Abstract
Plant viruses are excellent tools for studying microbial-plant interactions as well as the complexities of host activities. Our study focuses on the role of C2 encoded by Beet severe curly top virus (BSCTV) in the virus-plant interaction. Using BSCTV C2 as bait in a yeast two-hybrid screen, a C2-interacting protein, S-adenosyl-methionine decarboxylase 1 (SAMDC1), was identified from an Arabidopsis thaliana cDNA library. The interaction was confirmed by an in vitro pull-down assay and a firefly luciferase complemention imaging assay in planta. Biochemical analysis further showed that the degradation of the SAMDC1 protein was inhibited by MG132, a 26S proteasome inhibitor, and that C2 could attenuate the degradation of the SAMDC1 protein. Genetic analysis showed that loss of function of SAMDC1 resulted in reduced susceptibility to BSCTV infection and reduced viral DNA accumulation, similar to the effect of BSCTV C2 deficiency. Bisulfite sequencing analysis further showed that C2 deficiency caused enhanced DNA methylation of the viral genome in infected plants. We also showed that C2 can suppress de novo methylation in the FWA transgenic assay in the C2 transgene background. Overexpression of SAMDC1 can mimic the suppressive activity of C2 against green fluorescent protein-directed silencing. These results suggest that C2 interferes with the host defense mechanism of DNA methylation-mediated gene silencing by attenuating the 26S proteasome-mediated degradation of SAMDC1.
Highlights
The methods of the study have been previously reported.[4]
acute coronary syndromes (ACS) was defined according to contemporary criteria, which include an increase of troponin of . 0.2 mg/l with at least one of the following: ischaemic symptoms, development of pathological Q waves on the ECG, and ECG changes indicative of ischaemia
300 were randomly assigned to folic acid 0.5 mg once daily and 293 patients served as control group
Summary
Homocysteine has been regarded as a modest independent risk factor for atherosclerotic vascular disease.[1 2] folic acid can reduce homocysteine concentrations substantially, the value of folic acid intervention in primary and secondary prevention in terms of hard clinical end points is still uncertain. Many studies addressing this question are still underway. We analysed the data again according to contemporary definitions of acute coronary syndromes (ACS).[5]
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