Virus resistance and gene silencing: killing the messenger

Waterhouse, P. M.

doi:10.1016/s1360-1385(99)01493-4

Cited by 98 publications

(52 citation statements)

References 41 publications

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“…In the PTGS process, once a specific mRNA enters the cytoplasm, it is recognized by the RNA surveillance system and degraded. This phenomenon is observed in different organisms including plants, animals, and fungi (Waterhouse, 1999;Sijen and Kooter, 2000). When transgenic plants become infected with the virus that expresses the same sequence as the transgene, the mRNA, viral RNA, and transgene mRNA are degraded (Vaucheret and Fagard, 2001).…”

Section: Analysis Of Resistance To Plrv Infection In Transgenic Plantsmentioning

confidence: 99%

Replicase mediated resistance against Potato Leafroll Virus in potato Desirée plants

et al. 2004

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Potato leafroll virus (PLRV) is a major menace for the potato production all over the world. PLRV is transmitted by aphids, and until now, the only strategy available to control this pest has been to use large amounts of insecticides. Transgenic approaches involving the expression of viral replicases are being developed to provide protection for plants against viral diseases. The purpose of this study was to compare the protection afforded by the differential expression of PLRV replicase transgene in potato plants cv. Desirée. Plants were genetically modified to express the complete sense PLRV replicase gene. Two constructions were used, one containing the constitutive 35SCaMV promoter and the other the phloem-specific RolA promoter from Agrobacterium rhizogenes. Transgenic plants were infected with PLRV in vitro, using infested aphids. In plants in which 35SCaMV controlled the expression of the PLRV replicase gene, signs of infection were initially detected, although most plants later developed a recovery phenotype showing undetectable virus levels 40 days after infection. In turn, those plants with the RolA promoter displayed an initial resistance that was later overcome. Different molecular mechanisms are likely to participate in the response to PLRV infection of these two types of transgenic plants.

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Section: Analysis Of Resistance To Plrv Infection In Transgenic Plantsmentioning

confidence: 99%

Replicase mediated resistance against Potato Leafroll Virus in potato Desirée plants

et al. 2004

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“…The independence of RNA truncation on DNA methylation observed in this study is consistent with our previous finding that GUS gene silencing by a dsRNAencoding inverted-repeat transgene is associated with increased DNA methylation in the GUS sequence but is not reversed by demethylation treatment (Wang & Waterhouse, 2000)+ In both cases, the hypermethylation appears to be a footprint of dsRNA-mediated PTGS, but does not contribute to the reduction in RNA levels+ This suggests that, although PTGS and RdDM are likely to be induced by the same dsRNA, they may have distinct biological roles+ It has been suggested that PTGS is a natural mechanism developed by plants to fight against viral infection (Covey et al+, 1997;Kooter et al+, 1999;Waterhouse et al+, 1999)+ DNA methylation, on the other hand, has been suggested to play a role in plant defense against selfish DNA (i+e+, transposon elements) by silencing the transposons through methylation-induced chromatin condensation (Ashraf & Ip, 1998;Kooter et al+, 1999)+ It has been recently found that, in Caenorhabditis elegans, mutations of several genes involved in RNAi can cause reactivation of transposons (Tabara et al+, 1999)+ This indicates that dsRNA is involved in both RNA degradation and transposon silencing+ Our result suggests that this may also be the case in plants; dsRNA confers viral resistance by triggering PTGS against viral RNA, while it can silence the transposons by inducing RdDM in the target sequences+…”

Section: The Biological Role Of Rddmmentioning

confidence: 99%

Replicating satellite RNA induces sequence-specific DNA methylation and truncated transcripts in plants

Wang

Wesley

Finnegan

et al. 2001

RNA

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Tobacco plants were transformed with a chimeric transgene comprising sequences encoding b-glucuronidase (GUS) and the satellite RNA (satRNA) of cereal yellow dwarf luteovirus. When transgenic plants were infected with potato leafroll luteovirus (PLRV), which replicated the transgene-derived satRNA to a high level, the satellite sequence of the GUS:Sat transgene became densely methylated. Within the satellite region, all 86 cytosines in the upper strand and 73 of the 75 cytosines in the lower strand were either partially or fully methylated. In contrast, very low levels of DNA methylation were detected in the satellite sequence of the transgene in uninfected plants and in the flanking nonsatellite sequences in both infected and uninfected plants. Substantial amounts of truncated GUS:Sat RNA accumulated in the satRNA-replicating plants, and most of the molecules terminated at nucleotides within the first 60 bp of the satellite sequence. Whereas this RNA truncation was associated with high levels of satRNA replication, it appeared to be independent of the levels of DNA methylation in the satellite sequence, suggesting that it is not caused by methylation. All the sequenced GUS:Sat DNA molecules were hypermethylated in plants with replicating satRNA despite the phloem restriction of the helper PLRV. Also, small, sense and antisense ;22 nt RNAs, derived from the satRNA, were associated with the replicating satellite. These results suggest that the sequence-specific DNA methylation spread into cells in which no satRNA replication occurred and that this was mediated by the spread of unamplified satRNA and/or its associated 22 nt RNA molecules.

