An emerging question in plant biology is whether plants display analogous elements of mammalian-programmed cell death (apoptosis) during development and pathogen attack. With respect to plant-pathogen interactions, cell death occurs in both susceptible disease and resistant host responses. For example, in resistant reactions, specific recognition responses in plants trigger formation of the "hypersensitive response" (HR) and activation of host defense mechanisms. HR triggers a cell death pathway resulting in restriction of pathogen growth and disease development. Historically HR has been considered a product of necrosis, but several studies have suggested that cell death during HR involves activation of a plant-encoded program for cell suicide that may resemble apoptosis. Susceptible interactions also result in host cell death although it is unclear to what degree (if any) the host participates in this response. Recent data obtained in my laboratory strongly suggest that during disease development in pathogen infected susceptible tobacco plants, apoptosis is occurring. Hallmark characteristics of apoptosis, including discrete DNA fragmentation (e.g., DNA ladders) and nuclear condensation have been observed. These apoptotic responses do not occur in the transgenic, disease resistant tobacco. Based on these data, as well as reports from other laboratories, it appears that elements of animal cell suicide are functionally conserved in plants. The central hypothesis of this research is that plants share certain features of apoptosis with animals. The goal of this project are: (I) to identify and characterize plant genes which functionally resemble those found in animal apoptosis pathways and evaluate these genes in resolution, the cell death process in plants. An understanding of how plants regulate cellular suicide will provide information regarding plant response to environmental stress and have the potential to generate effective disease resistant plants.
