Abstract
RNA viruses exist as populations of genome variants. Virus-infected plants accumulate 21–24 nucleotide small interfering RNAs (siRNAs) derived from viral RNA (virus-derived siRNAs) through gene silencing. This paper describes the profile of mutations in virus-derived siRNAs for three members of the family Potyviridae: Turnip mosaic virus (TuMV), Papaya ringspot virus (PRSV) and Wheat streak mosaic virus (WSMV). For TuMV in Arabidopsis thaliana, profiles were obtained for mechanically inoculated rosette leaves and systemically infected cauline leaves and inflorescence. Results are consistent with selection pressure on the viral genome imposed by local and systemic movement. By genetically removing gene silencing in the plant and silencing suppression in the virus, our results showed that antiviral gene silencing imposes selection in viral populations. Mutations in siRNAs derived from a PRSV coat protein transgene in the absence of virus replication showed the contribution of cellular RNA-dependent RNA polymerases to the generation of mutations in virus-derived siRNAs. Collectively, results are consistent with two sources of mutations in virus-derived siRNAs: viral RNA-dependent RNA polymerases responsible for virus replication and cellular RNA-dependent RNA polymerases responsible for gene silencing amplification.
Highlights
In plants virus infection triggers antiviral gene silencing that results in the accumulation of virus-derived small interfering RNAs that are normally 21–24 nucleotides long and associate with argonaute proteins to form RNA-induced silencing complexes and guide translational repression or cleave of viral RNA targets based on sequence complementarity[1,2,3]
With respect to the Turnip mosaic virus (TuMV) reference genome, virus-derived small interfering RNAs (siRNAs) were classified into two groups: perfect match, and one or two mismatches
Results described above for TuMV, Wheat streak mosaic virus (WSMV), and Papaya ringspot virus (PRSV) showed that virus-derived siRNAs harbor mutations originating from two possible sources: viral RNA-dependent RNA polymerases responsible for virus replication and cellular RNA-dependent RNA polymerases responsible for gene silencing amplification
Summary
In plants virus infection triggers antiviral gene silencing that results in the accumulation of virus-derived small interfering RNAs (siRNAs) that are normally 21–24 nucleotides long and associate with argonaute proteins to form RNA-induced silencing complexes and guide translational repression or cleave of viral RNA targets based on sequence complementarity[1,2,3]. Small RNA profiles were generated for TuMV-infected Arabidopsis thaliana (Arabidopsis) ecotype Colombia, and comparisons were made between the mechanically inoculated rosette leaves, and systemically infected cauline leaves, or inflorescence. As they move across tissues, viruses face several selection pressures. Accumulation of mutations in virus-derived siRNAs is in agreement with antiviral gene silencing imposing selection pressure in viral populations. A subset of the viral RNA population targeted by siRNAs is used as a template by cellular by RNA-dependent RNA polymerases to synthesize dsRNA that is processed into secondary virus-derived siRNAs by DCL proteins[3,7,29]. Results support the contribution of cellular RNA-dependent RNA polymerases to the generation of mutations in virus-derived siRNAs
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