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 C2O42- ion on photosynthetic performance remain unknown. 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 C2O42- 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 C2O42- 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, K2C2O42 treatment did not further decrease photosynthetic performance, which infers that C2O42- inhibited PSII activity partly by repressing the carbon assimilation. In addition, it was showed that C2O42- treatment inhibited the PSII activity but not the PSI activity. 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 C2O42- which plays a much more important role in damaging the photosynthetic apparatus. C2O42- 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.

Background: Fall dormancy of alfalfa is significantly associated with its cold tolerance, while root, the main body of alfalfa for overwintering, is critical for the cold resistance of alfalfa. The effect of low temperature on mitochondrial ultrastructure and respiratory metabolism of alfalfa seedling root with different fall dormancy was examined, to study the root cold resistance mechanism by which fall dormancy affects alfalfa cold tolerance. Results: Low temperature induced mitochondrial swelling, and the decline of ATP and accumulation of H 2 O 2 in alfalfa seedling root. Both the Cytochrome pathway (CP) and Alternative pathway (AP) respiratory rate were restrained and mETC complex I, II, III and IV activities were inhibited directly by low temperature in both kinds of alfalfa seedling root, while the decline of mETC complex II and III activities were more serious in Gannong No. 5. These results indicated that the damage of mitochondrial structure and the inhibition of mETC complex I , II, III and IV activities directly by low temperature declined the ATP synthesis and aggravated the ROS accumulation, which inhibit the growth of alfalfa seedling root. Moreover, the lower damage on mitochondrial structure and mETC complex II, III activities and higher the percent of AP to total respiratory rate lead to the lower ATP lack and H 2 O 2 accumulation, which contributed to the root growth of Xinmu No.4 seedling. Conclusions: Low sensitivity of mitochondrial structural stability and mETC complex II, III and Alternative respiration to low temperature contributed to the root cold resistance of alfalfa with low fall dormancy grade.