended on suppressor of G2 allele of Skp1 (SGT1) and heat shock protein 90 (HSP90), but not on Mla12 resistance (RAR1) and somatic embryogenesis receptor-like kinase (SERK3). A natural variation that prevents the triggering of cell death in N. benthamiana was found in RsIA_NP8 in 25 R. solani AG1 IA strains. It is important to note that RsIA_NP8 induced the immune response in N. benthamiana leaves. Collectively, these results show that RsIA_NP8 is a possible effector that plays a key role in R. solani AG1 IA–host interactions.

Starch accumulation is key for the maturity of rice pollen grains; however, the regulatory mechanism underlying this process remains unknown. Here, we have isolated a male-sterile rice mutant, abnormal pollen 1 (ap1), which produces nonviable pollen grains with defective starch accumulation. Functional analysis revealed that AP1 encodes an active L-type lectin receptor-like kinase (L-LecRLK). AP1 is localized to the plasma membrane and its transcript is highly accumulated in pollen during the starch synthesis phase. RNA-seq and phosphoproteomic analysis revealed that the expression/phosphorylation levels of numerous genes/proteins involved in starch and sucrose metabolism pathway were significantly altered in the mutant pollen, including a known rice UDP-glucose pyrophosphorylase (OsUGP2). We further found that AP1 physically interacts with OsUGP2 to elevate its enzymatic activity, likely through targeted phosphorylation. These findings revealed a novel role of L-LecRLK in controlling pollen maturity via modulating sucrose and starch metabolism.

Tilletia horrida is a soil-borne, mononucleate basidiomycete fungus with a biotrophic lifestyle that causes rice kernel smut, a disease that is distributed throughout hybrid rice growing areas worldwide. Here we report on the high-quality genome sequence of T. horrida; it is composed of 23.2 Mb that encode 7,729 predicted genes and 6,973 genes supported by RNA-seq. The genome contains few repetitive elements that account for 8.45% of the total. Evolutionarily, T. horrida lies close to the Ustilago fungi, suggesting grass species as potential hosts, but co-linearity was not observed between T. horrida and the barley smut Ustilago hordei. Genes and functions relevant to pathogenicity were presumed. T. horrida possesses a smaller set of carbohydrate-active enzymes and secondary metabolites, which probably reflect the specific characteristics of its infection and biotrophic lifestyle. Genes that encode secreted proteins and enzymes of secondary metabolism, and genes that are represented in the pathogen-host interaction gene database genes, are highly expressed during early infection; this is consistent with their potential roles in pathogenicity. Furthermore, among the 131 candidate pathogen effectors identified according to their expression patterns and functionality, we validated two that trigger leaf cell death in Nicotiana benthamiana. In summary, we have revealed new molecular mechanisms involved in the evolution, biotrophy, and pathogenesis of T. horrida.