Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599 Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, North Carolina 27599 INTRODUCTION A nearly ubiquitous feature of plant-pathogen interactions is host cell death. In its most recognizable form, host cell death is manifested as the rapid collapse of tissue, termed the hypersensitive response (HR). This response accompanies âincompatible interactionsâ and leads to disease resistance. As detailed below, the HR is programmed genetically in the plant and is a consequenceof new host transcription and translation (Dixon et al., 1994; Godiard et al., 1994). The HR is a correlative feature of many but not all incompatible interactions controlled by classic disease resistance(R) genes (Dangl, 1995; Staskawicz et al., 1995; see also Bent, 1996, in this issue). A local HR is often associated with the onset of systemic acquired resistance (SAR; Chester, 1933; Enyedi et al., 1992; Ryals et al., 1994, 1996, in this issue) in dista1 plant tissues. In addition, sites of the HR are invariably focal points for transcriptional induction of plant defense genes in neighboring cells (Somssich et al., 1988; Schmelzer et al., 1989). Subsequent biosynthesis of protective secondary metabolites and cell
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