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Plant resistance and symptom modulation by a satellite RNA in turnip crinkle virus/Arabidopsis system
Abstract
In this dissertation, I report my studies on the resistance of Arabidopsis thaliana ecotype Dijon (Di-0) to turnip crinkle carmovirus (TCV), a simple, single-stranded, positive-sense, plant RNA virus. TCV efficiently replicated in protoplasts prepared from Di-0 callus culture, but it did not move long-distance in Di-0 plants (Simon et al., 1992). Cardamine chlorotic fleck virus (CCFV), the carmovirus most closely related to TCV, infected Di-0 plants systemically (Oh et al., 1995). I found that TCV with the coat protein open reading frame (ORF) from CCFV (TCV-CP$\rm\sb{CCFV})$ and TCV with a single base mutation in the initition codon (AUG to ACG) of the coat protein ORF (TCV-CPm) were infectious on ecotypes Columbia (Col-0, TCV-susceptible) and Di-0 (TCV-resistant). These results indicate that TCV coat protein is the viral determinant for resistance of Di-0 to TCV. In addition, my results suggest that the resistance of Di-0 to TCV is specific to TCV and may involve an RNA degradation activity. I also studied the movement of TCV, CCFV, and TCV-CP$\sb{\rm CCFV}$ in Col-0 and Di-0 plants using a whole plant in situ hybridization technique. The results indicate that TCV was restricted to within small areas around the initial infection sites on inoculated leaves of Di-0 plants, whereas TCV (in Col-0), CCFV and TCV-CP$\sb{\rm CCFV})$ (in Col-0 and Di-0) moved long-distance to metabolic sink tissues (young leaves and roots) at different rates. Many plant RNA viruses are associated with small subviral RNAs, including satellite (sat-) RNAs. Small subviral RNAs require a helper virus for replication and movement, and they often intensify or attenuate the symptoms caused by the helper virus. TCV is associated with sat-RNA C, a sat-RNA that normally intensifies the symptoms of the TCV-M isolate (Simon et al., 1988; Li and Simon, 1990). I will report my work on the mechanism of symptom modulation mediated by sat-RNA C in Arabidopsis plants. My results indicate that symptom modulation by sat-RNA C is mediated by the viral coat protein, and a putative interaction between the 3$\sp\prime$ end of sat-RNA C and the N-terminus of coat protein is involved. Symptom attenuation by sat-RNAs is widely believed to be mediated by inhibition of helper virus replication through competition for replication factors (Roossinck et al., 1992). My study shows that inhibition of virus long distance movement is involved in sat-RNA C-mediated symptom attenuation of TCV-CPm (and probably TCV-CP$\rm\sb{CCFV})$ and inhibition of helper virus replication is not important. In addition, symptom attenuation mediated by sat-RNA C is localized and does not involve the major plant defense pathway. A model that explains sat-RNA C-mediated symptom attenuation is proposed.
Subject Area
Plant pathology|Microbiology|Molecular biology
Recommended Citation
Kong, Qingzhong, "Plant resistance and symptom modulation by a satellite RNA in turnip crinkle virus/Arabidopsis system" (1996). Doctoral Dissertations Available from Proquest. AAI9709616.
https://scholarworks.umass.edu/dissertations/AAI9709616