Abstract

The V-satellite RNA (V-satRNA) of peanut stunt virus (PSV) has no effect on symptoms produced in tobacco by PSV. In contrast, the G-satRNA induced complete or nearly complete suppression of systemic symptom development. Because G-satRNA differs from V-satRNA in only five nucleotide positions, these two satRNAs provide excellent material for investigating the molecular basis of satRNA-mediated symptom attenuation. For this purpose, we constructed transcription vectors containing full-length cDNA clones from which infectious RNA transcripts can be synthesized in vitro, and produced chimeric and mutant satRNA molecules. Although an A → C substitution at position 362 of the V-satRNA molecule delayed systemic symptom development and reduced symptom severity, changes at both nucleotide positions 226 (C → U) and 362 (A → C) of V-satRNA were required for suppression of systemic symptom development. Our results are consistent with the idea that PSV satRNAs are noncoding molecules that exert their biological activities by directly interacting with host/viral components.

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