Abstract

IntroductionSeptoria nodorum blotch (SNB) is a complex fungal disease of wheat caused by the Dothideomycete fungal pathogen Parastagonospora nodorum. The fungus infects through the use of necrotrophic effectors (NEs) that cause necrosis on hosts carrying matching dominant susceptibility genes. The Western Australia (WA) wheatbelt is a SNB “hot spot” and experiences significant under favorable conditions. Consequently, SNB has been a major target for breeders in WA for many years.Materials and MethodsIn this study, we assembled a panel of 155 WA P. nodorum isolates collected over a 44-year period and compared them to 23 isolates from France and the USA using 28 SSR loci.ResultsThe WA P. nodorum population was clustered into five groups with contrasting properties. 80% of the studied isolates were assigned to two core groups found throughout the collection location and time. The other three non-core groups that encompassed transient and emergent populations were found in restricted locations and time. Changes in group genotypes occurred during periods that coincided with the mass adoption of a single or a small group of widely planted wheat cultivars. When introduced, these cultivars had high scores for SNB resistance. However, the field resistance of these new cultivars often declined over subsequent seasons prompting their replacement with new, more resistant varieties. Pathogenicity assays showed that newly emerged isolates non-core are more pathogenic than old isolates. It is likely that the non-core groups were repeatedly selected for increased virulence on the contemporary popular cultivars.DiscussionThe low level of genetic diversity within the non-core groups, difference in virulence, low abundance, and restriction to limited locations suggest that these populations more vulnerable to a population crash when the cultivar was replaced by one that was genetically different and more resistant. We characterize the observed pattern as a low-amplitude boom-and-bust cycle in contrast with the classical high amplitude boom-and-bust cycles seen for biotrophic pathogens where the contrast between resistance and susceptibility is typically much greater. Implications of the results are discussed relating to breeding strategies for more sustainable SNB resistance and more generally for pathogens with NEs.

Highlights

  • Septoria nodorum blotch (SNB) is a complex fungal disease of wheat caused by the Dothideomycete fungal pathogen Parastagonospora nodorum

  • A collection of 155 Western Australia (WA) and 23 non-Australian [this study; (Friesen et al, 2006; Syme et al, 2018; Richards et al, 2019)] P. nodorum isolates, plus single isolates of five closely-related species were used in this study (Figure 1)

  • WA isolates were collected from 24 known locations across the WA wheat belt

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Summary

Introduction

Septoria nodorum blotch (SNB) is a complex fungal disease of wheat caused by the Dothideomycete fungal pathogen Parastagonospora nodorum. The development of SNB is dictated by interactions between several proteinaceous necrotrophic effectors (NEs) secreted by P. nodorum and dominant susceptibility genes in the host (Friesen and Faris, 2010; Oliver et al, 2012). ToxA encode a protein that causes necrosis on wheat varieties that carry the dominant susceptibility gene Tsn (Friesen et al, 2006). Tox encodes a small cysteine-rich protein and sensitivity is controlled by Snn which is located on wheat chromosome 5BS (Shi et al, 2016). These effectors possess multiple protein isoforms (McDonald et al, 2013)

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