Objective
1. Assess resistance levels in the UBC B. napus TILLING population, Brassica rapa and Sinapis arvensis against V. longisporum.
2. Identify candidate susceptibility (S) genes and associated proteins.
3. Validate the function of a candidate susceptibility gene.
4. Develop molecular markers associated with susceptible genes.
Project Description
According to the 2014 soil survey by the Canadian Food Inspection Agency, V. longisporum was first found in Manitoba. A 2015 report revealed that the pathogen had also been detected in other provinces, including Saskatchewan. During the 2021 general canola disease survey, four suspicious samples from east central Saskatchewan (near the Manitoba border and further west) were confirmed to contain Verticillium sp. Thus, V. longisporum is increasingly prevalent across Saskatchewan and Manitoba, and research is ongoing to determine the exact extent of yield loss and how it correlates with the severity of infection. V. longisporum affects canola and other Brassica crops, causing significant yield losses and premature plant death by interfering with water and nutrient uptake, and is becoming increasingly prevalent in canola fields. There is no effective fungicide treatment to control any Verticillium diseases, and genetic resistance is the preferred strategy for disease management. However, there are no known resistance genes (R genes) available for Verticillium disease. Quantitative resistance exists mainly in the Brassica C-genome of parental cabbage lines and may be introgressed into oilseed rape breeding lines. While these are closely related species within the same mustard family, interspecific crosses (between different species) occur less frequently and are not as readily successful as intraspecific crosses (between the same species), making the development of desirable cultivars a potentially time-consuming process. An alternative way to manage Verticillium disease is by improving host resistance through the loss-of-function of susceptibility (S) genes. These S-genes encode proteins that enable pathogen compatibility with the host. In this proposed project, we aim to disrupt the function of these genes to improve host resistance and develop a disease management strategy.
