Poster: Plant-pathogen interactions
Abs #
529: Sclerotinia sclerotiorum produces oxalic acid to deregulate guard cells during infection
Sclerotinia sclerotiorum, which infects a broad range of plant species, uses oxalate to damage plant tissues and to cause wilting and necrosis. In this work we show that S. sclerotiorum alters stomatal movement by means of oxalate. Using a GFP tagged strain we show that infected Vicia faba leaves are wide open during darkness in the vicinity of the fungus, and that growing hyphae penetrate open stomata. This suggests that the fungus alters stomatal behavior to facilitate infection. Stomata of V. faba infected with oxalate-deficient S. sclerotiorum are significantly less open in darkness in comparison with a wild type isolate. We also demonstrate that oxalate induces stomatal opening in detached epidermal peels from V. faba leaves, and that at physiological concentrations of 10 mM, oxalate treatment 1) triggers guard cell potassium ion accumulation and starch breakdown; and 2) interferes with ABA-induced stomatal closure. In whole leaves, a wild type Sclerotinia strain caused significantly higher transpiration rates and reduced plant biomass when compared with an oxalate-deficient mutant.
The above results suggest that oxalate may act by two different mechanisms, one that triggers accumulation of osmotica in guard cells and another that inhibits ABA-induced stomatal closure. Simultaneous regulation of these two mechanisms by oxalate may explain the dramatic degree of stomatal opening in leaf lesions infected by wild type strains of S. sclerotiorum.
