Pathotypes and phylogenetic variation determine downy mildew epidemics in Brassica spp. in Australia

Abstract

Isolates of Hyaloperonospora brassicae inoculated onto cotyledons of 28 diverse Brassicaceae genotypes, 13 from Brassica napus, two from B. juncea, five from B. oleracea, two from Eruca vesicaria, and one each from B. nigra, B. carinata, B. rapa, Crambe abyssinica, Raphanus sativus and R. raphanistrum, showed significant effects (P ≤ 0.001) of isolate, host and their interaction. Host responses ranged from no visible symptom or a hypersensitive response, to systemic spread and abundant pathogen sporulation. Isolates were generally most virulent on their host of origin. Using an octal classification, six host genotypes were identified as suitable host differentials to characterize pathotypes of H. brassicae and distinguished eight distinct pathotypes. There were fewer, but more virulent, pathotypes in 2015–2016 isolates than 2006–2008 pathogen populations, probably explaining the increase in severity of canola downy mildew over the past decade. Phylogenetic relationships determined across 20 H. brassicae isolates collected in 2006–2008 and 88 isolates collected in 2015–2016 showed seven distinct clades, with 70% of 2006–2008 isolates distributed within clade I (bootstrap value (BVs) of 100%) and the remaining 30% in clade V (BVs 83.3%). This is the first study to define phylogenetic relationships of H. brassicae isolates in Australia, setting a benchmark for understanding current and future genetic shifts within pathogen populations; it is also the first to use octal classification to characterize pathotypes of H. brassicae, providing a novel basis for standardizing phenotypic characterization and monitoring of pathotypes on B. napus and some crucifer species in Australia.

Geographic location and year determine virulence, and year determines genetic change, in populations of Neopseudocercosporella capsellae

“…Scoop remained resistant to this 2016 isolate, in the same way as it was resistant to the 2005 N. capsellae isolates. As with the current study, Mohammed et al (2018a) found that current H. brassicae isolates from 2015-2016 were not only more virulent as compared to earlier H. brassicae isolates (2006)(2007)(2008), but that 70% of those isolates also grouped into a different clade from the earlier isolates. Hence, some clade segregations related to expressions of host resistance against N. capsellae in the current study were to be expected, as genetic variability would probably explain virulence differences between isolates (e.g.…”

“…Scoop remained resistant to this 2016 isolate, in the same way as it was resistant to the 2005 N. capsellae isolates. As with the current study, Mohammed et al () found that current H . brassicae isolates from 2015–2016 were not only more virulent as compared to earlier H .…”

“…Daverdin et al (2012) showed that in plant-pathogen interactions, enhanced mutability of fungal genes is directly related to their reproductive system and genomic environment. Similarly, in a study by Mohammed et al (2018a), phylogenetic association of 70% of Hyaloperonospora parasitica isolates from 2006-2008 were clustered separately from the more virulent pathotypes from 2015-2016. Such variation challenges the development and implementation of successful management strategies, as these are often predicated on understanding the pathogen's ability to respond to such practices, including in response to development and deployment of host resistance and even application of fungicides (Attanayake et al, 2013).…”

“…Virulence allele frequency was elevated in current compared to historical isolates of L. maculans and showed that genotype of cultivar dramatically influenced the frequencies of avirulence alleles (van de Wouw et al , ). Furthermore, for downy mildew ( H. brassicae ), Mohammed et al () noted more virulent pathotypes in 2015–2016 isolates compared to 2006–2008 populations, probably explaining the increase in downy mildew severity in rapeseed in Australia over the past decade. Clearly, resistance in Brassica cultivars to a range of different diseases faces a significant challenge from highly variable and rapidly evolving pathogen populations in Australia.…”

“…Hence, understanding the variation within the pathogen population is fundamental to successful implementation of management strategies, and, in particular, is critical to enable plant breeding programmes to generate cultivars with durable disease resistance. There is substantial variation in brassica pathogen populations in Australia, including distinct pathotypes of Sclerotinia sclerotiorum (Ge et al , ), pathotypes of Hyaloperonospora brassicae (Mohammed et al , ), races of Leptosphaeria maculans (Balesdent et al , ; Anonymous, ) and races of Albugo candida (Kaur et al , ). Various reasons have been suggested for this increasing diversity within brassica pathogen populations across southern Australia, including the increasingly variable climatic conditions as a consequence of climate change (Barbetti et al , ).…”