scholarly journals The viral silencing suppressor P19 interacts with the receptor‐like kinases BAM1 and BAM2 and suppresses the cell‐to‐cell movement of RNA silencing independently of its ability to bind sRNA

2020 ◽  
Author(s):  
Borja Garnelo Gόmez ◽  
Tabata Rosas‐Díaz ◽  
Chaonan Shi ◽  
Pengfei Fan ◽  
Dan Zhang ◽  
...  
Keyword(s):  
Rna Silencing ◽  
Cell Movement ◽  
Silencing Suppressor ◽  
Viral Silencing Suppressor

scholarly journals Identification and Functional Analysis of Four RNA Silencing Suppressors in Begomovirus Croton Yellow Vein Mosaic Virus

2022 ◽  
Vol 12 ◽  
Author(s):  
Ying Zhai ◽  
Anirban Roy ◽  
Hao Peng ◽  
Daniel L. Mullendore ◽  
Gurpreet Kaur ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Rna Silencing ◽  
Cell Movement ◽  
Yellow Vein ◽  
Silencing Suppressor ◽  
Monopartite Begomovirus ◽  
Yellow Vein Mosaic Virus ◽  
First Time ◽  
Leaf Curl Disease ◽  
Leaf Curl

Croton yellow vein mosaic virus (CYVMV), a species in the genus Begomovirus, is a prolific monopartite begomovirus in the Indian sub-continent. CYVMV infects multiple crop plants to cause leaf curl disease. Plants have developed host RNA silencing mechanisms to defend the threat of viruses, including CYVMV. We characterized four RNA silencing suppressors, namely, V2, C2, and C4 encoded by CYVMV and betasatellite-encoded C1 protein (βC1) encoded by the cognate betasatellite, croton yellow vein betasatellite (CroYVMB). Their silencing suppressor functions were verified by the ability of restoring the β-glucuronidase (GUS) activity suppressed by RNA silencing. We showed here for the first time that V2 was capable of self-interacting, as well as interacting with the V1 protein, and could be translocalized to the plasmodesmata in the presence of CYVMV. The knockout of either V2 or V1 impaired the intercellular mobility of CYVMV, indicating their novel coordinated roles in the cell-to-cell movement of the virus. As pathogenicity determinants, each of V2, C2, and C4 could induce typical leaf curl symptoms in Nicotiana benthamiana plants even under transient expression. Interestingly, the transcripts and proteins of all four suppressors could be detected in the systemically infected leaves with no correlation to symptom induction. Overall, our work identifies four silencing suppressors encoded by CYVMV and its cognate betasatellite and reveals their subcellular localizations, interaction behavior, and roles in symptom induction and intercellular virus movement.

RNA Silencing Suppressor p19 Regulates The Expressions of Cell Cycle Related Genes*

2009 ◽  
Vol 36 (5) ◽  
pp. 541-548 ◽  
Author(s):  
Li LIU ◽  
Jian LI ◽  
Yu-Ping XU ◽  
Wen-Tao QIAO ◽  
Qi-Min CHEN ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rna Silencing ◽  
Silencing Suppressor ◽  
Rna Silencing Suppressor

Identification of RNA silencing suppressor encoded by wheat blue dwarf (WBD) phytoplasma

Plant Biology ◽  
2021 ◽  
Author(s):  
Licheng Wang ◽  
Wenbao Chen ◽  
Huan Ma ◽  
Jingyuan Li ◽  
Xingan Hao ◽  
...  
Keyword(s):  
Rna Silencing ◽  
Silencing Suppressor ◽  
Rna Silencing Suppressor

scholarly journals Requirement for Host RNA-Silencing Components and the Virus-Silencing Suppressor when Second-Site Mutations Compensate for Structural Defects in the 3′ Untranslated Region

2015 ◽  
Vol 89 (22) ◽  
pp. 11603-11618 ◽  
Author(s):  
Maitreyi Chattopadhyay ◽  
Vera A. Stupina ◽  
Feng Gao ◽  
Christine R. Szarko ◽  
Micki M. Kuhlmann ◽  
...  
Keyword(s):  
Small Rnas ◽  
Rna Silencing ◽  
Untranslated Region ◽  
Higher Order ◽  
Order Structure ◽  
Silencing Suppressor ◽  
Turnip Crinkle Virus ◽  
Site Mutation ◽  
Primary Mutation ◽  
Positive Strand Rna

