A multi-institution team co-led by a Cornell University researcher has identified the genetic mechanisms that enable the production of a deadly toxin called Victorin — the causal agent for Victoria blight of oats, a disease that wiped out oat crops in the United States in the 1940s.
Victoria blight is caused by the fungus Cochliobolus victoriae, which produces the Victorin toxin, but until now no one has uncovered the genes and mechanisms involved.
“The oat varieties favoured by farmers in the 1940s were resistant to crown rust disease, but scientists later discovered this was the very trait that made those oat varieties susceptible to Victoria blight because the Victorin toxin was targeting that specific plant protein,” said co-senior author Gillian Turgeon, professor and chair of the Plant Pathology and Plant-Microbe Biology Section of the School of Integrative Plant Science, in Cornell’s College of Agriculture and Life Sciences.
“Unearthing the molecules involved in this fungus-plant interaction is fundamental to our understanding of how plants respond to attack by diverse microbes.”
Most fungal toxins are synthesized by large, multi-functional enzymes, and the small peptides created by these enzymes include both toxins and medicines, such as the antibiotic penicillin.
But Turgeon and co-author Heng Chooi, a researcher at the University of Western Australia, discovered the Victorin toxin is actually synthesized directly in the ribosome, which is an organelle in cells that makes most proteins.
These small molecules produced in ribosomes are known as ribosomally synthesized and post-translationally modified peptides, or RiPPs.
This alternate mechanism for producing small peptides like Victorin — coupled with the fact that fungal genomes likely contain many RiPP-associated genes — could lead to the discovery of additional small molecules, including both new toxins and beneficial compounds.
As well, first author Simon Kessler, a doctoral student at the University of Western Australia, confirmed the enzymatic function of several Victorin genes, including a novel enzyme that converts the Victorin peptide to its active form.
Surprisingly, the research team found that the Victorin genes encoding these enzymes are scattered across repetitive regions in the pathogen genome — a stark contrast to genes for most known small molecules, which are typically found in compact clusters on the fungal chromosomes.