The Samuel Roberts Noble Foundation, Inc.   How and why would a virus become a pathogen?
 

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Summary of genes that are down regulated (A) or up regulated (B) in the tomato plants infected with CMV/D satRNA compared with the plants infected with CMV/Dm satRNA (the attenuating mutant of D satRNA). C-E, symptoms of plants infected with CMV/Dm sat RNA (C), CMV alone (D), and CMV/D satRNA (E).

We are addressing this question by trying to understand the basis of pathogenesis of a lethal parasite of CMV, the D satRNA. D satRNA attenuates CMV symptoms in most hosts, but specifically induces systemic necrosis in tomato.

We are interested in the cellular and molecular mechanisms involved in this lethal disease that result in a run-away systemic necrosis. We are using molecular biological, genomic, functional genomic, genetic, biochemical and cell biological approaches to understand the mechanisms of virus-induced plant lethality and host specificity of plant death (Xu and Roossinck, 2000; Xu et al., 2003; Xu et al., 2004).

We know that we can change only 3 nt of the D satRNA, and change it from a pathogen to an attenuating satRNA. We have studied the changes in the transcriptome that are associated with infection by these two closely related satRNAs and find that expression of 400 genes is either enhanced or reduced (Irian et al., 2007).

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