ABSTRACTTurnip crinkle virus (TCV) contains a structured 3′ region with hairpins and pseudoknots that form a complex network of noncanonical RNA:RNA interactions supporting higher-order structure critical for translation and replication. We investigated several second-site mutations in the p38 coat protein open reading frame (ORF) that arose in response to a mutation in the asymmetric loop of a critical 3′ untranslated region (UTR) hairpin that disrupts local higher-order structure. All tested second-site mutations improved accumulation of TCV in conjunction with a partial reversion of the primary mutation (TCV-rev1) but had neutral or a negative effect on wild-type (wt) TCV or TCV with the primary mutation. SHAPE (selective 2′-hydroxylacylation analyzed byprimerextension) structure probing indicated that these second-site mutations reside in an RNA domain that includes most of p38 (domain 2), and evidence for RNA:RNA interactions between domain 2 and 3′UTR-containing domain 1 was found. However, second-site mutations were not compensatory in the absence of p38, which is also the TCV silencing suppressor, or indcl-2/dcl4orago1/ago2backgrounds. One second-site mutation reduced silencing suppressor activity of p38 by altering one of two GW motifs that are required for p38 binding to double-stranded RNAs (dsRNAs) and interaction with RNA-induced silencing complex (RISC)-associated AGO1/AGO2. Another second-site mutation substantially reduced accumulation of TCV-rev1 in the absence of p38 or DCL2/DCL4. We suggest that the second-site mutations in the p38 ORF exert positive effects through a similar downstream mechanism, either by enhancing accumulation of beneficial DCL-produced viral small RNAs that positively regulate the accumulation of TCV-rev1 or by affecting the susceptibility of TCV-rev1 to RISC loaded with viral small RNAs.IMPORTANCEGenomes of positive-strand RNA viruses fold into high-order RNA structures. Viruses with mutations in regions critical for translation and replication often acquire second-site mutations that exert a positive compensatory effect through reestablishment of canonical base pairing with the altered region. In this study, two distal second-site mutations that individually arose in response to a primary mutation in a critical 3′ UTR hairpin in the genomic RNA of turnip crinkle virus did not directly interact with the primary mutation. Although different second-site changes had different attributes, compensation was dependent on the production of the viral p38 silencing suppressor and on the presence of silencing-required DCL and AGO proteins. Our results provide an unexpected connection between a 3′ UTR primary-site mutation proposed to disrupt higher-order structure and the RNA-silencing machinery.

scholarly journals Identification and subcellular location of an RNA silencing suppressor encoded by mulberry crinkle leaf virus

Virology ◽  
2019 ◽  
Vol 526 ◽  
pp. 45-51 ◽  
Author(s):  
Quan-You Lu ◽  
Lei Yang ◽  
Jinshan Huang ◽  
Luping Zheng ◽  
Xin Sun
Keyword(s):  
Rna Silencing ◽  
Subcellular Location ◽  
Silencing Suppressor ◽  
Rna Silencing Suppressor ◽  
Leaf Virus

scholarly journals Cymbidium Ringspot Virus Harnesses RNA Silencing To Control the Accumulation of Virus Parasite Satellite RNA

2008 ◽  
Vol 82 (23) ◽  
pp. 11851-11858 ◽  
Author(s):  
Vitantonio Pantaleo ◽  
József Burgyán
Keyword(s):  
Rna Silencing ◽  
Sequence Similarity ◽  
Helper Virus ◽  
Ringspot Virus ◽  
Silencing Suppressor ◽  
Short Interfering Rna ◽  
Satellite Rna ◽  
The Cost ◽  
Interfering Rna ◽  
Rna Replicon

ABSTRACT Cymbidium ringspot virus (CymRSV) satellite RNA (satRNA) is a parasitic subviral RNA replicon that replicates and accumulates at the cost of its helper virus. This 621-nucleotide (nt) satRNA species has no sequence similarity to the helper virus, except for a 51-nt-long region termed the helper-satellite homology (HSH) region, which is essential for satRNA replication. We show that the accumulation of satRNA strongly depends on temperature and on the presence of the helper virus p19 silencing suppressor protein, suggesting that RNA silencing plays a crucial role in satRNA accumulation. We also demonstrate that another member of the Tombusvirus genus, Carnation Italian ringspot virus (CIRV), supports satRNA accumulation at a higher level than CymRSV. Our results suggest that short interfering RNA (siRNA) derived from CymRSV targets satRNA more efficiently than siRNA from CIRV, possibly because of the higher sequence similarity between the HSH regions of the helper and CIRV satRNAs. RNA silencing sensor RNA carrying the putative satRNA target site in the HSH region was efficiently cleaved when transiently expressed in CymRSV-infected plants but not in CIRV-infected plants. Strikingly, replacing the CymRSV HSH box2 sequence with that of CIRV restores satRNA accumulation both at 24°C and in the absence of the p19 suppressor protein. These findings demonstrate the extraordinary adaptation of this virus to its host in terms of harnessing the antiviral silencing response of the plant to control the virus parasite satRNA.

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