|Simon, Anne - UNIVERSITY OF MARYLAND|
Submitted to: Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 10, 2008
Publication Date: July 18, 2008
Citation: Manfre, A.J., Simon, A.E. 2008. Importance of coat protein and RNA silencing in satellite RNA/virus interactions. Virology. 379:161-167. Interpretive Summary: Plants and animals are susceptible to a wide variety of disease causing organisms including bacteria, viruses, and prions. Viruses are sub-microscopic agents that grow and reproduce within a host by taking over its cellular machinery and using it to benefit the virus rather than the host. In response to viral infections, plants have evolved defense mechanisms to fight an invading virus. One of these mechanisms used has been termed RNA silencing, a mechanism involving the targeted degradation of "foreign" RNA. In response, viruses have also evolved proteins to suppress the host RNA silencing pathway. The work presented here investigates how the silencing pathway interacts with the suppressor protein (CP) of the Turnip crinkle virus (TCV) and if a small satellite helper virus (satC) can change the amount of virus accumulating in plant cells. These findings are very important, because this is the first published study to suggest that a satellite virus (satC) may affect host plant immunity and therefore, disease resistance.
Technical Abstract: RNA silencing is a major defense mechanism that plants use to fight an invading virus. The silencing suppressor of Turnip crinkle virus (TCV) is the viral coat protein (CP), which obstructs the DCL2/DCL4 silencing pathway. TCV is associated with a virulent satellite RNA (satC) that represses the accumulation of TCV genomic RNA and whose accumulation is repressed by the TCV CP. To investigate if reduced TCV accumulation due to satC involves RNA silencing and/or the suppressor activity of the CP, TCV was altered to contain a mutation reported to target CP silencing suppressor activity (Deleris et al., Science 313, 68, 2006). However, the mutation did not cause a specific defect in silencing suppression but rather produced a generally non-functional protein. We demonstrate that a functional CP, but not DCL2/DCL4, is required for satC-mediated repression of TCV. In addition, enhancement of satC in the absence of a functional CP requires DCL2/DCL4.