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Histopathology of durable adult plant resistance to leaf rust in the Brazilian wheat variety Toropi

Wesp-Guterres, Caroline, Martinelli, José Antônio, Graichen, Felipe André Sganzerla, Chaves, Márcia Soares
European journal of plant pathology 2013 v.137 no.1 pp. 181-196
cell death, wheat, genes, appressoria, adults, hydrogen peroxide, disease severity, Triticum aestivum, genotype, Puccinia recondita, leaves, defense mechanisms, disease outbreaks, leaf rust, histopathology, races, environmental factors, genetic variation, fungi, South America
Leaf rust, caused by the fungus Puccinia triticina is a major disease of wheat (Triticum aestivum) worldwide. This disease is prevalent in southern South America where the environmental conditions and high genetic variability of P. triticina favour epidemics. The primary means of controlling pathogenic P. triticina races has been through using wheat varieties containing race-specific resistance genes. The defence mechanisms involved in durable race non-specific resistance to P. triticina are probably distinct from those involved in non-durable race-specific resistance. We investigated the histological components of resistance to P. triticina present in three wheat genotypes: the race non-specific resistant Brazilian variety Toropi; the race-specific resistant line RL6010 Lr9; and the susceptible Brazilian variety BRS 194. Plants of these three genotypes were inoculated with P. triticina race MFP and tissue samples excised from flag leaves at various times after inoculation to assess the number of infective structures, frequency of cell death and the accumulation of autofluorescent cells and hydrogen peroxide. The genotypes showed different resistance mechanisms active at different times during the infection process. Our results for Toropi indicate that there was a reduction in the extent of formation of stomatal appressoria and all subsequent structures. During attempted penetration we also observed the production of autofluorescent compounds and late cell death, but not peroxide formation. This non-specific resistance to P. triticina involves both pre-haustorial and post-haustorial mechanisms which may be responsible for maintaining the low disease severity observed in this variety even under high inoculum pressure.