scholarly journals RNA Silencing and Plant Viral Diseases

2012 ◽  
Vol 25 (10) ◽  
pp. 1275-1285 ◽  
Author(s):  
Ming-Bo Wang ◽  
Chikara Masuta ◽  
Neil A. Smith ◽  
Hanako Shimura
Keyword(s):  
Rna Silencing ◽  
Defense Mechanisms ◽  
Critical Role ◽  
Viral Disease ◽  
Rna Degradation ◽  
Degradation Pathway ◽  
Plant Viruses ◽  
Direct Role ◽  
Dna Viruses ◽  
Disease Induction

RNA silencing plays a critical role in plant resistance against viruses, with multiple silencing factors participating in antiviral defense. Both RNA and DNA viruses are targeted by the small RNA-directed RNA degradation pathway, with DNA viruses being also targeted by RNA-directed DNA methylation. To evade RNA silencing, plant viruses have evolved a variety of counter-defense mechanisms such as expressing RNA-silencing suppressors or adopting silencing-resistant RNA structures. This constant defense–counter defense arms race is likely to have played a major role in defining viral host specificity and in shaping viral and possibly host genomes. Recent studies have provided evidence that RNA silencing also plays a direct role in viral disease induction in plants, with viral RNA-silencing suppressors and viral siRNAs as potentially the dominant players in viral pathogenicity. However, questions remain as to whether RNA silencing is the principal mediator of viral pathogenicity or if other RNA-silencing-independent mechanisms also account for viral disease induction. RNA silencing has been exploited as a powerful tool for engineering virus resistance in plants as well as in animals. Further understanding of the role of RNA silencing in plant–virus interactions and viral symptom induction is likely to result in novel anti-viral strategies in both plants and animals.

scholarly journals The influenza A virus NS1 protein binds small interfering RNAs and suppresses RNA silencing in plants

2004 ◽  
Vol 85 (4) ◽  
pp. 983-991 ◽  
Author(s):  
Etienne Bucher ◽  
Hans Hemmes ◽  
Peter de Haan ◽  
Rob Goldbach ◽  
Marcel Prins
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Rna Silencing ◽  
Influenza A ◽  
Rna Degradation ◽  
Plant Viruses ◽  
Sequence Specificity ◽  
Ns1 Protein ◽  
Rna Molecules ◽  
Wide Range

RNA silencing comprises a set of sequence-specific RNA degradation pathways that occur in a wide range of eukaryotes, including animals, fungi and plants. A hallmark of RNA silencing is the presence of small interfering RNA molecules (siRNAs). The siRNAs are generated by cleavage of larger double-stranded RNAs (dsRNAs) and provide the sequence specificity for degradation of cognate RNA molecules. In plants, RNA silencing plays a key role in developmental processes and in control of virus replication. It has been shown that many plant viruses encode proteins, denoted RNA silencing suppressors, that interfere with this antiviral response. Although RNA silencing has been shown to occur in vertebrates, no relationship with inhibition of virus replication has been demonstrated to date. Here we show that the NS1 protein of human influenza A virus has an RNA silencing suppression activity in plants, similar to established RNA silencing suppressor proteins of plant viruses. In addition, NS1 was shown to be capable of binding siRNAs. The data presented here fit with a potential role for NS1 in counteracting innate antiviral responses in vertebrates by sequestering siRNAs.

scholarly journals Effects of the Crinivirus Coat Protein–Interacting Plant Protein SAHH on Post-Transcriptional RNA Silencing and Its Suppression

2013 ◽  
Vol 26 (9) ◽  
pp. 1004-1015 ◽  
Author(s):  
M. Carmen Cañizares ◽  
Rosa Lozano-Durán ◽  
Tomás Canto ◽  
Eduardo R. Bejarano ◽  
David M. Bisaro ◽  
...  
Keyword(s):  
Coat Protein ◽  
Rna Silencing ◽  
Rna Degradation ◽  
Plant Viruses ◽  
Plant Protein ◽  
Transcriptional Gene Silencing ◽  
Small Interfering Rnas ◽  
Post Transcriptional Gene Silencing ◽  
Secondary Sirnas ◽  
Tomato Chlorosis Virus

