PLANT VIRUS SATELLITE AND DEFECTIVE INTERFERING RNAS: New Paradigms for a New Century

Abstract

Although many subviral RNAs reduce or intensify disease symptoms caused by the helper virus, only recently have clues concerning the mechanism of disease modulation been revealed. New models for DI RNA-mediated reduction in helper virus levels and symptom attenuation include DI RNA enhancement of posttranscriptional gene silencing (PTGS), which is an antiviral defense mechanism in plants. Symptom enhancement by the satRNA of Cucumber mosaic virus is caused by minus-strand induction of the programmed cell death pathway. In contrast, symptom enhancement by satC of Turnip crinkle virus is due to satC interference with virion formation, leading to increased levels of free coat protein, which is the viral suppressor of PTGS. Mutualism between satRNA and helper virus can be seen for the satRNA of Groundnut rosette virus, which contributes to the virus by allowing virion assembly. These novel findings are leading to re-evaluation of the relationships between subviral RNAs, helper viruses, and hosts.

Mimicry of molecular pretenders: The terminal structures of satellites associated with plant RNA viruses

“…Together with the observations of mutualisms in certain satRNA/helper virus systems, 2 our views of satellites are gradually adjusting: satellites are no longer seen as purely parasitic on the respective helper viruses. Instead, the satellites could be thought of simply as molecular mimicries of their respective helper viruses, which evolved similar but sometimes more efficient ways to utilize the resources provided by the helper viruses and host plants.…”

“…1,2,4,5 Several excellent reviews have detailed the general characteristics of satRNAs and satellite viruses, such as RNA structures, pathogenicity, replication, variability and evolution, as well as the molecular interactions among satellites, helper viruses and host plants. 1,2,[4][5][6][7] However, relatively little emphasis has been placed on the similarities and differences between the cis-acting elements required for efficient replication and replicase complexes that satRNAs and cognate helper viruses use. Recent technical advances have facilitated the preparation of replicase complexes of several viruses and the determination of higher-order structures of certain satRNAs.…”

“…By definition, satRNAs are phylogenetically unrelated small RNA molecules that depend on the helper viruses for replication, encapsidation and dissemination; 1,2 and those satRNAs that encode and are encapsidated in their own coat proteins (CPs) are termed satellite viruses. Most satellites do not encode any replication-related protein and thus rely on the replicase complexes provided by the respective helper viruses for replication, although a few satRNAs associated with nepoviruses do encode nonstructural proteins involved in their replication.…”

“…2,23 Therefore, this system provides an example of mutualism between the satRNA and helper virus, which alters our views of satRNAs as being pure parasites on the helper viruses and led to the re-evaluation of the trilateral relationship among satellites, helper viruses, and host plants.…”

“…[36][37][38] D4-satRNA contains a necrogenic domain that forms a conserved stem-loop structure in all necrogenic CMV satRNAs, as revealed by covariation analysis. 38 This element is located in the 3' terminus of satRNA and is likely involved in enhancing satRNA minus-strand accumulation and inducing programmed cell death in tomato, 2,29 which might explain the pathogenicity of D4-satRNA.…”