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Host-induced avirulence of hibiscus chlorotic ringspot virus mutants correlates with reduced gene-silencing suppression activity

¹ Department of Biological Sciences, 14 Science Drive 4, National University of Singapore, Singapore 117545, Singapore
² Functional Genomics Laboratory, Institute of Molecular and Cell Biology, Singapore 138673, Singapore
³ Temasek Life Sciences Laboratory, 1 Research Link, Singapore 117604, Singapore

Correspondence
Sek-Man Wong
dbswsm{at}nus.edu.sg

Post-transcriptional gene silencing (PTGS) and virus-encoded gene-silencing suppressors are defence and counterdefence strategies developed by host and pathogens during evolution. Using a green fluorescence protein-based transient suppression system, the coat protein (CP) of Hibiscus chlorotic ringspot virus (HCRSV) was identified as a strong gene-silencing suppressor. CP suppressed sense RNA-induced but not dsRNA-induced local and systemic PTGS. This is different from another virus in the genus Carmovirus, Turnip crinkle virus (TCV), the CP of which strongly suppresses dsRNA-induced PTGS. HCRSV CP domain deletion mutants lost their suppression function, indicating that the complete CP is essential for suppression of PTGS. When CP was expressed from a Potato virus X (PVX) vector, it was able to enhance the symptom severity and to increase the accumulation of PVX RNA. Here, it is proposed that HCRSV CP suppresses PTGS at the initiation step, which is different from TCV CP. In addition, a previous study demonstrated that CP mutants resulting from serial passage of HCRSV in its local lesion host also showed a significantly reduced suppression function, indicating that host-induced mutations that lead to avirulence of HCRSV in kenaf correlate with its reduced ability to suppress PTGS.

A phylogenetic tree based on the Tombusviridae CP sequence is available as supplementary material in JGV Online.

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