Relevant bibliographies by topics / PTGS (posttranscriptional gen silencing)

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Academic literature on the topic 'PTGS (posttranscriptional gen silencing)'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "PTGS (posttranscriptional gen silencing)"

1

Hoffer, Paul, Sergey Ivashuta, Olga Pontes, Alexa Vitins, Craig Pikaard, Andrew Mroczka, Nicholas Wagner, and Toni Voelker. "Posttranscriptional gene silencing in nuclei." Proceedings of the National Academy of Sciences 108, no. 1 (December 20, 2010): 409–14. http://dx.doi.org/10.1073/pnas.1009805108.

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In plants, small interfering RNAs (siRNAs) with sequence homology to transcribed regions of genes can guide the sequence-specific degradation of corresponding mRNAs, leading to posttranscriptional gene silencing (PTGS). The current consensus is that siRNA-mediated PTGS occurs primarily in the cytoplasm where target mRNAs are localized and translated into proteins. However, expression of an inverted-repeat double-stranded RNA corresponding to the soybeanFAD2-1Adesaturase intron is sufficient to silenceFAD2-1, implicating nuclear precursor mRNA (pre-mRNA) rather than cytosolic mRNA as the target of PTGS. SilencingFAD2-1using intronic or 3′-UTR sequences does not affect transcription rates of the target genes but results in the strong reduction of target transcript levels in the nucleus. Moreover, siRNAs corresponding to pre-mRNA–specific sequences accumulate in the nucleus. In Arabidopsis, we find that two enzymes involved in PTGS, Dicer-like 4 and RNA-dependent RNA polymerase 6, are localized in the nucleus. Collectively, these results demonstrate that siRNA-directed RNA degradation can take place in the nucleus, suggesting the need for a more complex view of the subcellular compartmentation of PTGS in plants.
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Kubota, Kenji, Shinya Tsuda, Atsushi Tamai, and Tetsuo Meshi. "Tomato Mosaic Virus Replication Protein Suppresses Virus-Targeted Posttranscriptional Gene Silencing." Journal of Virology 77, no. 20 (October 15, 2003): 11016–26. http://dx.doi.org/10.1128/jvi.77.20.11016-11026.2003.

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ABSTRACT Posttranscriptional gene silencing (PTGS), a homology-dependent RNA degradation system, has a role in defending against virus infection in plants, but plant viruses encode a suppressor to combat PTGS. Using transgenic tobacco in which the expression of green fluorescent protein (GFP) is posttranscriptionally silenced, we investigated a tomato mosaic virus (ToMV)-encoded PTGS suppressor. Infection with wild-type ToMV (L strain) interrupted GFP silencing in tobacco, coincident with visible symptoms, whereas some attenuated strains of ToMV (L11 and L11A strains) failed to suppress GFP silencing. Analyses of recombinant viruses containing the L and L11A strains revealed that a single base change in the replicase gene, which causes an amino acid substitution, is responsible for the symptomless and suppressor-defective phenotypes of the attenuated strains. An agroinfiltration assay indicated that the 130K replication protein acts as a PTGS suppressor. Small interfering RNAs (siRNAs) of 21 to 25 nucleotides accumulated during ToMV infection, suggesting that the major target of the ToMV-encoded suppressor is downstream from the production of siRNAs in the PTGS pathway. Analysis with GFP-tagged recombinant viruses revealed that the suppressor inhibits the establishment of the ToMV-targeted PTGS system in the inoculated leaves but does not detectably suppress the activity of the preexisting, sequence-specific PTGS machinery there. Taken together, these results indicate that it is likely that the ToMV-encoded suppressor, the 130K replication protein, blocks the utilization of silencing-associated small RNAs, so that a homology-dependent RNA degradation machinery is not newly formed.
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Qu, Feng, Tao Ren, and T. Jack Morris. "The Coat Protein of Turnip Crinkle Virus Suppresses Posttranscriptional Gene Silencing at an Early Initiation Step." Journal of Virology 77, no. 1 (January 1, 2003): 511–22. http://dx.doi.org/10.1128/jvi.77.1.511-522.2003.

