abstract
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Septoria leaf blotch disease is caused by closely related but different species on cereal crops: Zymoseptoria tritici affects wheat but not barley, while Z. passerinii infects barley but not wheat. To test for differences between susceptible, R-gene incompatible and non-host resistance responses, wheat and barley cultivars were inoculated with isolates of Z. tritici or Z. passerinii and analyzed for gene expression at 1, 3, 6, 10 and 17 days after inoculation (DAI).
The highest numbers of differentially expressed genes for the R-gene interaction on barley occurred at 1 and 10 DAI, corresponding to the times of initial penetration by the pathogen and its transition from biotrophic to necrotrophic growth, while for the non-host interaction it occurred only at 1 DAI. Very few differentially expressed genes relative to the water controls were conserved across all five time points indicating large changes in gene expression over time. The highest numbers of differentially expressed genes across all time points was with the R-gene interactions.
The two R genes tested in wheat, Stb2 and Stb3, each had very different patterns of expression in response to pathogen inoculation, but how much of this is due to resistance genes versus other differences between the cultivars is not known. GO and KEGG analyses were performed to try to identify possible biological functions of the differentially expressed genes. One gene for a possible SCP-like extracellular protein showed differential expression between the susceptible and non-host responses at all time points except for 1 DAI and could be a possible candidate gene for resistance.
Large differences in expression between the two resistance genes in wheat plus the wheat and barley non-host responses compared to susceptible interactions likely indicate that the different types of resistance response occur by disparate mechanisms. Lack of similarity among homologous genes in wheat and barley for the same type of response indicate that resistance mechanisms likely are species specific.
Ultimately, we hope that analyses between responses of closely related pathosystems to compatible and non-host pathogens could identify broad-spectrum resistance genes that could function across species to improve resistance in the future.