Induced Resistance Responses

A number of resistance responses by plants are induced by pathogen invasion or insect attack (Hutcheson 1998). The hypersensitive response (HR) results after R-gene-mediated, race-specific recognition of a pathogen. The HR in a natural infection is often limited to relatively few cells around the initial infection site. It can also be triggered nonspecifically by various elicitor compounds, such as fungal cell-wall components. The HR involves a cascade of reactions that result in production of reactive oxygen intermediates, antimicrobial compounds (termed phytoalexins), and degradative enzymes; alteration of cell membranes and cell walls; and ultimately cell death. The result of the HR in infected tissues is usually localized necrosis, inhibition of pathogen growth, and limitation of the disease. The HR can occur in plants that contain race-specific R genes effective against all types of viruses, fungi, and bacteria.

The HR leads to a number of other localized and systemic processes that result in increased generalized resistance to a wide array of pathogens. The systemic-acquired-resistance response results in activation of genes that encode defensive proteins, such as glucanases and chitinases, and antimicrobial biosynthetic pathways throughout the plant (Ryals et al. 1996). Defensive proteins can also be induced during the natural course of development of some plants; for example, pathogenesis-related proteins (such as several chitinases and osmotin) with antifungal activity are the predominant proteins that accumulate in the ripening fruit of grape plants (Salzman et al. 1998).

Insect herbivore activity can lead to a systemic defense response (Ryan 1990). This response can be triggered by biotic damage, such as that caused by chewing insects, or by mechanical damage. Insect feeding on a single leaf can result in production of defensive chemicals in all of a plant's leaves (Rosenthal and Berenbaum 1991). An important component of this wound-induced response is activation of genes that encode proteins, such as proteinase inhibitors, that have insecticidal activity. Proteinase inhibitors prevent digestion of plant material in the insect gut, and so result in starvation. Thus, plants exposed to chewing insects gain resistance to additional insect feeding through the wound response.

Viruses activate a defensive response that resembles post-transcriptional gene silencing (PTGS) (Carrington and Whitham 1998). PTGS response is adaptive in providing a customized antiviral response to each new virus that the plant encounters. Silencing in response to viruses with a RNA-based genetic code involves degradation of the genome itself. For viruses with a DNA-based genetic code, the PTGS results in degradation of the transcription products (mRNA). In either case this results in lower virus accumulation or in recovery of the plant. PTGS response can be

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