In plants, post-transcriptional gene silencing (PTGS) is a sequence-specific mechanism of RNA degradation induced by double-stranded RNA (dsRNA), which is processed into small interfering RNAs (siRNAs). siRNAs are methylated and, thereby, stabilized by the activity of the S-adenosylmethionine-dependent RNA methyltransferase HEN1. PTGS is amplified by host-encoded RNA-dependent RNA polymerases (RDR), which generate dsRNA that is processed into secondary siRNAs. To counteract this RNA silencing-mediated response of the host, plant viruses express proteins with silencing suppression activity. Here, we report that the coat protein (CP) of crinivirus (family Closteroviridae, genus Crinivirus) Tomato chlorosis virus, a known suppressor of silencing, interacts with S-adenosylhomocysteine hydrolase (SAHH), a plant protein essential for sustaining the methyl cycle and S-adenosylmethionine-dependent methyltransferase activity. Our results show that, by contributing to an increased accumulation of secondary siRNAs generated by the action of RDR6, SAHH enhances local RNA silencing. Although downregulation of SAHH prevents local silencing, it enhances the spread of systemic silencing. Our results also show that SAHH is important in the suppression of local RNA silencing not only by the crinivirus Tomato chlorosis virus CP but also by the multifunctional helper component-proteinase of the potyvirus Potato virus Y.

scholarly journals The Coat Protein of Turnip Crinkle Virus Suppresses Posttranscriptional Gene Silencing at an Early Initiation Step

2003 ◽  
Vol 77 (1) ◽  
pp. 511-522 ◽  
Author(s):  
Feng Qu ◽  
Tao Ren ◽  
T. Jack Morris
Keyword(s):  
Coat Protein ◽  
Gene Silencing ◽  
Rna Silencing ◽  
Rna Degradation ◽  
Plant Viruses ◽  
Early Initiation ◽  
Turnip Crinkle Virus ◽  
Small Interfering Rnas ◽  
Posttranscriptional Gene Silencing ◽  
Initiation Step

ABSTRACT Posttranscriptional gene silencing (PTGS), or RNA silencing, is a sequence-specific RNA degradation process that targets foreign RNA, including viral and transposon RNA for destruction. Several RNA plant viruses have been shown to encode suppressors of PTGS in order to survive this host defense. We report here that the coat protein (CP) of Turnip crinkle virus (TCV) strongly suppresses PTGS. The Agrobacterium infiltration system was used to demonstrate that TCV CP suppressed the local PTGS as strongly as several previously reported virus-coded suppressors and that the action of TCV CP eliminated the small interfering RNAs associated with PTGS. We have also shown that the TCV CP must be present at the time of silencing initiation to be an effective suppressor. TCV CP was able to suppress PTGS induced by sense, antisense, and double-stranded RNAs, and it prevented systemic silencing. These data suggest that TCV CP functions to suppress RNA silencing at an early initiation step, likely by interfering the function of the Dicer-like RNase in plants.

scholarly journals RNA silencing and viral disease induction in plants

Uirusu ◽  
2012 ◽  
Vol 62 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Hanako SHIMURA ◽  
Chikara MASUTA
Keyword(s):  
Rna Silencing ◽  
Viral Disease ◽  
Disease Induction

scholarly journals Autophagic degradation of the Cucumber mosaic virus virulence factor 2b balances antiviral RNA silencing with proviral plant fitness and virus seed transmission

2020 ◽  
Author(s):  
Aayushi Shukla ◽  
Gesa Hoffmann ◽  
Silvia López-González ◽  
Daniel Hofius ◽  
Anders Hafrén
Keyword(s):  
Cucumber Mosaic Virus ◽  
Mosaic Virus ◽  
Rna Silencing ◽  
Seed Transmission ◽  
Degradation Pathway ◽  
Plant Viruses ◽  
Cellular Reprogramming ◽  
Pathway Engineering ◽  
Dependent Manner ◽  
Selective Degradation

