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- Title
TYMV and TRV infect Arabidopsis thaliana by expressing weak suppressors of RNA silencing and inducing host RNASE THREE LIKE1.
- Authors
Sehki, Hayat; Yu, Agnès; Elmayan, Taline; Vaucheret, Hervé
- Abstract
Post-Transcriptional Gene Silencing (PTGS) is a defense mechanism that targets invading nucleic acids of endogenous (transposons) or exogenous (pathogens, transgenes) origins. During plant infection by viruses, virus-derived primary siRNAs target viral RNAs, resulting in both destruction of single-stranded viral RNAs (execution step) and production of secondary siRNAs (amplification step), which maximizes the plant defense. As a counter-defense, viruses express proteins referred to as Viral Suppressor of RNA silencing (VSR). Some viruses express VSRs that totally inhibit PTGS, whereas other viruses express VSRs that have limited effect. Here we show that infection with the Turnip yellow mosaic virus (TYMV) is enhanced in Arabidopsis ago1, ago2 and dcl4 mutants, which are impaired in the execution of PTGS, but not in dcl2, rdr1 and rdr6 mutants, which are impaired in the amplification of PTGS. Consistently, we show that the TYMV VSR P69 localizes in siRNA-bodies, which are the site of production of secondary siRNAs, and limits PTGS amplification. Moreover, TYMV induces the production of the host enzyme RNASE THREE-LIKE 1 (RTL1) to further reduce siRNA accumulation. Infection with the Tobacco rattle virus (TRV), which also encodes a VSR limiting PTGS amplification, induces RTL1 as well to reduce siRNA accumulation and promote infection. Together, these results suggest that RTL1 could be considered as a host susceptibility gene that is induced by viruses as a strategy to further limit the plant PTGS defense when VSRs are insufficient. Author summary: RNA silencing is a conserved defense mechanism directed against viruses in various eukaryotic kingdoms. As a counter-defense, viruses generally express proteins referred to as viral suppressor of RNA silencing (VSR), which promote infection by inhibiting one or the other component of the RNA silencing machinery. So far, most of the work on VSRs has concentrated on those that strongly inhibit RNA silencing, causing severe infections and plant death. However, situations where VSRs only partially inhibit RNA silencing could be considered as advantageous for both partners of the infection because infected plants survive, flower and produce seeds despite virus multiplication. In this study, we show that Turnip yellow mosaic virus (TYMV) encodes a weak VSR, P69, which partially inhibits the amplification but not the execution of RNA silencing. In addition, TYMV induces the expression of the endogenous enzyme RNASE THREE-LIKE 1 (RTL1) to further reduce siRNA accumulation. Similarly, Tobacco rattle virus (TRV), which also encodes a weak VSR, induces RTL1 to reduce siRNA accumulation and promote infection. We propose that the limited effect of some VSRs on RNA silencing together with the ability of the corresponding viruses to induce the host RTL1 results in a tight balance between virus propagation and plant development, allowing a virus to propagate without killing its host. In the light of these results, RTL1 could be considered as a susceptibility gene induced by viruses encoding weak VSRs.
- Subjects
ARABIDOPSIS thaliana; TURNIP mosaic virus; RNA; NUCLEIC acids; PLANT viruses; NICOTIANA benthamiana
- Publication
PLoS Pathogens, 2023, Vol 18, Issue 1, p1
- ISSN
1553-7366
- Publication type
Article
- DOI
10.1371/journal.ppat.1010482