The occurrence of host-, pathogen- and interaction-specific proteins in the apoplast of Cladosporium fulvum (syn. Fulvia fulva) infected tomato leaves

Abstract

The interaction between the intercellularly growing fungus Cladosporium fulvum and tomato was used as a model system to study the accumulation of host-, pathogen- and interaction-specific proteins in intercellular fluids in various compatible and incompatible combinations. Electrophoresis of intercellular fluids under low pH non-denaturing conditions revealed the accumulation of five host coded proteins (proteins 2, 3, 4, 5 and 6) which accumulate 2–4- days earlier in incompatible interactions than in the compatible ones but litde at all in healthy controls. Three of these proteins are most likely charged isomers of the pathogenesis-related, protein P14. In compatible interactions, in addition to these five proteins, two others, most likely fungal proteins (proteins 1 and 7), accumulated. Protein 7 is the necrosis-inducing peptide, a putative product of avirulence gene A9 . Proteins 1 and 7 accumulated concomitantly in all compatible interactions with the exception of the interaction Cf2Cf4Cf9 /racc 2.4.5.9, where only protein 1 was detected. Electrophoresis of intercellular fluids under high pH non-denaturing conditions revealed the accumulation of at least four proteins (I, III, IV and V) in compatible interactions, which were barely detectable in incompatible interactions, The origin of these proteins is not known but there are indications that some are fungal in origin. Electrophoresis of intercellular fluids under denaturing conditions on SDS-polyacrylamide gels revealed no qualitative differences between the protein profiles obtained from compatible and incompatible interactions. However, four of the proteins (W, X, Y and P14) accumulated earlier in the intercellular fluids from incompatible interactions. Western blots incubated with antiserum raised against intercellular fluids from compatible and incompatible interactions showed that only a limited number of the proteins in the intercellular fluids appeared to be antigenic. No differences in protein profiles additional to those detected by Coomassie brilliant blue staining could be detected by immunoautoradiography.