Host-selective toxins: agents of compatibility.

Abstract

20 HSTs have been documented. In general, HSTs are deter? minants of host range or specificity in that plant species, varieties, or genotypes sensitive to an HST are those that are susceptible to the producing pathogen. HSTs have been criti? cal factors in two major epidemics of crops in the United States in the 20th century, including the Southern corn leaf blight epidemic of 1970 that destroyed ~15% of that year's crop. They are also important factors in several other economically sig? nificant diseases throughout the world. Studies of diseases involving HSTs led to the first elucidation of the molecular ba? sis of disease susceptibility in any interaction (Southern corn leaf blight; Dewey et al., 1988) and to the first cloning and func? tional characterization of a Mendelian disease resistance gene (Northern corn leaf spot; Johal and Briggs, 1992). Some HSTs have highly unusual chemical structures and unusual biolog? ical activities. Although some HSTs are extremely toxic, the reaction to them is often controlled by single plant genes. The study of HSTs and the diseases in which they occur continues to contribute fundamental knowledge about the processes and regulation of disease susceptibility and resistance, about ba? sic plant biochemistry through their use as specific metabolic inhibitors, about the structure and organization of secondary metabolite pathways, and about the organization of fungal ge? nomes and the evolution of new pathogen races. Because cell death is a symptom of many plant diseases, it was hypothesized early on that phytotoxic compounds con? tribute to the virulence or pathogenicity of plant pathogens. Although it is now well established that many plant pathogenic bacteria and fungi produce phytotoxic compounds, the majority of these compounds are nonselective. That is, these com? pounds affect a broader range of organisms than the producing organism infects. Some nonselective toxins, such as fusicoc? cin, trichothecene, coronatine, phaseolotoxin, syringomycin, and tabtoxin, contribute to virulence or symptom development in the diseases in which they occur (Stoessl, 1981; Ballio and