The role or programmed plant cell death in susceptibility and resistance to necrotrophic plant pathogens

Programmed cell death (PCD) is now recognized to play an important part in plant disease. Understanding the impact of blocking PCD elicited by compatible and incompatible plant pathogens will provide means to better engineer plants to resist pathogen infection.; When expressed in various vertebrate and invertebrate systems, baculovirus p35 protein prevents PCD, by blocking the actions of caspases. When expressed in tomato plants, a phenotype consistent with p35 function in animal cell systems was observed. Furthermore, tomato plants expressing p35 were less susceptible to infection by the necrotrophic fungus Alternaria alternata f. sp. lycopersici (Aal), which has been shown to cause cell death in susceptible tomato plants. Reduced susceptibility to Aal cosegregated with the presence of the transgene in T2 progeny derived from a self of a p35-transformed parent. The expression of p35 transcript in T3 tomato plants homozygous for p35 was linked with reduced susceptibility to a number of necrotrophic tomato pathogens including Sclerotinia sclerotiorum, Collectotrichum coccodes, Alternaria alternata, and Pseudomonas syringae pv. tomato.; Tetrapeptide aldehyde caspase inhibitors have been shown to block PCD of animals cells by specifically diminishing the proteolytic ability of caspases. Disease symptoms induced by Pseudomonas syringae and Xanthamonas campestris in tobacco, bean and tomato were greatly reduced by the co-infiltration of tetrapeptide inhibitors with the bacteria. Reduced disease symptoms were correlated with diminished growth of the causal organism.; Hypersensitive plant cell death is often associated with resistance to plant pathogenic bacteria. To test whether hypersensitive plant cell death is necessary for resistance, the cell death pathway must be specifically impeded without interfering with other components of the resistance response. When co-infiltrated with incompatible Pseudomonas syringae pv. phaseolicola, tetrapeptide caspase inhibitors blocked hypersensitive cell death in tobacco leaves and greatly decreased the growth of the bacteria in tobacco leaf tissue. The inhibitors also blocked hypersensitive cell death in the gene-for-gene interaction between tomato with the Pto gene and Pseudomonas syringae pv. tomato strain T1 with avrPto. However, the resistant plants did not become susceptible to the pathogen. Thus, the inhibitors blocked both non-host and host specific hypersensitive cell death without compromising resistance.