Role of toxins in evolution and ecology of plant pathogenic fungi

Many fungal pathogens of plants adapt readily to changes in agriculture. Among the most revealing is a fungal group whose species produce host-selective toxins as key determinants of disease. Several lines of evidence support the hypothesis that these fungi evolved from opportunistic, low-grade pathogens by gaining new genetic information leading to toxin production; in some species, toxin production is known to be under single gene control. as a result of this evolution, these fungi became virulent and host-specialized. The best-known model cases belong to the generaCochliobolus andAlternaria; there are suggestions of evolutionary lines among these genera, with species that range from saprophytes to opportunists to specialized pathogens. Host specialization can lead to genetic isolation, a first step in speciation. Ability to produce host-selective toxin has allowed these fungi to exploit the monocultures and genetic uniformity of modern agriculture. Destructive epidemics have been the result.     

Bacterial phytotoxins: Mechanisms of action

Many species of phytopathogenic procaryotes produce toxins that appear to function in disease development. The affect the plant in different ways, the end result of which is the elicitation of chlorosis, necrosis, watersoaking, growth abnormalities or wilting. The most extensively studied toxins cause chlorosis. They specifically inhibit diverse enzymes, all critical to the plant cell. This inhibition results in a complex series of metabolic dysfunctions ultimately resulting in symptom expression. Substances causing growth abnormalities consist of known phytohormones and other compounds with plant hormone-like activities, but which have no structural relationship to the known hormones. The former act in the usual manner but, because of their elevated levels and imbalances, the host's regulatory mechanisms are overwhelmed and abnormal growth results (hyperplasia, shoot or root formation); the mechanisms of action of the latter group are unknown. High molecular weight, carbohydrate-containing substances, also acting in unknown ways, cause tissue watersoaking or wilting. Likewise, we know little about toxins causing necrosis except for syringomycin which affects ion transport across the plasmalemma.     

Genetics of toxin production and resistance in phytopathogenic bacteria

Genes for phytotoxin production have been identified and cloned from several phytopathogenic pseudomonads. These genes comprise physically linked clusters that have been located both on the chromosome and on endogenous plasmids. Contained within these genetic regions are resistance genes specific to those toxins that have a bactericidal component to their activity. DNA sequences required for toxin production are often conserved among bacteria with divergent host specificities, suggesting the ability of toxin genes to be transferred between bacteria. Toxins are usually modulators of plant pathogenicity, their production causing a significant increase in disease severity. In one case, however, toxin production appears to be a major contributor to the basic pathogenicity of a plant pathogenic bacterium.