The discovery of the virulence gene ToxA in the wheat and barley pathogen Bipolaris sorokiniana

Abstract

Bipolaris sorokiniana is the causal agent of multiple diseases on wheat and barley and is the primary constraint to cereal production throughout South Asia. Despite its significance, the molecular basis of disease is poorly understood. To address this, the genomes of three Australian isolates of B. sorokiniana were sequenced and screened for known pathogenicity genes. Sequence analysis revealed that the isolate BRIP10943 harboured the ToxA gene, which has been associated previously with disease in the wheat pathogens Parastagonospora nodorum and Pyrenophora tritici-repentis. Analysis of the regions flanking ToxA within B. sorokiniana revealed that it was embedded within a 12-kb genomic element nearly identical to the corresponding regions in P. nodorum and P. tritici-repentis. A screen of 35 Australian B. sorokiniana isolates confirmed that ToxA was present in 12 isolates. Sequencing of the ToxA genes within these isolates revealed two haplotypes, which differed by a single non-synonymous nucleotide substitution. Pathogenicity assays showed that a B. sorokiniana isolate harbouring ToxA was more virulent on wheat lines that contained the sensitivity gene when compared with a non-ToxA isolate. This work demonstrates that proteins that confer host-specific virulence can be horizontally acquired across multiple species. This acquisition can dramatically increase the virulence of pathogenic strains on susceptible cultivars, which, in an agricultural setting, can have devastating economic and social impacts.

The inconspicuous gatekeeper: endophytic Serendipita vermifera acts as extended plant protection barrier in the rhizosphere

“…S6d; Table S7), suggesting that the pathogen is likely to be starving in the nutrient‐poor soil in the absence of the host. Together, these findings indicate that, similar to leaves (McDonald et al ., ), B. sorokiniana utilises secondary metabolites and potentially detoxifies phytoalexins to successfully infect host roots. Interestingly, by contrast with the gene expression changes in B. sorokiniana during fungal confrontation, genes involved in DHN−melanin biosynthesis were not activated during barley root colonisation, suggesting that this pathway is not required during compatible interaction with the plant host.…”

Vavilov wheat accessions provide useful sources of resistance to tan spot (syn. yellow spot) of wheat

“…This study provides significant implications in wheat breeding for resistance. For necrotrophic pathogens, breeding strategies include elimination or avoidance of sensitivity/susceptibility genes, or introgression of broad‐spectrum resistance genes (Pavan et al ., ; Faris et al ., ; McDonald et al ., ). In the wheat– P. tritici‐repentis pathosystem, ToxA– Tsn1 interaction is the most common, and eliminating Tsn1 in the breeding programme is recommended as there is no yield penalty observed in the insensitive cultivars (Faris et al ., ; Oliver et al ., ).…”

Evaluating the importance of the tan spot ToxA–Tsn1 interaction in Australian wheat varieties

“…To date, three Ptr effectors have been identified: ToxA, ToxB and ToxC. Of these, ToxA is the most prevalent and the most studied, and is also produced by the septoria nodorum blotch (SNB) wheat fungal pathogen, Parastagonospora nodorum (Friesen et al ., ; Liu et al ., ) and the spot blotch cereal necrotroph, Bipolaris sorokiniana (McDonald et al ., ). The tan spot disease system is governed primarily by inverse gene‐for‐gene, race‐specific interactions, which involve the recognition of necrotrophic fungal effectors by corresponding wheat sensitivity genes (Tan et al ., ).…”