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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.
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Havelda, Zoltán, Csaba Hornyik, Aniello Crescenzi, and József Burgyán. "In Situ Characterization of Cymbidium Ringspot Tombusvirus Infection-Induced Posttranscriptional Gene Silencing in Nicotiana benthamiana." Journal of Virology 77, no. 10 (May 15, 2003): 6082–86. http://dx.doi.org/10.1128/jvi.77.10.6082-6086.2003.

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ABSTRACT In plants, posttranscriptional gene silencing (PTGS) is an ancient and effective defense mechanism against viral infection. A number of viruses encode proteins that suppress virus-activated PTGS. The p19 protein of tombusviruses is a potent PTGS suppressor which interferes with the onset of PTGS-generated systemic signaling and is not required for viral replication or for viral movement in Nicotiana benthamiana. This unique feature of p19 suppressor allowed us to analyze the mechanism of PTGS-based host defense and its viral suppression without interfering with other viral functions. In contrast to the necrotic symptoms caused by wild-type tombusvirus, the infection of p19-defective mutant virus results in the development of a typical PTGS-associated recovery phenotype in N. benthamiana. In this report we show the effect of PTGS on the viral infection process for N. benthamiana infected with either wild-type Cymbidium Ringspot Tombusvirus (CymRSV) or a p19-defective mutant (Cym19stop). In situ analyses of different virus-derived products revealed that PTGS is not able to reduce accumulation of virus in primary infected cells regardless of the presence of p19 PTGS suppressor. We also showed that both CymRSV and Cym19stop viruses move systemically in the vasculature, with similar efficiencies. However, in contrast to the uniform accumulation of CymRSV throughout systemically infected leaves, the presence of Cym19stop virus was confined to and around the vascular bundles. These results suggest that the role of p19 is to prevent the onset of mobile signal-induced systemic PTGS ahead of the viral infection front, leading to generalized infection.
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Havelda, Zoltán, Csaba Hornyik, Anna Válóczi, and József Burgyán. "Defective Interfering RNA Hinders the Activity of a Tombusvirus-Encoded Posttranscriptional Gene Silencing Suppressor." Journal of Virology 79, no. 1 (January 1, 2005): 450–57. http://dx.doi.org/10.1128/jvi.79.1.450-457.2005.

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ABSTRACT Defective interfering (DI) RNAs are subviral replicons originating from the viral genome and are associated with many plant RNA viruses and nearly all animal RNA viruses. The presence of DI RNAs in tombusvirus-infected plants reduces the accumulation of helper virus RNA and results in the development of attenuated symptoms similar to those caused by tombusviruses defective in p19, the posttranscriptional gene silencing (PTGS) suppressor. In situ analysis of infected plants containing DI RNAs revealed that the extent of virus infection was spatially restricted as was found for p19-defective tombusvirus. Previously, p19 was shown to suppress PTGS by sequestering the small interfering RNAs (siRNAs), which act as the specificity determinant for PTGS. Our results demonstrate that DI RNAs dramatically elevate the level of virus-specific siRNAs in viral infections, resulting in the saturation of p19 and the accumulation of unbound siRNAs. Moreover, we showed that, at low temperature, where PTGS is inhibited, DI RNAs are not able to efficiently interfere with virus accumulation and protect the plants. These data show that the activation of PTGS plays a pivotal role in DI RNA-mediated interference. Our data also support a role for 21-nucleotide siRNAs in PTGS signaling.
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Dong, Xiangli, Rene van Wezel, John Stanley, and Yiguo Hong. "Functional Characterization of the Nuclear Localization Signal for a Suppressor of Posttranscriptional Gene Silencing." Journal of Virology 77, no. 12 (June 15, 2003): 7026–33. http://dx.doi.org/10.1128/jvi.77.12.7026-7033.2003.

