Abstract

In this study, the recovery phenomenon following infection with Potato virus Y (PVY) was investigated in tobacco (Nicotiana tobaccum), tomato (Solanum lycopersicum) and potato (Solanum tuberosum) plants. In tobacco plants, infection of severe strains of PVY (PVYN or PVYN:O) induced conspicuous vein clearing and leaf deformation in the first three leaves above the inoculated leaves, but much milder symptoms in the upper leaves. The recovery phenotype was not obvious in tobacco plants infected with PVY strain that induce mild symptoms (PVYO). However, regardless of the virus strains, reduction in PVY RNA levels was similarly observed in the upper leaves of these plants. Removal of the first three leaves above the inoculated leaves interfered with the occurrence of recovery, suggesting that the signal(s) mediating the recovery is likely generated in these leaves. In PVYN or PVYN:O but not in PVYO-infected tobacco plants, the expression of PR-1a transcripts were correlated with the accumulation level of PVY RNA. Reduced level of PVY RNA in the upper leaves was also observed in infected tomato plants, whereas such phenomenon was not observed in potato plants. PVY-derived small RNAs were detected in both tobacco and potato plants and their accumulation levels were correlated with PVY RNA levels. Our results demonstrate that the recovery phenotype following PVY infection is host-specific and not necessarily associated with the expression of PR-1a and generation of PVY small RNAs.

Highlights

  • Multiple strategies are employed by plants to cope with virus invasion

  • Using the virus level as an indicator, the recovery was revealed to occur in tomato but not in potato plants, demonstrating that the recovery phenotype is host-dependent

  • Potato virus Y (PVY) genome-derived small RNAs of ~21 nt were detected in both tobacco and potato plants

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Summary

Introduction

Multiple strategies are employed by plants to cope with virus invasion. These strategies include the inherited and pathogen-specific resistance conferred by a resistance (R) gene [1], the induced and pathogen-nonspecific resistance brought about by systemic acquired resistance (SAR) [2,3,4,5], and the pathogen-derived and pathogen-specific resistance mediated by RNA silencing [4]. The R gene-mediated resistance is the classical mode of resistance in host plants against incompatible pathogens including viruses [1], falling into the gene-for-gene model [6]. The SAR, on the other hand, is a basal defense mechanism mediated by signal molecules such as salicylic acid (SA), ethylene and jasmonic acid against a broad spectrum of pathogens [2]. The RNA silencing-directed resistance is mediated by small interfering RNAs (siRNA) of ~21–26 nucleotides (nt) in length [7,8,9], generated through the cleavage of a double-stranded, or an imperfect stem-loop, RNA molecule by a

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