A multi-institution team, co-led by a Cornell University researcher, has identified genetic mechanisms that enable the production of a deadly toxin called Victorin – the causative agent of oats, a disease that wiped out oat crops in the 1940s.
Victoria is badly affected by the fungus Cochliobolus victoriae, which produces the toxin Victorin, but so far no one has discovered the genes and mechanisms involved.
“The oat varieties that favored farmers in the 1940s were resistant to Crown Rust, but scientists later discovered that it was this characteristic that made those oats susceptible to the ill effects of Victoria, because the toxin Victorin directed him to that specific plant protein, ”said Kovich author Ilyan Turgeon, Professor and Chair of the Department of Plant Pathology and Plant-Microbiology at the School of Integrative Plant Science, Cornell College of Agriculture and Life Sciences (CALS). ). “Excavation of the molecules involved in this interaction between fungi and plants is fundamental to our understanding of how plants respond to attack by different microbes.”
Most fungal toxins are synthesized by large, multi-functional enzymes, and the small peptides created by these enzymes include toxins and drugs, such as the antibiotic penicillin. But Turjon and co-author Heng Choi, a researcher at the University of Western Australia, found that the toxin Victorin was actually synthesized directly in the ribosome, which is an organelle in the cells that make most proteins. These small molecules produced in ribosomes are known as ribosomally synthesized and post-translationally modified peptides or RiPPs.
This alternative mechanism for producing small peptides such as Victorin – along with the fact that fungal genomes likely contain many RiPP-related genes – could lead to the discovery of additional small molecules, including new toxins and beneficial compounds.
Furthermore, the first author, Simon Kessler, a doctoral student at the University of Western Australia, confirmed the enzymatic function of several Victorine genes, including a new enzyme that converts the Victorine peptide into active form. Surprisingly, the research team found that the Victorin genes encoding these enzymes are scattered across repetitive regions in the pathogen’s genome – a stark contrast to the genes for most known small molecules typically found in compact clusters of fungal chromosomes.
The discovery could help researchers better understand the evolutionary origins of molecules such as Victorine peptides, which determine the virulence of growing crop diseases and how to better prevent them in the future.
Turjon notes that Victorine peptides have been shown to interact with targets in plant cells called thioredoxins, which are also found in humans and have the potential as a site for cancer therapy.
“The discovery that these genes are not found in closely related fungi gives us insight into how virulence factors are acquired and transmitted,” Turgeon said. “Our findings from this study significantly expand the potential for detecting small molecules in fungal organisms, which will increase our repertoire of knowledge about their beneficial and harmful activities.”
Materials provided by Cornell University. Original written by Krishna Ramanujan. Note: Content can be edited by style and length.