Background: Sclerotinia sclerotiorum (Lib.) de Bary is a necrotrophic fungal pathogen which causes disease in a wide range of plants. An observed decrease in photosynthetic performance is the primary reason for the reduction of crop yield induced by S. sclerotiorum. The H2C2O4 is the main pathogenic material secreted by S. sclerotiorum, but the effects of H2C2O4 acidity and the C2O4 2- ion on photosynthetic performance remain unknown.
Results: S. sclerotiorum infection significantly decreased photosynthetic O2 evolution and the maximum quantum yield of photosystem II (Fv/Fm) in tobacco leaves under high-light. H2C2O4 (the main pathogenic material secreted by S. sclerotiorum) with pH 4.0 also significantly decreased photosynthetic performance. However, treatment with H3PO4 and HCl at the same pH as H2C2O4 caused much less decrease in photosynthetic performance than H2C2O4 did. These results verify that the acidity of the H2C2O4 secreted by S. sclerotiorum was only partially responsible for the observed decreases in photosynthesis. Treatment with 40 mM K2C2O4 decreased Fv/Fm by about 70% of the levels observed under 40 mM H2C2O4, which further demonstrates that C2O4(2-) was the primary factor that impaired photosynthetic performance during S. sclerotiorum infection. K2C2O4 treatment did not further decrease photosynthetic performance when D1 protein synthesis was fully inhibited, indicating that C2O4(2-) inhibited PSII by repressing D1 protein synthesis. It was observed that K2C2O4 treatment inhibited the rate of RuBP regeneration and carboxylation efficiency. In the presence of a carbon assimilation inhibitor, K2C2O4 2 treatment did not further decrease photosynthetic performance, which infers that C2O4(2-) inhibited PSII activity partly by repressing the carbon assimilation. In addition, it was showed that C2O4(2-) treatment inhibited the PSII activity but not the PSI activity.
Conclusions: This study demonstrated that the damage to the photosynthetic apparatus induced by S. sclerotiorum is not only caused by the acidity of H2C2O4, but also by C2O4(2-) which plays a much more important role in damaging the photosynthetic apparatus. C2O4(2-) inhibits PSII activity, as well as the rate of RuBP regeneration and carboxylation efficiency, leading to the over production of reactive oxygen species (ROS). By inhibiting the synthesis of D1, ROS may further accelerate PSII photoinhibition.