1. Oxaloacetate acetylhydrolase gene mutants of Sclerotinia sclerotiorum do not accumulate oxalic acid, but do produce limited lesions on host plants.
- Author
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Liang, Xiaofei, Liberti, Daniele, Li, Moyi, Kim, Young‐Tae, Hutchens, Andrew, Wilson, Ron, and Rollins, Jeffrey A.
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SCLEROTINIA sclerotiorum ,PLANT mutation ,OXALIC acid ,BIOACCUMULATION ,PLANT cloning ,MICROBIAL virulence - 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 Δ 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 Δ 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 Δss-oah1 mutants established very restricted lesions in which the infectious hyphae gradually lost viability. Cytological comparisons of WT and Δ 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. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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