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Oxaloacetate acetylhydrolase gene mutants of Sclerotinia sclerotiorum do not accumulate oxalic acid, but do produce limited lesions on host plants.

ABSTRACT: The oxaloacetate acetylhydrolase (OAH, EC 3.7.1.1)-encoding gene Ss-oah1 was cloned and functionally characterized from Sclerotinia sclerotiorum. Ss-oah1 transcript accumulation mirrored oxalic acid (OA) accumulation with neutral pH induction dependent on the pH-responsive transcriptional regulator Ss-Pac1. Unlike previously characterized ultraviolet (UV)-induced oxalate-deficient mutants ('A' mutants) which retain the capacity to accumulate OA, gene deletion ?ss-oah1 mutants did not accumulate OA in culture or during plant infection. This defect in OA accumulation was fully restored on reintroduction of the wild-type (WT) Ss-oah1 gene. The ?ss-oah1 mutants were also deficient in compound appressorium and sclerotium development and exhibited a severe radial growth defect on medium buffered at neutral pH. On a variety of plant hosts, the ?ss-oah1 mutants established very restricted lesions in which the infectious hyphae gradually lost viability. Cytological comparisons of WT and ?ss-oah1 infections revealed low and no OA accumulation, respectively, in subcuticular hyphae. Both WT and mutant hyphae exhibited a transient association with viable host epidermal cells at the infection front. In summary, our experimental data establish a critical requirement for OAH activity in S.?sclerotiorum?OA biogenesis and pathogenesis, but also suggest that factors independent of OA contribute to the establishment of primary lesions.

SUBMITTER: Liang X

PROVIDER: S-EPMC6638444 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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Oxaloacetate acetylhydrolase gene mutants of Sclerotinia sclerotiorum do not accumulate oxalic acid, but do produce limited lesions on host plants.

Liang Xiaofei X Liberti Daniele D Li Moyi M Kim Young-Tae YT Hutchens Andrew A Wilson Ron R Rollins Jeffrey A JA

Molecular plant pathology 20141215 6

The oxaloacetate acetylhydrolase (OAH, EC 3.7.1.1)-encoding gene Ss-oah1 was cloned and functionally characterized from Sclerotinia sclerotiorum. Ss-oah1 transcript accumulation mirrored oxalic acid (OA) accumulation with neutral pH induction dependent on the pH-responsive transcriptional regulator Ss-Pac1. Unlike previously characterized ultraviolet (UV)-induced oxalate-deficient mutants ('A' mutants) which retain the capacity to accumulate OA, gene deletion Δss-oah1 mutants did not accumulate ...[more]

PMID: 25285668

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Project description: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.

Dataset Information

Oxaloacetate acetylhydrolase gene mutants of Sclerotinia sclerotiorum do not accumulate oxalic acid, but do produce limited lesions on host plants.

Publications

Oxaloacetate acetylhydrolase gene mutants of Sclerotinia sclerotiorum do not accumulate oxalic acid, but do produce limited lesions on host plants.

Similar Datasets

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