Role of hypersensitive cell death in conditioning elicitation competency and defense potentiation

Abstract

A plant’s capacity for the recognition of an incompatible pathogen (mediated by non-host or race-specific resistance) leads initially to a nearly universal defense reaction, the programmed hypersensitive death of cells in immediate contact with the pathogen. This hypersensitive response (HR), in turn, is complemented by the expression of several other forms of induced resistance, including both local and systemic acquired resistance (LAR, SAR). In some species, LAR responses have been further delineated into discrete reactions that are immediately proximal or distal to the HR lesion [see, e.g., 12, 13, 37, 41]. Furthermore, an additional form of induced systemic resistance (ISR) has been described in some plants. Although not as fully characterized as SAR [19, 30, 38, 42, 43], ISR is often associated with host resistance induced by rhizosphere micro-organisms [31]. The spatial and temporal coordination of these various plant defense responses has been the subject of careful study in a number of systems. From these studies, it is clear that the regulation of the various cellular responses involves a very complex array and interplay of signals from the pathogen, the environment and from the host itself [see, e.g. 14, 41]. In the latter area, it is apparent that the host takes a very active role in the orchestration of its defense reactions through the generation of signals that both initiate and condition the responses of specific cell populations. Recent work in several plant species has suggested that signaling processes associated with or initiated during the HR may actively program or condition downstream LAR and SAR reactions. This coordinating