Role of RNA Silencing in Plants

I want to know exatly How the process of RNA silencing is used by the
plants against the invading viruses? What all proteins and genes
regulate the activity of RNA silencing.

Does mutations in the gene sequences result in inhibition of the
activity and make the plant more suceptible to various kinds of plant
viruses?

How does the knowledge of RNA Silencing in plants help us in
develpoing new viral resistant varities ?

In article <[Only registered users see links. ]> ,
[Only registered users see links. ] [Raghavendra] wrote...

Don't know anything about the subject, but for whatever it's
worth, here's some results of a quick Biological Abstracts
database search [for "RNA silencing" and "plants" and "virus"].
Hope it's relevant [recent research often seems to concern how
successful viruses can turn off a plant's RNA-silencing defense].

Title: The capacity of transgenic tobacco to send a systemic RNA
silencing signal depends on the nature of the inducing transgene locus.
Author, Editor, Inventor: Mallory-Allison-C; Mlotshwa-Sizolwenkosi;
Bowman-Lewis-H; Vance-Vicki-B {a}
Source: Plant-Journal. [print] July 2003 2003; 35 (1): 82-92.
Abstract: RNA silencing is a conserved eukaryotic pathway in which
double-stranded RNA (dsRNA) triggers destruction of homologous target
RNA via production of short-interfering RNA (siRNA). In plants, at
least some cases of RNA silencing can spread systemically. The signal
responsible for systemic spread is expected to include an RNA component
to account for the sequence specificity of the process, and transient
silencing assays have shown that the capacity for systemic silencing
correlates with the accumulation of a particular class of small RNA.
Here, we report the results of grafting experiments to study
transmission of silencing from stably transformed tobacco lines in the
presence or absence of helper component-proteinase (HC-Pro), a viral
suppressor of silencing. The studied lines carry either a tail-to-tail
inverted repeat, the T4-IR transgene locus, or one of two different
amplicon transgene loci encoding replication-competent viral RNA. We
find that the T4-IR locus, like many sense-transgene-silenced loci, can
send a systemic silencing signal, and this ability is not detectably
altered by HC-Pro. Paradoxically, neither amplicon locus effectively
triggers systemic silencing except when suppressed for silencing by
HC-Pro. In contrast to results from transient assays, these grafting
experiments reveal no consistent correlation between capacity for
systemic silencing and accumulation of any particular class of small
RNA. In addition, although all transgenic lines used to transmit
systemic silencing signals were methylated at specific sites within
the transgene locus, silencing in grafted scions occurred without
detectable methylation at those sites in the target locus of the scion.

Title: Suppressor of RNA silencing encoded by Beet yellows virus.
Author, Editor, Inventor: Reed-Jonathan-C; Kasschau-Kristin-D;
Prokhnevsky-Alexey-I; Gopinath-Kodetham; Pogue-Gregory-P;
Carrington-James-C; Dolja-Valerian-V {a}
Source: Virology-. [print] February 15 2003 2003; 306 (2): 203-209.
Abstract: Using an Agrobacterium-mediated transient assay, we screened
the 15.5-kb genome of the Beet yellows virus for proteins with RNA
silencing suppressor activity. Among eight proteins tested, only a
21-kDa protein (p21) was able to suppress double-stranded (ds)
RNA-induced silencing of the green fluorescent protein (GFP) mRNA.
Restoration of GFP expression by p21 under these conditions had no
apparent effect on accumulation of the small interfering RNAs. In
addition, p21 elevated the transient expression level of the GFP mRNA
in the absence of dsRNA inducer. Similar activities were detected using
homologs of p21 encoded by other members of the genus Closterovirus.
Computer analysis indicated that p21-like proteins constitute a novel
protein family that is unrelated to other recognized suppressors of
RNA silencing. Examination of the subcellular distribution in
BYV-infected plants revealed that p21 is partitioned between soluble
cytoplasmic form and proteinaceous inclusion bodies at the cell
periphery.

