Abstract

Rhynchosporium secalis (Oud.) J.J. Davis, causal agent of scald of barley (Hordeum vulgare L.), was isolated from barley, couch grass (Elymus repens L.) and rye (Secale cereale L.). Isolates were used to inoculate seedlings of a differential barley series containing several sources of major gene resistance to the disease. The series included Atlas46, (resistance gene Rrs1) and the isogenic line Atlas, which lacks the gene (rrs1). The necrosis-inducing peptide NIP1 has been suggested to be the product of the avirulence gene AvrRrs1 (NIP1) that with the barley resistance gene Rrs1 determines the incompatibility of the pathogen-host interaction. All R. secalis isolates were virulent only on the susceptible barley cultivars Arve and Chan, irrespective of spore concentration or original host species. There were no indications of redundant virulence among the R. secalis isolates. The NIP1 gene was sequenced from each isolate and there was no correlation with source of the isolate or sequence modification and virulence. Four isolates, from barley and couch grass, were characterised by a basic Type I NIP1sequence. The recorded NIP1 sequence changes are consistent withR. secalis populations not receiving selection through deployment of the Rrs1 gene in commercial barley cultivars in Finland.

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