RESUMEN
Alternaria is a ubiquitous fungal genus in many ecosystems, consisting of species and strains that can be saprophytic, endophytic, or pathogenic to plants or animals, including humans. Alternaria species can produce a variety of secondary metabolites (SMs), especially low molecular weight toxins. Based on the characteristics of host plant susceptibility or resistance to the toxin, Alternaria phytotoxins are classified into host-selective toxins (HSTs) and non-host-selective toxins (NHSTs). These Alternaria toxins exhibit a variety of biological activities such as phytotoxic, cytotoxic, and antimicrobial properties. Generally, HSTs are toxic to host plants and can cause severe economic losses. Some NHSTs such as alternariol, altenariol methyl-ether, and altertoxins also show high cytotoxic and mutagenic activities in the exposed human or other vertebrate species. Thus, Alternaria toxins are meaningful for drug and pesticide development. For example, AAL-toxin, maculosin, tentoxin, and tenuazonic acid have potential to be developed as bioherbicides due to their excellent herbicidal activity. Like altersolanol A, bostrycin, and brefeldin A, they exhibit anticancer activity, and ATX V shows high activity to inhibit the HIV-1 virus. This review focuses on the classification, chemical structure, occurrence, bioactivity, and biosynthesis of the major Alternaria phytotoxins, including 30 HSTs and 50 NHSTs discovered to date.
RESUMEN
The necrotrophic fungus Alternaria alternata contains different pathotypes that produce different mycotoxins. The pathotype Ageratina adenophora secretes the non-host-selective toxin tenuazonic acid (TeA), which can cause necrosis in many plants. Although TeA is thought to be a central virulence factor of the A. adenophora pathotype, the precise role of TeA in different stages of host infection by pathogens remains unclear. Here, an A. alternata wild-type and the toxin-deficient mutant ΔHP001 with a 75% reduction in TeA production were used. It was observed that wild-type pathogens could induce the reactive oxygen species (ROS) bursts in host leaves and killed photosynthetic cells before invading hyphae. The ROS interceptor catalase remarkably inhibited hyphal penetration and invasive hyphal growth and expansion in infected leaves and suppressed necrotic leaf lesion. This suggests that the production of ROS is critical for pathogen invasion and proliferation and disease symptom formation during infection. It was found that the mutant pathogens did not cause the formation of ROS and cell death in host leaves, showing an almost complete loss of disease susceptibility. In addition, the lack of TeA resulted in a significant reduction in the ability of the pathogen to penetrate invasive hyphal growth and spread. The addition of exogenous TeA, AAL-toxin, and bentazone to the mutant ΔHP001 pathogens during inoculation resulted in a significant restoration of pathogenicity by increasing the level of cell death, frequency of hyphal penetration, and extent of invasive hyphal spread. Our results suggest that cell death triggered by TeA is the essential requirement for successful colonization and disease development in host leaves during infection with A. adenophora pathogens.