Title: Turnip crinkle virus coat protein mediates suppression of RNA
silencing in Nicotiana benthamiana.
Author, Editor, Inventor: Thomas-Carole-L; Leh-V; Lederer-Carsten;
Maule-Andrew-J {a}
Source: Virology-. [print] February 1 2003 2003; 306 (1): 33-41.
Abstract: All of the protein products of Turnip crinkle virus (TCV;
Tombusviridae, Carmovirus) were tested for their ability to suppress
RNA silencing of a reporter gene after transient expression in
Agrobacterium-infiltrated Nicotiana benthamiana leaves. Only the capsid
protein, P38, showed suppression activity, although this was not
obvious when P38 was expressed as part of a TCV infection of the same
tissues. When P38 was expressed from a PVX vector, symptoms with
enhanced severity that correlated with increased PVX RNA accumulation
were observed. This contradiction between ectopic expression of P38 and
TCV infection could be accounted for if the active determinant of
suppressor activity within P38 was sequestered within the capsid
protein structure. The N-terminal 25 amino acids were shown to be
important for this activity. This region forms part of the unexposed
R-domain that interacts with the RNA within the virus particle. This
observation throws light on some of the complex biology exhibited by
TCV.

Title: RNA target sequences promote spreading of RNA silencing.
Author, Editor, Inventor: Van-Houdt-Helena; Bleys-Annick; Depicker-Anna
Source: Plant-Physiology-Rockville. [print] January 2003 2003; 131 (1):
245-253.
Abstract: It is generally recognized that a silencing-inducing locus
can efficiently reduce the expression of genes that give rise to
transcripts partially homologous to those produced by the silencing-
inducing locus (primary targets). Interestingly, the expression of
genes that produce transcripts without homology to the silencing-
inducing locus (secondary targets) can also be decreased dramatically
via transitive RNA silencing. This phenomenon requires primary target
RNAs that contain sequences homologous to secondary target RNAs.
Sequences upstream from the region homologous to the silencing inducer
in the primary target transcripts give rise to approximately
22-nucleotide small RNAs, coinciding with the region homologous to the
secondary target. The presence of these small RNAs corresponds with
reduced expression of the secondary target whose transcripts are not
homologous to the silencing inducer. The data suggest that in transgenic
plants, targets of RNA silencing are involved in the expansion of the
pool of functional small interfering RNAs. Furthermore, methylation of
target genes in sequences without homology to the initial silencing
inducer indicates not only that RNA silencing can expand across target
RNAs but also that methylation can spread along target genes.

Title: P1/HC-Pro, a viral suppressor of RNA silencing, interferes with
Arabidopsis development and miRNA function.
Author, Editor, Inventor: Kasschau-Kristin-D; Xie-Zhixin; Allen-Edwards;
Llave-Cesar; Chapman-Elisabeth-J; Krizan-Kate-A; Carrington-James-C {a}
Source: Developmental-Cell. [print] February 2003 2003; 4 (2): 205-217.
Abstract: The molecular basis for virus-induced disease in plants has
been a long-standing mystery. Infection of Arabidopsis by Turnip mosaic
virus (TuMV) induces a number of developmental defects in vegetative
and reproductive organs. We found that these defects, many of which
resemble those in miRNA-deficient dicerlike1 (dcl1) mutants, were due
to the TuMV-encoded RNA-silencing suppressor, P1/HC-Pro. Suppression of
RNA silencing is a counterdefensive mechanism that enables systemic
infection by TuMV.The suppressor interfered with the activity of miR171
(also known as miRNA39), which directs cleavage of several mRNAs coding
for Scarecrow-like transcription factors, by inhibiting miR171-guided
nucleolytic function. Out of ten other mRNAs that were validated as
miRNA-guided cleavage targets, eight accumulated to elevated levels in
the presence of P1/HC-Pro. The basis for TuMV- and other virus-induced
disease in plants may be explained, at least partly, by interference
with miRNA-controlled developmental pathways that share components with
the antiviral RNA-silencing pathway.

