Abstract
Sclerotinia sclerotiorum is a necrotrophic ascomycete fungus with an extremely broad host range. This pathogen produces the non-specific phytotoxin and key pathogenicity factor, oxalic acid (OA). Our recent work indicated that this fungus and more specifically OA, can induce apoptotic-like programmed cell death (PCD) in plant hosts, this induction of PCD and disease requires generation of reactive oxygen species (ROS) in the host, a process triggered by fungal secreted OA. Conversely, during the initial stages of infection, OA also dampens the plant oxidative burst, an early host response generally associated with plant defense. This scenario presents a challenge regarding the mechanistic details of OA function; as OA both suppresses and induces host ROS during the compatible interaction. In the present study we generated transgenic plants expressing a redox-regulated GFP reporter. Results show that initially, Sclerotinia (via OA) generates a reducing environment in host cells that suppress host defense responses including the oxidative burst and callose deposition, akin to compatible biotrophic pathogens. Once infection is established however, this necrotroph induces the generation of plant ROS leading to PCD of host tissue, the result of which is of direct benefit to the pathogen. In contrast, a non-pathogenic OA-deficient mutant failed to alter host redox status. The mutant produced hypersensitive response-like features following host inoculation, including ROS induction, callose formation, restricted growth and cell death. These results indicate active recognition of the mutant and further point to suppression of defenses by the wild type necrotrophic fungus. Chemical reduction of host cells with dithiothreitol (DTT) or potassium oxalate (KOA) restored the ability of this mutant to cause disease. Thus, Sclerotinia uses a novel strategy involving regulation of host redox status to establish infection. These results address a long-standing issue involving the ability of OA to both inhibit and promote ROS to achieve pathogenic success.
Highlights
Sclerotinia sclerotiorum is a devastating and economically important necrotrophic fungal pathogen capable of infecting more than 400 species of dicotyledonous plants worldwide [1,2] causing annual crop losses exceeding $200 million in the United States alone [2]
We showed that oxalic acid (OA), secreted by Sclerotinia, is a pathogenicity determinant and elicitor of plant programmed cell death [12]
Challenge with the non-pathogenic OAdeficient A2 mutant resulted in restricted growth, reminiscent of an HR-like response (Figure 1A, 1B)
Summary
Sclerotinia sclerotiorum is a devastating and economically important necrotrophic fungal pathogen capable of infecting more than 400 species of dicotyledonous plants worldwide [1,2] causing annual crop losses exceeding $200 million in the United States alone [2]. Necrotrophic plant pathogens require dead host tissue in order to obtain nourishment. The resulting disease symptoms have been attributed to direct killing of host tissue via secretion of toxic metabolites by the pathogen. We have been investigating the role of fungal secreted oxalic acid (OA) in pathogenicity of S. sclerotiorum [5,6,7,8,9]. OA (dicarboxylic acid) is remarkably multifunctional and contributes to numerous physiological processes (e.g. reduction in pH, acidity-induced activation of enzymes, elevation of Ca2+, guard cell regulation, vascular plugging with oxalate crystals) that augment fungal colonization of host plants (reviewed in [10]). We have shown that OA is a fungal elicitor that induces cell death in host plant tissue resulting in hallmark apoptotic-like features including cell shrinkage, DNA laddering, and TUNEL reactive cells in a time and dose dependent manner. Oxalic acid aids Sclerotinia pathogenicity indirectly acting as a signaling molecule, via manipulation of host ROS [12]
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