Plants possess inducible systemic defense responses when locally infected by pathogens. Bacterial infection results in the increased accumulation of the mobile metabolite azelaic acid, a nine-carbon dicarboxylic acid, in the vascular sap of Arabidopsis that confers local and systemic resistance against the pathogen Pseudomonas syringae . Azelaic acid primes plants to accumulate salicylic acid (SA), a known defense signal, upon infection. Mutation of the AZELAIC ACID INDUCED 1 (AZI1) gene, which is induced by azelaic acid, results in the specific loss of systemic immunity triggered by pathogen or azelaic acid and of the priming of SA induction in plants. Furthermore, the predicted secreted protein AZI1 is also important for generating vascular sap that confers disease resistance. Thus, azelaic acid and AZI1 are components of plant systemic immunity involved in priming defenses.

It is commonly known that animal pathogens often target and suppress programmed cell death (pcd) pathway components to manipulate their hosts. In contrast, plant pathogens often trigger pcd. In cases in which plant pcd accompanies disease resistance, an event called the hypersensitive response, the plant surveillance system has learned to detect pathogen‐secreted molecules in order to mount a defence response. In plants without genetic disease resistance, these secreted molecules serve as virulence factors that act through largely unknown mechanisms. Recent studies suggest that plant bacterial pathogens also secrete antiapoptotic proteins to promote their virulence. In contrast, a number of fungal pathogens secrete pcd‐promoting molecules that are critical virulence factors. Here, we review recent progress in determining the role and regulation of plant pcd responses that accompany both resistance and susceptible interactions. We also review progress in discerning the mechanisms by which plant pcd occurs during these different interactions.

Escherichia coli responds to superoxide-generating agents by inducing approximately 40 proteins. We have identified a genetic locus, soxR (superoxide response), that positively regulates 9 of these proteins during superoxide stress. Induction under soxR control is at the transcriptional level, as shown with lac fusions to five paraquat-inducible promoters. Members of the soxR regulon include at least three proteins with demonstrable antioxidant roles: Mn-containing superoxide dismutase (which destroys superoxide radicals), endonuclease IV (which repairs radical-induced damages in DNA), and glucose-6-phosphate dehydrogenase (which produces NADPH). Induction of the soxR regulon also leads to diminished levels of the major outer membrane protein OmpF and alteration of the small-subunit ribosomal protein S6. These latter changes confer resistance to a variety of antibiotics. The soxR regulon may thus operate as an inducible defense against xenobiotics in general.

Cell death in higher plants has been widely observed in predictable patterns throughout development and in response to pathogenic infection. Genetic, biochemical, and morphological evidence suggests that these cell deaths occur as active processes and can be defined formally as examples of programmed cell death (PCD). Intriguingly, plants have at least two types of PCD, an observation that is also true of PCD in animals [Schwartz, L. M., Smith, W.W., Jones, M. E. E. & Osborne, B. A. (1993) Proc. Natl. Acad. Sci. USA 90, 980-984]. Thus, in plants, PCD resembles either a common form of PCD seen in animals called apoptosis or it resembles a morphologically distinct form of cell death. The ubiquitous occurrence and necessity of PCD for plant development and defense suggest that the underlying mechanisms of regulation and execution of these processes merit further examination.

▪ Abstract Plants cope with pathogen attacks by using mechanisms of resistance that rely both on preformed protective defenses and on inducible defenses. The latter are the most well studied, and progress is being made in determining which induced responses are responsible for limiting pathogen growth. Many plant-pathogen interactions are accompanied by plant cell death. Recent evidence suggests that this cell death is often programmed and results from an active process on the part of the host. The review considers the roles and possible mechanisms of plant cell death in response to pathogens.