Genetic dissection of acquired resistance to disease.

Abstract

Plants come in frequent contact with potentially pathogenic fungi, bacteria, and viruses, yet disease results from relatively few of these exposures. In many cases an encounter leaves no obvious trace of its occurrence and the microbe fails to establish itself due to a lack in activation of pathogenicity functions or to highly effective plant defense mechanisms. Other encounters leave evidence of an intense plant-microbe interaction that results in the arrest of pathogen development after attempted colonization. In these cases plant tissues often display activated defense functions that produce antimicrobial compounds, enzymes, and structural reinforcements that may limit pathogen growth (Dixon and Lamb, 1990). These reactions may also be associated with the HR, a localized region of plant cell death around infection sites. An HR may involve just a single cell or it can produce death of extensive regions of tissue. The combination of defense activities can limit infection and prevent it from spreading to other tissues. The effectiveness of these defense strategies is determined both by the rate of host activation of defenses and by the rate of expansion of the pathogen colony. Therefore, in the evolution of plants and their pathogens, traits that permit rapid and effective defense responses should be favored in the evolution of the host, whereas desirable pathogen traits are those that enable rapid growth or facilitate evasion, suppression, or tolerance of host reactions. Host defense reactions are activated by sensing of the pathogen, and are sometimes mediated by plant R genes that recognize pathogens that possess corresponding avr genes (Keen, 1990). Although R genes have obvious adaptive value to plants, the maintenance of avr genes by pathogens may seem paradoxical, since their presence can trigger host defense responses. However, in several cases avr gene products have been shown to contribute to pathogen virulence on hosts that lack corresponding R genes (see Dangl, 1994, and refs. therein), indicating that, whereas a particular avr gene may expose a pathogen to the defenses of one host, it may more importantly enhance its pathogenicity on other susceptible hosts. In cases in which host defenses are inadequate to constrain pathogen development, multiplication and growth of the invading microbe will tap host resources and can lead to tissue damage and ultimately to pathogen reproduction, any of which can contribute to both immediate and delayed symptoms of disease. Whether a diseased plant succumbs to or recovers from infection depends on both its ability to assemble effective defenses against an established disease-causing organism and on the pathogenic strategy of the etiologic agent. Under conditions favorable for disease, some pathogens cause massive destruction of host tissues, against which there is little defense. By contrast, many intimate biotrophic pathogens produce much less damage and are highly sensitive to host defenses if triggered (Collmer and Bauer, 1994). Furthermore, some pathogens use a fast in-fast out strategy, completing their life cycle in a short time, which may enable evasion of host defenses.