Ensnaring microbes: the components of plant disease resistance

Abstract

SUMMARYPlants activate an array of co-ordinated defence responses to restrict microbial attack. Timely perception of foreign molecules appears to be critical for the success of these defences. However, the nature of the molecular events required for resistance is largely unknown. Recent isolation of disease resistance (R) genes, has revealed that R gene products have several features in common. This finding suggests that plants have evolved several common or similar signal transduction pathways to activate resistance to a range of unrelated microbes. R gene isolation and the genetic identification of other loci required for R function permits analysis of the structure and evolution of microbe-perception mechanisms. Numerous types of activated defence responses are recognized. .4 requirement for salicylic acid in resistance has been established in some systems. Roles for other events, like reactive oxygen species and the hypersensitive (host cell death) response, remain enigmatic. A thorough understanding of the components leading to pathogen recognition and the expression of resistance should permit the design of novel strategies to engineer broad-spectrum and durable plant disease control.

Collateral gene expression changes induced by distinct plant viruses during the hypersensitive resistance reaction in Chenopodium amaranticolor

“…Generally, pathogen infection induces a complex series of biochemical and physiological changes that mediate resistance against a range of pathogens throughout the tissues of the plant (Dixon and Lamb, 1990; Fritig et al ., 1987; Hammond‐Kosack and Jones, 1996; Lamb et al ., 1989; Ryals et al ., 1994). One of the earliest detectable signs of the HR is a rapid oxidative burst that precedes the appearance of visible necrosis by several hours and plays an important role in regulating other aspects of the defense response (Dangl et al ., 1996; Dixon et al ., 1994; Hammond‐Kosack and Jones, 1996; Low and Merida, 1996; Mehdy, 1994). Reactive oxygen intermediates (ROIs) that may be generated by the action of a membrane‐bound NADPH oxidase complex (Desikan et al ., 1996) are produced in the area of tissue where the local necrotic lesion forms and accumulate within that region to levels that may have a direct toxic effect on the cells of the plant and the invading pathogen (Peng and Kuc, 1992).…”

“…A number of hypersensitive disease resistance systems has been studied and much progress has been made recently in characterizing R (resistance) genes and their cognate pathogen‐encoded avirulence genes (Bent, 1996; Boyes et al ., 1996; Dangl, 1995; Hammond‐Kosack et al ., 1996; Jones, 1996; Staskawicz et al ., 1995). Subsequent to recognition of the pathogen by the host, a complex series of biochemical and physiological changes is induced that mediates intercellular signaling, apoptosis in the vicinity of the infection sites, attack of the microbe directly, and establishment of a persistent state of heightened sensitivity and resistance against a range of pathogens throughout the tissues of the plant (Dixon and Lamb, 1990; Fritig et al ., 1987; Hammond‐Kosack and Jones, 1996; Lamb et al ., 1989; Ryals et al ., 1994).…”

“…Subsequent to recognition of the pathogen by the host, a complex series of biochemical and physiological changes is induced that mediates intercellular signaling, apoptosis in the vicinity of the infection sites, attack of the microbe directly, and establishment of a persistent state of heightened sensitivity and resistance against a range of pathogens throughout the tissues of the plant (Dixon and Lamb, 1990; Fritig et al ., 1987; Hammond‐Kosack and Jones, 1996; Lamb et al ., 1989; Ryals et al ., 1994). Many of the biochemical and physiological changes that take place during hypersensitive resistance (HR) have been well defined, and advances have begun to elucidate the signal‐transduction events that coordinate this form of plant defense (Dangl et al ., 1996; Dangl, 1995; Hammond‐Kosack and Jones, 1996; Jones, 1996; Lamb et al ., 1989; Lamb, 1994). Despite the high degree of pathogen specificity of R gene‐mediated pathogen recognition, the consequent HR appears to be very similar for a variety of host–pathogen interactions.…”

Overexpression of the plasma membrane‐localized NDR1 protein results in enhanced bacterial disease resistance in Arabidopsis thaliana

“…The HR involves rapid necrosis of infected cells and concomitant production of reactive oxygen species (Bolwell, 1999). Production of an HR is also associated with induction of pathogenesis-related (PR) genes and various anti-microbial agents, lignification of the cell wall, alkalization of the apoplast, and activation of systemic-acquired resistance (SAR) (Hammond-Kosack et al, 1996). Recognition of bacterial effector molecules occurs within the plant cell by products of specific plant-derived genes known as resistance or R proteins.…”

Novel Type of Receptor-like Protein Kinase from a Higher Plant (Catharanthus roseus)

“…There is considerable interest also in the other RLK because they are thought to be involved in extracellular signal perception, in particular in plant development, plant/microbe interactions, and disease resistance phenomena (reviewed in Ref. 8).…”