Abstract
Fusarium head blight (FHB) is a major disease in wheat causing severe economic losses globally by reducing yield and contaminating grain with mycotoxins. In Canada, Fusarium graminearum is the principal etiological agent of FHB in wheat, producing mainly the trichothecene mycotoxin, deoxynivalenol (DON) and its acetyl derivatives (15-acetyl deoxynivalenol (15ADON) and 3-acetyl deoxynivalenol (3ADON)). Understanding the population biology of F. graminearum such as the genetic variability, as well as mycotoxin chemotype diversity among isolates is important in developing sustainable disease management tools. In this study, 570 F. graminearum isolates collected from commercial wheat crops in five geographic regions in three provinces in Canada in 2018 and 2019 were analyzed for population diversity and structure using 10 variable number of tandem repeats (VNTR) markers. A subset of isolates collected from the north-eastern United States was also included for comparative analysis. About 75% of the isolates collected in the Canadian provinces of Saskatchewan and Manitoba were 3ADON indicating a 6-fold increase in Saskatchewan and a 2.5-fold increase in Manitoba within the past 15 years. All isolates from Ontario and those collected from the United States were 15ADON and isolates had a similar population structure. There was high gene diversity (H = 0.803–0.893) in the F. graminearum populations in all regions. Gene flow was high between Saskatchewan and Manitoba (Nm = 4.971–21.750), indicating no genetic differentiation between these regions. In contrast, less gene flow was observed among the western provinces and Ontario (Nm = 3.829–9.756) and USA isolates ((Nm = 2.803–6.150). However, Bayesian clustering model analyses of trichothecene chemotype subpopulations divided the populations into two clusters, which was correlated with trichothecene types. Additionally, population cluster analysis revealed there was more admixture of isolates among isolates of the 3ADON chemotypes than among the 15ADON chemotype, an observation that could play a role in the increased virulence of F. graminearum. Understanding the population genetic structure and mycotoxin chemotype variations of the pathogen will assist in developing FHB resistant wheat cultivars and in mycotoxin risk assessment in Canada.
Highlights
Fusarium head blight (FHB) is a global disease affecting small grain cereals including wheat, barley and oat [1,2,3,4] The disease is caused by several Fusarium species of whichFusarium graminearum Schwabe is the primary etiological agent in wheat crops in Canada based on the frequency of isolation and impact on grain yield and quality [5,6,7,8]
Epidemics of FHB in western Canada started in the early 1980s when grain samples of wheat from Manitoba showed symptoms of bleached kernels and detectable levels of DON mycotoxin [11,12]
Increasingly frequent FHB epidemic years occurred in Canadian prairies with the worst outbreak in 2016 in Saskatchewan (SK) and Manitoba (MB) [13]
Summary
Fusarium head blight (FHB) is a global disease affecting small grain cereals including wheat, barley and oat [1,2,3,4] The disease is caused by several Fusarium species of which. Epidemics of FHB is enhanced by rapid evolution of Fusarium pathogens and the ability of the disease to spread through airborne ascospores over large areas [17]. Several surveys and molecular mycotoxin profiling over the last 20 years have shown a temporal and spatial increase in the 3ADON isolates compared to the 15ADON isolates, with a 3ADON vs 15ADON frequency of 10.7% and 31% 3ADON in Saskatchewan and Manitoba, respectively, between 1984 and 2004 [7,9,20] These studies did not consider the mycotoxin sub-structuring profile within the geographic locations in the provinces in Canada. The specific objectives were to: (i) investigate the genetic variability and population structure of F. graminearum, and the patterns of relatedness of the populations in Manitoba and Saskatchewan, (ii) investigate the level of gene flow and to determine the correlation of genetic distance with genetic identity, and (iii) determine the DON chemotype distribution within and between the provinces and their relationship with population genetic structure
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