European Journal of Plant Pathology

, Volume 128, Issue 1, pp 7–19 | Cite as

ABA signaling inhibits oxalate-induced production of reactive oxygen species and protects against Sclerotinia sclerotiorum in Arabidopsis thaliana

  • Xiaomei Guo
  • Henrik U. Stotz


Oxalic acid is an essential virulence factor of Sclerotinia sclerotiorum that elicits wilting symptoms in infected host plants. Foliar wilting in response to oxalic acid is known to be dependent on an increase in stomatal conductance. To determine whether stomatal regulation controls susceptibility to S. sclerotiorum, abscisic acid-insensitive and open stomata mutants of Arabidopsis thaliana were analyzed. Whereas abscisic acid-insensitive mutants were hypersusceptible to S. sclerotiorum, open stomata mutants were as susceptible as wild type. It was concluded that stomatal regulation does not control susceptibility to S. sclerotiorum because open stomata mutants are known to only impair guard cells whereas abscisic acid-insensitive mutants also affect other cell types. Guard cell-independent processes also control sensitivity to oxalic acid because oxalic acid was more toxic to abscisic acid-insensitive mutants than to open stomata mutants. To explore a possible mechanism of toxicity, production of reactive oxygen species was measured in plant cells after exposure to oxalic acid. Oxalic acid was found to elicit reactive oxygen species production independently of abscisic acid. Nevertheless, cancellation of reactive oxygen species elicitation after co-stimulation of wild-type guard cells with oxalic acid and abscisic acid provided evidence for antagonistic interaction between both molecules.


Disease Guard cell H2O2 Hypersusceptible Stomatal aperture 



abscisic acid




2′,7′-dichlorofluorescein diacetate


programmed cell death


reactive oxygen species



We thank D. Zhang and Y. Kamiya for using their epifluorescence microscopes; G. Tallman for critical reading of the manuscript.


This work was supported by National Sclerotinia Initiative Special Grants program U.S. Department of Agriculture [Grant number 58-5442-7-226].

Supplementary material

10658_2010_9623_MOESM1_ESM.xls (16 kb)
ESM 1 (XLS 15 kb)
10658_2010_9623_MOESM2_ESM.doc (1.3 mb)
Supplemental Figure 1 Images of pathogen-infected wild-type and mutant plants. Pictures were taken 2 days after inoculation with wild-type S. sclerotiorum. Note increased lesion sizes of the abi1 mutant. Original excel file used for figure 1 was included in this supplementary figure 1 to demonstrate that the lesion diameters of abi1 mutant are significant larger than those of Ler. (DOC 1335 kb)
10658_2010_9623_MOESM3_ESM.doc (33 kb)
Supplemental Figure 2 Stomatal apertures (width/length) after inoculation of wild-type (Ler) or abi1-1 mutant plants with S. sclerotiorum. Epidermis was removed from uninfected leaves and measured. Means and standard errors are shown (n > 160). Letters indicate significant differences (P < 0.01). (DOC 33 kb)
10658_2010_9623_MOESM4_ESM.doc (729 kb)
Supplemental Figure 3 Vanadate-sensitive stomatal opening in response to oxalic acid (OA) indicative of P-type ATPase activation. Epidermal strips of Vicia faba were incubated in the presence or absence of 2 mM vanadate (Van) prior to treatment with 10 mM OA (Schwartz et al., 1991). As a positive control, 1 μM fusicoccin (FC), a fungal toxin and activator of the plasma membrane H+-ATPase, was used. Means and standard errors are shown. Asterisks indicate significant differences (P < 0.001). The experiment was repeated six times following published procedures (Guimaraes and Stotz, 2004). (DOC 729 kb)


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Copyright information

© KNPV 2010

Authors and Affiliations

  1. 1.E306 Beadle CenterUniversity of Nebraska-LincolnLincolnUSA
  2. 2.Julius-von-Sachs-Institute für Biowissenschaften, Pharmazeutische Biologie, BiozentrumUniversitaet WuerzburgWuerzburgGermany

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