Malectin Domain Protein Kinase (MDPK) Promotes Rice Resistance to Sheath Blight via IDD12, IDD13, and IDD14.

Sheath blight (ShB) caused by Rhizoctonia solani is a major disease of rice, seriously affecting yield; however, the molecular defense mechanism against ShB remains unclear. A previous transcriptome analysis of rice identified that R. solani inoculation significantly induced MDPK. Genetic studies using MDPK RNAi and overexpressing plants identified that MDPK positively regulates ShB resistance. This MDPK protein was found localized in the endoplasmic reticulum (ER) and Golgi apparatus. Yeast one-hybrid assay, electrophoresis mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP) showed that the intermediate domain proteins IDD12, IDD13, and IDD14 bind to the MDPK promoter. Moreover, IDD14 was found to interact with IDD12 and IDD13 to form a transcription complex to activate MDPK expression. The three IDDs demonstrated an additive effect on MDPK activation. Further genetic studies showed that the IDD13 and IDD14 single mutants were more susceptible to ShB but not IDD12, while IDD12, IDD13, and IDD14 overexpressing plants were less susceptible than the wild-type plants. The IDD12, IDD13, and IDD14 mutants also proved the additive effect of the three IDDs on MDPK expression, which regulates ShB resistance in rice. Notably, MDPK overexpression maintained normal yield levels in rice. Thus, our study proves that IDD12, IDD13, and IDD14 activate MDPK to enhance ShB resistance in rice. These results improve our knowledge of rice defense mechanisms and provide a valuable marker for resistance breeding.

Genomic analysis of Elsinoë arachidis reveals its potential pathogenic mechanism and the biosynthesis pathway of elsinochrome toxin.

Elsinochromes (ESCs) are virulence factors produced by Elsinoë arachidis which is the cause of peanut scab. However, the biosynthesis pathway of ESCs in E. arachidis has not been elucidated and the potential pathogenic mechanism of E. arachidis is poorly understood. In this study, we report a high-quality genome sequence of E. arachidis. The size of the E. arachidis genome is 33.18Mb, which is comparable to the Ascomycota genome (average 36.91 Mb), encoding 9174 predicted genes. The self-detoxification family including transporters and cytochrome P450 enzymes were analysis, candidate effectors and cell wall degrading enzymes were investigated as the pathogenicity genes by using PHI and CAZy databases. Additionally, the E. arachidis genome contains 24 secondary metabolism gene clusters, in which ESCB1 was identified as the core gene of ESC biosynthesis. Taken together, the genome sequence of E. arachidis provides a new route to explore its potential pathogenic mechanism and the biosynthesis pathway of ESCs.

Elsinochrome phytotoxin production and pathogenicity of Elsinoë arachidis isolates in China.

Peanut scab caused by Elsinoë arachidis is found throughout China's peanut-growing areas. Elsinochrome produced by E. arachidis is a perylenequinone photosensitive mycotoxin vital to the pathogenic process of the pathogen. In this study, the complex mechanism underlying the regulation of elsinochrome biosynthesis by E. arachidis was investigated based on various nutritional and environmental factors. The initiation of elsinochrome biosynthesis depends on light. E. arachidis produced substantially more quantities of elsinochrome when grown on a semi-synthetic medium (PDA) than when grown on synthetic media with defined ingredients in the presence of light. Elsinochrome accumulation decreased when adjusted with either citrate or phosphate buffers and changing pH suppressed the radical growth. At temperatures ranging from 10°C to 25°C, the production of elsinochrome increased, peaking at 28°C, and it decreased slightly at 30°C. 63 field-collected isolates from China were assessed for the level of elsinochrome production, and pathogenicity analysis was conducted by selecting 12 strains from each 3 of the 4 groups with different levels of elsinochrome production. A direct correlation was observed between elsinochrome production and pathogenicity among the isolates. The results showed elsinochrome biosynthesis to be controlled by E. arachidis and showed elsinochrome to be a vital virulence factor of E. arachidis, required for disease severity.