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ABSTRACT The nucleus-localized C2 protein of Tomato yellow leaf curl virus-China (TYLCV-C) is an active suppressor of posttranscriptional gene silencing (PTGS). Consistently, infection with TYLCV-C resulted in PTGS arrest in plants. The C2 protein possesses a functional, arginine-rich nuclear localization signal within the basic amino acid-rich region 17KVQHRIAKKTTRRRR31. When expressed from potato virus X, C2-RRRR31DVGG (in which the four consecutive arginine residues 28RRRR31 were replaced with DVGG) that had been tagged with a green fluorescent protein (GFP) failed to transport GFP into nuclei and was dysfunctional in inducing necrosis and suppressing PTGS in plants. Amino acid substitution mutants C2-K17D-GFP, C2-HR21DV-GFP, and C2-KK25DI-GFP localized to nuclei and produced necrosis, but only C2-K17D-GFP suppressed PTGS. The N-terminal portions C21-31 and C217-31 fused in frame to GFP were capable of targeting GFP to nuclei, but neither caused necrosis nor affected PTGS. Our data establish that nuclear localization is likely required for C2 protein to function in C2-mediated induction of necrosis and suppression of PTGS, which may follow diverse pathways in plants. Possible mechanisms of how the C2 protein involves these biological functions are discussed.
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Bazzini, A. A., H. E. Hopp, R. N. Beachy, and S. Asurmendi. "Posttranscriptional Gene Silencing Does Not Play a Significant Role in Potato virus X Coat Protein-Mediated Resistance." Phytopathology® 96, no. 11 (November 2006): 1175–78. http://dx.doi.org/10.1094/phyto-96-1175.

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The expression of a gene that encodes coat protein (CP) of Potato virus X (PVX) in transgenic tobacco plants confers a high level of CP-mediated rresistance (CP-MR) against PVX infection. To determine if posttranscriptional gene silencing (PTGS) plays a role in resistance, transgenic plants expressing PVX CP were challenged against PVX under conditions in which PTGS was suppressed by low temperatures or using viruses carrying PTGS suppressors. The data demonstrate that PTGS does not play a significant role in PVX CP-MR.
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8

Zhang, Xinyan, Ying Zhu, Xiaodan Liu, Xinyu Hong, Yang Xu, Ping Zhu, Yang Shen, et al. "Suppression of endogenous gene silencing by bidirectional cytoplasmic RNA decay in Arabidopsis." Science 348, no. 6230 (April 2, 2015): 120–23. http://dx.doi.org/10.1126/science.aaa2618.

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Plant immunity against foreign gene invasion takes advantage of posttranscriptional gene silencing (PTGS). How plants elaborately avert inappropriate PTGS of endogenous coding genes remains unclear. We demonstrate in Arabidopsis that both 5′-3′ and 3′-5′ cytoplasmic RNA decay pathways act as repressors of transgene and endogenous PTGS. Disruption of bidirectional cytoplasmic RNA decay leads to pleiotropic developmental defects and drastic transcriptomic alterations, which are substantially rescued by PTGS mutants. Upon dysfunction of bidirectional RNA decay, a large number of 21- to 22-nucleotide endogenous small interfering RNAs are produced from coding transcripts, including multiple microRNA targets, which could interfere with their cognate gene expression and functions. This study highlights the risk of unwanted PTGS and identifies cytoplasmic RNA decay pathways as safeguards of plant transcriptome and development.
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9

Pfeffer, S., P. Dunoyer, F. Heim, K. E. Richards, G. Jonard, and V. Ziegler-Graff. "P0 of Beet Western Yellows Virus Is a Suppressor of Posttranscriptional Gene Silencing." Journal of Virology 76, no. 13 (July 1, 2002): 6815–24. http://dx.doi.org/10.1128/jvi.76.13.6815-6824.2002.

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ABSTRACT Higher plants employ a homology-dependent RNA-degradation system known as posttranscriptional gene silencing (PTGS) as a defense against virus infection. Several plant viruses are known to encode proteins that can suppress PTGS. Here we show that P0 of beet western yellows virus (BWYV) displays strong silencing suppressor activity in a transient expression assay based upon its ability to inhibit PTGS of green fluorescent protein (GFP) when expressed in agro-infiltrated leaves of Nicotiana benthamiana containing a GFP transgene. PTGS suppressor activity was also observed for the P0s of two other poleroviruses, cucurbit aphid-borne yellows virus and potato leafroll virus. P0 is encoded by the 5′-proximal gene in BWYV RNA but does not accumulate to detectable levels when expressed from the genome-length RNA during infection. The low accumulation of P0 and the resulting low PTGS suppressor activity are in part a consequence of the suboptimal translation initiation context of the P0 start codon in viral RNA, although other factors, probably related to the viral replication process, also play a role. A mutation to optimize the P0 translation initiation efficiency in BWYV RNA was not stable during virus multiplication in planta. Instead, the P0 initiation codon in the progeny was frequently replaced by a less efficient initiation codon such as ACG, GTG, or ATA, indicating that there is selection against overexpression of P0 from the viral genome.
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10

