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Oat stem rust, caused by Puccinia graminis f. sp. avenae, is one of the most devastating diseases of oat. The most cost-effective and environmentally friendly strategy to control this disease is the use of resistant cultivars. However, P. graminis f. sp. avenae can overcome the resistance of cultivars by rapidly changing its virulence. Thus, information on the virulence of P. graminis f. sp. avenae populations and resistance of cultivars is critical to control the disease. The current study was conducted to monitor the virulence composition and dynamics of the P. graminis f. sp. avenae population in China and to evaluate resistance of oat cultivars. Oat leaves naturally infected by P. graminis f. sp. avenae were collected in 2018 and 2019, and 159 isolates were derived from single uredinia. The isolates were tested on 12 international differential lines, and eight races, TJJ, TBD, TJB, TJD, TJL, TJN, TGD, and TKN, were identified for the first time in China. The predominant race was TJD, virulent against Pg1, Pg2, Pg3, Pg4, Pg8, Pg9, and Pg15, accounting for 35.8 and 37.8% in 2018 and 2019, respectively. The sub-predominant races were TJN (30.2% in 2018, 28.3% in 2019) and TKN (20.8% in 2018, 12.3% in 2019). All isolates were virulent to Pg1, Pg2, Pg3, and Pg4, and avirulent to Pg6 and Pg16. The three predominant races (TJD, TJN, and TKN) were used to evaluate resistance in 30 Chinese oat cultivars at the seedling and adult plant stages. Five cultivars, Bayan 1, Baiyan 2, Baiyan 3, Baiyan 5, and Baiyan 9, were highly resistant to the three races at both seedling and adult plant stages. The results of the virulences and frequencies of P. graminis f. sp. avenae races and the resistant cultivars will be useful in elucidating the pathogen migration and evolution and for breeding oat cultivars with stem rust resistance.

Sheath blight (ShB) significantly threatens rice yield production. However, the underlying mechanism of ShB defence in rice remains largely unknown. Here, we identified a highly ShB-susceptible mutant Ds-m which contained a mutation at the ammonium transporter 1;1 (AMT1;1) D

Sheath blight (ShB) is one of the most common diseases in rice that significantly affects yield production. However, the underlying mechanisms of rice defense remain largely unknown. Our previous transcriptome analysis identified that infection with Rhizoctonia solani significantly induced the expression level of SWEET2a, a member of the SWEET sugar transporter. The sweet2a genome-editing mutants were less susceptible to ShB. Further yeast-one hybrid, ChIP, and transient assays demonstrated that WRKY53 binds to the SWEET2a promoter to activate its expression. WRKY53 is a key brassinosteroid (BR) signaling transcription factor. Similar to the BR receptor gene BRI1 and biosynthetic gene D2 mutants, the WRKY53 mutant and overexpressor were less and more susceptible to ShB compared to wild-type, respectively. Inoculation with R. solani induced expression of BRI1, D2, and WRKY53, but inhibited MPK6 (a BR-signaling regulator) activity. Also, MPK6 is known to phosphorylate WRKY53 to enhance its transcription activation activity. Transient assay results indicated that co-expression of MPK6 and WRKY53 enhanced WRKY53 trans-activation activity to SWEET2a. Furthermore, expression of WRKY53 SD (the active phosphorylated forms of WRKY53) but not WRKY53 SA (the inactive phosphorylated forms of WRKY53), enhanced WRKY53-mediated activation of SWEET2a compared to expression of WRKY53 alone. Taken together, our analyses showed that R. solani infection may activate BR signaling to induce SWEET2a expression via WRKY53 through negative regulation of ShB resistance in rice.