AbstractAutophagy is a conserved intracellular degradation pathway that has recently emerged as an integral part of plant responses to virus infection. The elucidated mechanisms of autophagy range from the selective degradation of viral components to a more general attenuation of disease symptoms. In addition, several viruses are able to manipulate the autophagy machinery and counteract autophagy-dependent resistance. Despite these findings, the complex interplay of autophagy activities, viral pathogenicity factors, and host defence pathways in disease development remains poorly understood. In the current study, we analysed the interaction between autophagy and Cucumber mosaic virus (CMV) in Arabidopsis thaliana. We show that autophagy is induced during CMV infection and promotes the turnover of the major CMV virulence protein and RNA silencing suppressor 2b. Intriguingly, 2b itself dampens plant autophagy. In accordance with 2b degradation, we found that autophagy provides resistance against CMV by reducing viral RNA accumulation in an RNA silencing-dependent manner. Moreover, autophagy and RNA silencing pathways contribute to plant longevity and fecundity of CMV infected plants in an additive manner, uncoupling it from resistance. In addition to reduced fecundity, autophagy-deficient plants also failed to support seed transmission of the virus. We propose that autophagy attenuates CMV virulence via 2b degradation and thereby increases both plant and virus fitness with a trade-off penalty arising from increased RNA silencing-mediated resistance.Author summaryThe capacity of plants to fight pathogenic viruses in order to survive and minimize damage relies on profound cellular reprogramming events. These include the synthesis of new as well as the degradation of pre-existing cellular components, together shifting cellular homeostasis towards a better tolerance of disease and fortification of antiviral defence mechanisms. Autophagy is a prominent and highly conserved cellular degradation pathway that supports plant stress resilience. Autophagy functions vary broadly and range from rather unspecific renewal of cytoplasm to highly selective degradation of a wide collection of specific substrates. Autophagy is well established to be involved during virus infections in animals, and its importance has also recently emerged in virus diseases of plants. However, we are still far from a comprehensive understanding of the complexity of autophagy activities in host-virus interactions and how autophagy pathway engineering could be applied against viruses. Here, we have analyzed one of the traditional model plant viruses, Cucumber mosaic virus (CMV), and its interactions with autophagy. Our study revealed that autophagy is tightly integrated into CMV disease, influencing processes from plant health to CMV epidemiology.

scholarly journals The RNA Degradation Pathway Regulates the Function of GAS5 a Non-Coding RNA in Mammalian Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e55684 ◽  
Author(s):  
Hidenori Tani ◽  
Masaki Torimura ◽  
Nobuyoshi Akimitsu
Keyword(s):  
Mammalian Cells ◽  
Rna Degradation ◽  
Degradation Pathway ◽  
Non Coding Rna

scholarly journals Stages of in vitro phagocytosis of Plasmodium falciparum-infected erythrocytes by human monocytes

2009 ◽  
Vol 42 (2) ◽  
pp. 103-106 ◽  
Author(s):  
Maria Imaculada Muniz-Junqueira ◽  
Carlos Eduardo Tosta
Keyword(s):  
Plasmodium Falciparum ◽  
Blood Circulation ◽  
Defense Mechanisms ◽  
Healthy Adult ◽  
Critical Role ◽  
Immune Serum ◽  
Human Monocytes ◽  
Malaria Parasites

Monocytes/macrophages play a critical role in the defense mechanisms against malaria parasites, and are the main cells responsible for the elimination of malaria parasites from the blood circulation. We carried out a microscope-aided evaluation of the stages of in vitro phagocytosis of Plasmodium falciparum-infected erythrocytes, by human monocytes. These cells were obtained from healthy adult individuals by means of centrifugation through a cushion of Percoll density medium and were incubated with erythrocytes infected with Plasmodium falciparum that had previously been incubated with a pool of anti-plasmodial immune serum. We described the stages of phagocytosis, starting from adherence of infected erythrocytes to the phagocyte membrane and ending with their destruction within the phagolisosomes of the monocytes. We observed that the different erythrocytic forms of the parasite were ingested by monocytes, and that the process of phagocytosis may be completed in around 30 minutes. Furthermore, we showed that phagocytosis may occur continuously, such that different phases of the process were observed in the same phagocyte.

scholarly journals The RNA degradation pathway is involved in PPARα-modulated anti-oral tumorigenesis

BioMedicine ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 27
Author(s):  
Nai-Wen Chang ◽  
Yi-Ping Huang
Keyword(s):  
Oral Cancer ◽  
Enrichment Analysis ◽  
Rna Degradation ◽  
Degradation Pathway ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
New Strategy ◽  
Tramp Complex ◽  
Oral Cancer Cells ◽  
Next Generation Sequencing Ngs