Martínez de Alba, A. E., R. Flores, and C. Hernández. "Two Chloroplastic Viroids Induce the Accumulation of Small RNAs Associated with Posttranscriptional Gene Silencing." Journal of Virology 76, no. 24 (December 15, 2002): 13094–96. http://dx.doi.org/10.1128/jvi.76.24.13094-13096.2002.

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ABSTRACT In plants, posttranscriptional gene silencing (PTGS) has been reported for cytoplasmic RNAs from endogenous nuclear genes, transgenes, viruses, and, recently, for a viroid with nuclear replication and accumulation. However, phenomena of this kind have not been described for mitochondrial or chloroplastic RNAs. Here we show that viroids that replicate and accumulate in the chloroplast are also targets of PTGS and this process may control viroid titer.
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Dissertations / Theses on the topic "PTGS (posttranscriptional gen silencing)"

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Růžičková, Adéla. "Vliv způsobu indukce RNA interference na umlčování reportérového genu pro GFP u Arabidopsis thaliana." Master's thesis, 2015. http://www.nusl.cz/ntk/nusl-353799.

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RNA interference (RNAi) is one of the key mechanisms that are involved in many biological processes such as control of plant gene expression, influence on chromatin arrangement or providing protection against invasive DNA or RNA transposons, viruses and transgenes. In plants, RNAi is triggered by double stranded RNA (dsRNA) that is cleaved by DICER LIKE (DCL) proteins to small RNAs (sRNAs). The size of these sRNAs is in range of 21 - 24 nucleotides (nt). Small RNA acts in the place of origin and they are also a mobile signal which in plants can move to a short distance through plasmodesmata and to a long distance trough phloem. sRNA and Argonaute (AGO) protein form RNA-induced silencing complex (RISC). Together, they recognize the target RNA molecule and contribute to an efficient RNAi phase which may be exhibited by gene silencing at posttranscriptional level (PTGS) or transcriptional level (TGS). The purpose of this study was to compare the effects of silencing constructs, witch in a controlled way differently trigger RNAi directed against the expression of the GFP reporter gene in the model organism Arabidopsis thaliana. Silencing constructs were placed under an inducible promoter activated by the presence of 17-β-estradiol (XVE system). They differed in the way of the dsRNA formation and in the...
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Čermák, Vojtěch. "Studium mechanismu posttranskripčního a transkripčního umlčování transgenů v buněčné linii tabáku BY-2." Master's thesis, 2012. http://www.nusl.cz/ntk/nusl-306690.

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The RNA interference is a mechanism, which allows cells to regulate their genes functions, to establish and maintain heterochromatin and to defend them against invasive nucleic acids. In plants, RNA interference is initiated by double-stranded RNA, which is processed by Dicer into small RNAs, usually 20-24nt long. These small RNAs form a complex with Argonaut protein that participates in different processes based on sequence complementarity. This complex can guide mRNA cleavage, translation blocking and chromatin modifications, resulting either into posttranscriptional silencing (by preventing translation of already existing mRNA, PTGS) or transcriptional silencing (by preventing transcription of mRNA, TGS). The first step of this thesis was to establish different ways of triggering PTGS and to evaluate their functionality and efficiency. The next step was a preparation of a system which would allow to study the transition from posttrancriptional to transcriptional silencing. These so called "indicator lines" should allow to observe the timing and dynamics of this process by utilizing fluorescent proteins. This system is also going to enable to evaluate, how different factors are involved in this process - one of the factors is RNA-dependent RNA polymerase 6 (RDR6) which plays an essential role in...
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