Phytochrome (Phy)-regulated light signaling plays important roles in plant growth, development, and stress responses. However, its function in rice defense against sheath blight disease (ShB) remains unclear. Here, we found that PhyB mutation or shade treatment promoted rice resistance to ShB, while resistance was reduced by PhyB overexpression. Further analysis showed that PhyB interacts with phytochrome-interacting factor-like 15 (PIL15), brassinazole resistant 1 (BZR1), and vascular plant one-zinc-finger 2 (VOZ2). Plants overexpressing PIL15 were more susceptible to ShB in contrast to bzr1-D-overexpressing plants compared with the wild-type, suggesting that PhyB may inhibit BZR1 to negatively regulate rice resistance to ShB. Although BZR1 is known to regulate brassinosteroid (BR) signaling, the observation that BR signaling negatively regulated resistance to ShB indicated an independent role for BZR1 in controlling rice resistance. It was also found that the BZR1 ligand NAC028 positively regulated resistance to ShB. RNA sequencing showed that cinnamyl alcohol dehydrogenase 8B (CAD8B), involved in lignin biosynthesis was up-regulated in both bzr1-D- and NAC028-overexpressing plants compared with the wild-type. Yeast-one hybrid, ChIP, and transactivation assays demonstrated that BZR1 and NAC028 activate CAD8B directly. Taken together, the analyses demonstrated that PhyB-mediated light signaling inhibits the BZR1-NAC028-CAD8B pathway to regulate rice resistance to ShB. This article is protected by copyright. All rights reserved.

Phytochrome B (PhyB), a red-light receptor, plays important roles in diverse biological processes in plants; however, its function in NH

Rhizoctonia solani, the causative agent of the sheath blight disease (ShB), invades rice to obtain nutrients, especially sugars; however, the molecular mechanism via which R. solani hijacks sugars from rice remains unclear.In this study, rice-R. solani interaction model was used to explore whether pathogen effector proteins affect plant sugar absorption during infection.Yeast one-hybrid assay was used to identify Activator of SWEET2a (AOS2) from R. solani. Localization and invertase secretion assays showed that nuclear localization and secreted function of AOS2. Hexose transport assays verified the hexose transporter activity of SWEET2a and SWEET3a. Yeast two-hybrid assays, Bimolecular fluorescence complementation (BiFC) and transactivation assay were conducted to verify the AOS2-WRKY53-Grassy tiller 1 (GT1) transcriptional complex and its activation of SWEET2a and SWEET3a. Genetic analysis is used to detect the response of GT1, WRKY53, SWEET2a, and SWEET3a to ShB infestation. Also, the soluble sugar contents were measured in the mutants and overexpression plants before and after the inoculation of R. solani.The present study found that R. solani protein AOS2 activates rice SWEET2a and localized in the nucleus of tobacco cells and secreted in yeast. AOS2 interacts with rice transcription factor WRKY53 and GT1 to form a complex that activates the hexose transporter gene SWEET2a and SWEET3a and negatively regulate rice resistance to ShB.These data collectively suggest that AOS2 secreted by R. solani interacts with rice WRKY53 and GT1 to form a transcriptional complex that activates SWEETs to efflux sugars to apoplast; R. solani acquires more sugars and subsequently accelerates host invasion.

Rice bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) seriously affects rice yield production. The discovery and application of broad-spectrum resistance genes are of great advance for disease resistance breeding. Previously, we identified that multiple receptor-like kinase (RLK) family gene deletions induced by the Ac/Ds system resulted in a lesion mimic symptom. In this study, the mutant #29 showed that this lesion mimic symptom was isolated. Further analysis identified that four RLK genes (RLK19-22) were deleted in the #29 mutant. The #29 mutant exhibited broad-spectrum resistance to Xoo and subsequent analyses identified that pathogenesis-related genes PR1a, PBZ1, and cellular H2O2 levels were significantly induced in the mutant compared to wild-type plants. A genetic analysis revealed that reconstruction of RLK20, RLK21, or RLK22 rescued the lesion mimic symptom of the #29 mutant, indicating that these three RLKs are responsible for broad-spectrum resistance in rice. Further yeast two hybrid and bimolecular fluorescence complementation assays demonstrated that RLK20 interacts with RBOHB, which is a ROS producer in plants. Compared to wild-type plants, the #29 mutant was more, while #29/RLK20ox was less, susceptible to MV (methyl-viologen), an ROS inducer. Co-expression of RLK20 and RBOHB reduced RBOHB-promoted H2O2 accumulation in the cells. Taken together, our research indicated that the RLKs may inhibit RBOHB activity to negatively regulate rice resistance to Xoo. These results provide the theoretical basis and valuable information about the target genes necessary for the successful breeding of rice cultivars resistant to bacterial blight.