Recently, Associate Professor Zhang Xianghui of the Faculty of Plant Sciences, Cornell University in the United States and the University of Western Australia in Australia jointly researched a paper entitled "Victorin, the host-selective cyclic peptide toxin from the oat pathogen Cochliobolus victoriae, is ribosomally encoded" online on PNAS Published. The study reported that the oat leaf blight host-selective toxin-Vitaly Toxin is not synthesized by Nonribosomal Peptide Synthetase (NRPS), but is formed by ribosomes.
In the 1940s, oat leaf blight occurred in a large area in oat growing areas. Later, it was discovered that the epidemic and occurrence of this disease were closely related to the host-selective toxin secreted by a pathogenic fungus. Oat leaf blight is caused by a dead vegetative pathogenic fungus, Cochliobolus victoriae, which secretes a host-selective toxin victorin. The virulence of C. victoriae to susceptible varieties depends entirely on the toxin victorin. Later, it was discovered that the target of the toxin victorin in susceptible varieties was the Vb gene, and the Vb gene and the Pc-2 gene of the oats resistant to crown rust (Puccinia coronata) It's the same gene. Since C. victoriae contains multiple non-protein amino acids, and C. victoriae is closely related to Cochliobolus carbonum, and the cyclic tetrapeptide HC-toxin produced by C. carbonum is synthesized by NRPS, victorin has always been assumed It is also synthesized by the NRPS pathway.
In the article, the author explained that victorin is a product of the Ribosomally synthesized and posttranslationally modified peptide (RiPP) family. Through the analysis of the new genome sequence after the assembly of long-sequence sequencing, it was found that the entire genome sequence of C. victoriae contains 3 copies of the precursor peptide synthesis gene (vicA1-3), and each copy contains the core peptide that constitutes the victorin peptide backbone ( GLKLAF) The number of repetitions is different. vicA1-3 is located in a highly repetitive and gene-sparse region of the genome, and forms a gene cluster with several genes that may be related to the formation of victorin. Knockout of one copy of vicA gene resulted in a great decrease in victorin production. Knock out the gene encoding DUF3328 protein (VicYb) in the gene cluster, and victorin cannot be produced at all, which also proves that DUF3328 protein is responsible for the oxidative cyclization of victorin. In addition, the author revealed that the knockout of copper amine oxidase (Copper amine oxidase) encoded by vicK resulted in a large accumulation of victorin precursor (HV-toxin), which indicates that the role of vicK converts HV-toxin into victorin.
Associate Professor Zhang Xianghui of Jilin University and Dr. Simon C. Kessler of the University of Western Australia in Australia are the co-first authors of this article. Professor Gillian Turgeon of Cornell University in the United States and Yit-Heng Chooi of the University of Western Australia in Australia are the co-corresponding authors of this article. This research provides a new target for the prevention and control of oat leaf blight, and at the same time is of great significance to the yield and quality of oats.