Death Don't Have No Mercy: Cell Death Programs in Plant-Microbe Interactions.

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 "incompatible interactions" and leads to disease resistance. As detailed below, the HR is programmed genetically in the plant and is a consequence of new host transcription and trans? lation (Dixon et al., 1994; Godiard et al., 1994). The HR is a correlative feature of many but not all incompatible interac? tions controlled by classic disease resistance (R) genes (Dangl, 1995; Staskawicz et al., 1995; see also Bent, 1996, in this is? sue). 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 distal plant tissues. In addition, sites of the HR are invariably focal points for tran? scriptional induction of plant defense genes in neighboring cells (Somssich et al., 1988; Schmelzer et al., 1989). Subse? quent biosynthesis of protective secondary metabolites and cell wall buttressing around the HR site are also thought to contribute to overall pathogen containment. Signals derived from cells undergoing the HR apparently contribute signifi? cantly to the induction of defense gene transcription in adjacent cells. However, certain bacterial mutants unable to elicit an HR are still competent to trigger the transcription of defense genes that are normally induced during both incompatible and compatible interactions (Jakobek and Lindgren, 1993). Whether the cell death that constitutes the HR actually causes disease resistance by depriving the incoming patho? gen of nutrients or by releasing microbiocidal compounds from dying cells is unclear. Alternatively, the HR could be the con? sequence of a mechanism that is actually killing both host and microbe cells. In fact, recent evidence discussed below sug? gests that HR cell death is not required to stop pathogen growth in at least some cases (Century et al., 1995; Hammond-Kosack et al., 1996). If this separation of resistance per se and cell death is generalizable, can we glean insight from the mecha? nism by which host cells die that is relevant to the mechanism that kills or stops an invading pathogen?