Background: The activation of peroxisome proliferator-activated receptor alpha (PPARα) has been shown to reprogram tumor metabolism and exhibits great potential for treating anti-oral tumorigenesis. Methods: In this study, we used a pathway-based strategy to explore possible functional pathways involved in the anticancer activity of PPARα in oral cancer cells through next-generation sequencing (NGS) and bioinformatic approaches. Results: We found that 3919 genes were upregulated and 1060 genes were downregulated through PPARα activation. These genes were mainly involved in the proteasomal, mRNA surveillance, spliceosomal, RNA transport, and RNA degradation pathways, as indicated by GO and KEGG enrichment analysis. Importantly, a total of 13 upregulated genes in the RNA degradation pathway were identified including 3 core exosome factor genes (RRP43, RRP42, and CSL4), 2 TRAMP complex genes (TRF4 and Mtr4), 2 exosome cofactor genes (RRP6 and MPP6), 2 CCR4-NOT complex genes (CNOT2 and CNOT3), 2 Ski complex genes (SKI2 and Ski3), 1 decapping complex gene (EDC4), and 1 gene involved in 5’ exoribonuclease activity (XRN1). Conclusion: Our findings suggest that the activation of PPARα to upregulate the RNA degradation pathway might provide a new strategy for oral cancer treatment.

scholarly journals Insights Into the Antiviral Pathways of the Silkworm Bombyx mori

2021 ◽  
Vol 12 ◽  
Author(s):  
Liang Jiang
Keyword(s):  
Signaling Pathways ◽  
Bombyx Mori ◽  
Defense Mechanisms ◽  
Critical Role ◽  
Janus Kinase ◽  
Economic Losses ◽  
Phosphatidylinositol 3 Kinase ◽  
Extracellular Signal ◽  
Immune Pathways ◽  
Insect Innate Immunity

The lepidopteran model silkworm, Bombyx mori, is an important economic insect. Viruses cause serious economic losses in sericulture; thus, the economic importance of these viruses heightens the need to understand the antiviral pathways of silkworm to develop antiviral strategies. Insect innate immunity pathways play a critical role in the outcome of infection. The RNA interference (RNAi), NF-kB-mediated, immune deficiency (Imd), and stimulator of interferon gene (STING) pathways, and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway are the major antiviral defense mechanisms, and these have been shown to play important roles in the antiviral immunity of silkworms. In contrast, viruses can modulate the prophenol oxidase (PPO), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), and the extracellular signal-regulated kinase (ERK) signaling pathways of the host to elevate their proliferation in silkworms. In this review, we present an overview of the current understanding of the main immune pathways in response to viruses and the signaling pathways modulated by viruses in silkworms. Elucidation of these pathways involved in the antiviral mechanism of silkworms furnishes a theoretical basis for the enhancement of virus resistance in economic insects, such as upregulating antiviral immune pathways through transgenic overexpression, RNAi of virus genes, and targeting these virus-modulated pathways by gene editing or inhibitors.

scholarly journals NUDT2 initiates viral RNA degradation by removal of 5′-phosphates

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Beatrice T. Laudenbach ◽  
Karsten Krey ◽  
Quirin Emslander ◽  
Line Lykke Andersen ◽  
Alexander Reim ◽  
...  
Keyword(s):  
Rna Degradation ◽  
Degradation Pathway ◽  
Immune Defense ◽  
Viral Rna ◽  
Rna Turnover ◽  
Nudix Hydrolase ◽  
Cellular Mechanisms ◽  
Independent Manner ◽  
Viral Rnas ◽  
Bacterial Rna

AbstractWhile viral replication processes are largely understood, comparably little is known on cellular mechanisms degrading viral RNA. Some viral RNAs bear a 5′-triphosphate (PPP-) group that impairs degradation by the canonical 5′-3′ degradation pathway. Here we show that the Nudix hydrolase 2 (NUDT2) trims viral PPP-RNA into monophosphorylated (P)-RNA, which serves as a substrate for the 5′-3′ exonuclease XRN1. NUDT2 removes 5′-phosphates from PPP-RNA in an RNA sequence- and overhang-independent manner and its ablation in cells increases growth of PPP-RNA viruses, suggesting an involvement in antiviral immunity. NUDT2 is highly homologous to bacterial RNA pyrophosphatase H (RppH), a protein involved in the metabolism of bacterial mRNA, which is 5′-tri- or diphosphorylated. Our results show a conserved function between bacterial RppH and mammalian NUDT2, indicating that the function may have adapted from a protein responsible for RNA turnover in bacteria into a protein involved in the immune defense in mammals.

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