Leaves of near isogenic barley lines containing the race-specific resistance alleles. Mla1 or mla1 were subjected to double inoculation treatments with virulent and avirulent Blumeria graminis isolates. Attack by the avirulent isolate alone frequently caused hypersensitive death of individual Mla1 epidermal cells, but underlying mesophyll cells survived. Virulent and avirulent B. graminis isolates Were inoculated sequentially (inducer followed by challenger) in all possible combinations. As shown previously, where a papilla formed due to inducer attacks, the attacked epidermal cell, and to some extent its neighbours, showed highly increased resistance to challenger penetration. When epidermal cells died in response to avirulent inducer attack, adjacent cells also showed increased penetration resistance. By contrast, where the virulent inducer formed a haustorium, invaded epidermal cells, and to some extent their neighbours, showed induced penetration susceptibility to later challenger attack. Furthermore, when virulent inducer haustoria formed in Mla1 epidermal cells, these cells became highly susceptible to successful infection by the avirulent isolate and vigorous colonies developed. It appears that suppressive factors released during virulent inducer infection prevented the hypersensitive epidermal cell death that normally is induced by the race-specific avirulence elicitor. However, suppression of Mla1 race-specific resistance vas confined to the epidermis. The presence of successful avirulent fungus infection of the epidermis often: led to the death of the underlying mesophyll cells, thus generating a novel cellular response phenotype in B. graminis attacked Mla1 barley. (C) 2001 Academic Press.