Fungal Resistance to Plant Antibiotics as a Mechanism of Pathogenesis

Abstract

SUMMARY Many plants produce low-molecular-weight compounds which inhibit the growth of phytopathogenic fungi in vitro. These compounds may be preformed inhibitors that are present constitutively in healthy plants (also known as phytoanticipins), or they may be synthesized in response to pathogen attack (phytoalexins). Successful pathogens must be able to circumvent or overcome these antifungal defenses, and this review focuses on the significance of fungal resistance to plant antibiotics as a mechanism of pathogenesis. There is increasing evidence that resistance of fungal pathogens to plant antibiotics can be important for pathogenicity, at least for some fungus-plant interactions. This evidence has emerged largely from studies of fungal degradative enzymes and also from experiments in which plants with altered levels of antifungal secondary metabolites were generated. Whereas the emphasis to date has been on degradative mechanisms of resistance of phytopathogenic fungi to antifungal secondary metabolites, in the future we are likely to see a rapid expansion in our knowledge of alternative mechanisms of resistance. These may include membrane efflux systems of the kind associated with multidrug resistance and innate resistance due to insensitivity of the target site. The manipulation of plant biosynthetic pathways to give altered antibiotic profiles will also be valuable in telling us more about the significance of antifungal secondary metabolites for plant defense and clearly has great potential for enhancing disease resistance for commercial purposes.

Activation of quiescent infections by postharvest pathogens during transition from the biotrophic to the necrotrophic stage

“…The host's natural preformed and inducible fungistatic molecules or defense responses constitute a major barrier to the quiescent pathogen. Pathogens have developed several strategies to cope with these molecules (Morrisey & Osbourn, 1999): (i) detoxification of antifungal compounds (Mathews & Van Etten, 1983;Van Etten et al, 1989;Osbourn, 1996;Mayer & Staples, 2002;Schouten et al, 2002); (ii) efflux transport of antifungal compounds from the pathogen's cells (Jones & George, 2004); and (iii) suppression of the host's defenses (Williamson, 1994;Morrisey & Osbourn, 1999).…”

Gaeumannomyces graminis, the take‐all fungus and its relatives

“…Cyclic hydroxamic acids are found almost exclusively in the Gramineae (Frey et al, 1997). They have a 4-hydroxy-1,4-benzoxazin-3-one structure, and are found constitutively in wheat, rye, triticale, maize and sorghum, but are not present in barley, rice or oats (Morrissey and Osbourn, 1999;Niemeyer, 1988). In planta, hydroxamic acids are sequestered as inactive glucosides, but are hydrolysed after infection or tissue damage to aglucones, e.g.…”

Phytohormones and Plant–herbivore–pathogen Interactions: Integrating the Molecular With the Ecological

“…Perhaps more intriguing is that a highly dynamic defense strategy may limit consumers' own phenotypic plasticity to counteract host resistances. Such plasticity is evident, for example, in the ability of some insects to modify digestive enzymes to reduce the impact of proteinase inhibitors (Cloutier et al 2000, Paulillo et al 2000, or the induction in some pathogens of enzymes that degrade phytoalexins (Morrissey and Osbourn 1999), induced defense mechanisms (Heath 2002), or indeed to alter constitutive antifungal compounds and use them to interfere with induced defense responses (Bouarab et al 2002). It is intriguing that recent evidence (Li et al 2002) shows that some herbivores induce detoxification systems not in response to defensive end products but to signaling molecules (SA and JA).…”