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“…PTGS is triggered efficiently by dsRNA intermediates of cytoplasmically replicating viruses. The RNA genome of the invading virus is targeted and eliminated specifically when this natural antiviral mechanism is activated (Waterhouse et al, 1998(Waterhouse et al, , 1999Baulcombe, 1999;Smith et al, 2000;. In higher plants, PTGS is not limited to the cells in which it is activated, because mobile signals produced by PTGS can spread and confer sequence-specific RNA degradation in distant tissues (Palauqui et al, 1997;Voinnet and Baulcombe, 1997).…”

Section: Introductionmentioning

confidence: 99%

Short Defective Interfering RNAs of Tombusviruses Are Not Targeted but Trigger Post-Transcriptional Gene Silencing against Their Helper Virus

et al. 2002

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Post-transcriptional gene silencing (PTGS) is INTRODUCTIONPost-transcriptional gene silencing (PTGS), first identified in plants, is now thought to be an ancient self-defense mechanism acting against molecular parasites (Waterhouse et al., 2001). Introduction of double-stranded RNA (dsRNA) into plant cells triggers PTGS, resulting in the degradation of dsRNA and cognate mRNAs (Schweizer et al., 2000). A similar mechanism appears to operate in a wide variety of organisms, including filamentous fungi, nematodes, Drosophila , mice, and cultured HeLa cells, and generally is referred to as RNA interference (RNAi) (Cogoni and Macino, 1999a;Fire, 1999;Grant, 1999;Sharp and Zamore, 2000;Elbashir et al., 2001a;Svoboda et al., 2000). Recently, homologous genes required for PTGS were identified from different organisms, demonstrating the conservation of the gene-silencing machinery Macino, 1999a, 1999b;Ketting et al., 1999;Tabara et al., 1999;Catalanotto et al., 2000;Dalmay et al., 2000Dalmay et al., , 2001Domeier et al., 2000;Fagard et al., 2000;Mourrain et al., 2000;Smardon et al., 2000;Wu-Scharf et al., 2000). The accumulation of 21-to 25-nucleotide RNAs corresponding to both sense and antisense strands of target RNA occurs during PTGS in plant and animal cells (Hamilton and Baulcombe, 1999;Hammond et al., 2000;Parrish et al., 2000). These 21-to 25-nucleotide RNAs are generated by an RNase III-like enzyme (DICER) as the initiation step of RNAi, providing the specificity of a second RNase complex (RISC) that targets the cognate single-stranded (ss) RNAs (Bernstein et al., 2001).In plants, PTGS has evolved as an antiviral system. PTGS is triggered efficiently by dsRNA intermediates of cytoplasmically replicating viruses. The RNA genome of the invading virus is targeted and eliminated specifically when this natural antiviral mechanism is activated (Waterhouse et al., 1998(Waterhouse et al., , 1999Baulcombe, 1999;Smith et al., 2000;. In higher plants, PTGS is not limited to the cells in which it is activated, because mobile signals produced by PTGS can spread and confer sequence-specific RNA degradation in distant tissues (Palauqui et al., 1997;Voinnet and Baulcombe, 1997).Consistent with the importance of PTGS as an antiviral response, many viruses encode gene-silencing suppressor proteins (Anandalakshmi et al., 1998;Beclin et al., 1998;Brigneti et al., 1998;Kasschau and Carrington, 1998;Voinnet et al., 1999Voinnet et al., , 2000. However, not all viruses are able to suppress PTGS, and some virus-infected plants recover after the development of the first systemic viral symptoms (e.g., 1 These authors contributed equally to this work. 2 To whom correspondence should be addressed. E-mail burgyan@ abc.hu; fax 36-28-430-416. Article, publication date, and citation information can be found at www.plantcell.org/cgi/doi/10.1105/tpc.010366. 360The Plant Cell nepovirus-infected tobacco plants; Ratcliff et al., 1997). Upper leaves of recovered plants lack symptoms (or show attenuated symptoms), and the virus content in these leav...

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Virus resistance and gene silencing: killing the messenger

Cited by 98 publications

References 41 publications

Replicase mediated resistance against Potato Leafroll Virus in potato Desirée plants

Replicase mediated resistance against Potato Leafroll Virus in potato Desirée plants

Replicating satellite RNA induces sequence-specific DNA methylation and truncated transcripts in plants

Short Defective Interfering RNAs of Tombusviruses Are Not Targeted but Trigger Post-Transcriptional Gene Silencing against Their Helper Virus

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