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

摘要: A nearly ubiquitous feature of plant-pathogen interactions is host cell death. In its most recognizable form, death manifested as the rapid collapse tissue, termed hypersensitive response (HR). This accompanies "incompatible interactions" and leads to disease resistance. As detailed below, HR programmed genetically in plant a consequence new transcription trans? lation (Dixon et al., 1994; Godiard 1994). The correlative many but not all incompatible interac? tions controlled by classic resistance (R) genes (Dangl, 1995; Staskawicz see also Bent, 1996, this is? sue). local often associated with onset systemic acquired (SAR; Chester, 1933; Enyedi 1992; Ryals 1994, issue) distal tissues. addition, sites are invariably focal points for tran? scriptional induction defense neighboring cells (Somssich 1988; Schmelzer 1989). Subse? quent biosynthesis protective secondary metabolites wall buttressing around site thought contribute overall pathogen containment. Signals derived from undergoing apparently signifi? cantly gene adjacent cells. However, certain bacterial mutants unable elicit an still competent trigger that normally induced during both compatible (Jakobek Lindgren, 1993). Whether constitutes actually causes depriving incoming patho? gen nutrients or releasing microbiocidal compounds dying unclear. Alternatively, could be con? sequence mechanism killing microbe fact, recent evidence discussed below sug? gests required stop growth at least some cases (Century Hammond-Kosack 1996). If separation per se generalizable, can we glean insight mecha? nism which die relevant kills stops invading pathogen?