Mechanisms by which the infection of Sclerotinia sclerotiorum (Lib.) de Bary affects the photosynthetic performance in tobacco leaves

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 H(2)C(2)O(4) is the main pathogenic material secreted by S. sclerotiorum, but the effects of H(2)C(2)O(4) acidity and the C(2)O(4)(2−) ion on photosynthetic performance remain unknown. RESULTS: S. sclerotiorum infection significantly decreased photosynthetic O(2) evolution and the maximum quantum yield of photosystem II (F(v)/F(m)) in tobacco leaves under high-light. H(2)C(2)O(4) (the main pathogenic material secreted by S. sclerotiorum) with pH 4.0 also significantly decreased photosynthetic performance. However, treatment with H(3)PO(4) and HCl at the same pH as H(2)C(2)O(4) caused much less decrease in photosynthetic performance than H(2)C(2)O(4) did. These results verify that the acidity of the H(2)C(2)O(4) secreted by S. sclerotiorum was only partially responsible for the observed decreases in photosynthesis. Treatment with 40 mM K(2)C(2)O(4) decreased F(v)/F(m) by about 70% of the levels observed under 40 mM H(2)C(2)O(4), which further demonstrates that C(2)O(4)(2−) was the primary factor that impaired photosynthetic performance during S. sclerotiorum infection. K(2)C(2)O(4) treatment did not further decrease photosynthetic performance when D1 protein synthesis was fully inhibited, indicating that C(2)O(4)(2−) inhibited PSII by repressing D1 protein synthesis. It was observed that K(2)C(2)O(4) treatment inhibited the rate of RuBP regeneration and carboxylation efficiency. In the presence of a carbon assimilation inhibitor, K(2)C(2)O(4)(2) treatment did not further decrease photosynthetic performance, which infers that C(2)O(4)(2−) inhibited PSII activity partly by repressing the carbon assimilation. In addition, it was showed that C(2)O(4)(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 H(2)C(2)O(4), but also by C(2)O(4)(2−) which plays a much more important role in damaging the photosynthetic apparatus. C(2)O(4)(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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12870-014-0240-4) contains supplementary material, which is available to authorized users.