Title: Low temperature inhibits RNA silencing-mediated defence by the
control of siRNA generation.
Author, Editor, Inventor: Szittya-Gyorgy; Silhavy-Daniel; Molnar-Attila;
Havelda-Zoltan; Lovas-Agnes; Lakatos-Lorant; Banfalvi-Zsofia;
Burgyan-Jozsef {a}
Source: EMBO-European-Molecular-Biology-Organization-Journal. [print]
February 3 2003 2003; 22 (3): 633-640.
Abstract: Temperature dramatically affects plant-virus interactions.
Outbreaks of virus diseases are frequently associated with low
temperature, while at high temperature viral symptoms are often
attenuated (heat masking) and plants rapidly recover from virus
diseases. However, the underlying mechanisms of these well-known
observations are not yet understood. RNA silencing is a conserved
defence system of eukaryotic cells, which operates against molecular
parasites including viruses and transgenes. Here we show that at low
temperature both virus and transgene triggered RNA silencing are
inhibited. Therefore, in cold, plants become more susceptible to
viruses, and RNA silencing-based phenotypes of transgenic plants are
lost. Consistently, the levels of virus- and transgene-derived small
(21-26 nucleotide) interfering (si) RNAs-the central molecules of RNA
silencing-mediated defence pathways-are dramatically reduced at low
temperature. In contrast, RNA silencing was activated and the amount
of siRNAs gradually increased with rising temperature. However,
temperature does not influence the accumulation of micro (mi) RNAs,
which play a role in developmental regulation, suggesting that the
two classes of small (si and mi) RNAs are generated by different
nuclease complexes.

Title: Wyciszanie RNA; naturalny system obronny roslin przeciw infekcji
wirusowej. [RNA silencing as a plant innate system against viral
infection.]
Author, Editor, Inventor: Lehmann-Przemyslaw {a}
Source: Postepy-Biologii-Komorki. [print] 2003; 30 (1): 75-86.
Language: Polish; Non-English
Abstract: RNA silencing is a newly discovered mechanism of gene
regulation and defence against viruses. The mechanism is based on
sequence-specific targeting and degradation of RNA. It appears to
be directed by double-stranded RNA, associated with the production of
short 21 to 25 nt RNAs, and spread through the plant by a mobile
signal. It is not know what is the signal. Many of plant viruses
encode suppressors of RNA silencing, which inhibits of an antiviral
defence system in plants. RNA silencing is conceptually similar to
classical humoral immunity.

Title: RNA-mediated RNA degradation in transgene- and virus-induced
gene silencing.
Author, Editor, Inventor: Metzlaff-Michael {a}
Source: Biological-Chemistry. [print] October 2002 2002; 383 (10):
1483-1489.
Abstract: In the 'RNA world' hypothesis it is postulated that RNA was
the first genetic molecule. Recent discoveries in gene silencing
research on plants, fungi and animals show that RNA indeed plays a
key role not only in controlling invading nucleic acids, like viruses
and transposable elements, but also in regulating the expression of
transgenes and endogenous genes. Double-stranded RNAs were identified
to be the triggering structures for the induction of a specific and
highly efficient RNA silencing system, in which enzyme complexes, like
Dicer and RISC, facilitate as 'molecular machines' the processing of
dsRNA into characteristic small RNA species. RNA silencing can be
transmitted rapidly from silenced to non-silenced cells by short and
long distance signaling. There is evidence that at least one component
of the signal is a specific, degradation-resistant RNA.

Title: Negative-strand tospoviruses and tenuiviruses carry a gene for
a suppressor of gene silencing at analogous genomic positions.
Author, Editor, Inventor: Bucher-Etienne; Sijen-Titia; de-Haan-Peter;
Goldbach-Rob; Prins-Marcel {a}
Source: Journal-of-Virology. [print] January 2003 2003; 77 (2):
1329-1336.
Abstract: Posttranscriptional silencing of a green fluorescent protein
(GFP) transgene in Nicotiana benthamiana plants was suppressed when
these plants were infected with Tomato spotted wilt virus (TSWV), a
plant-infecting member of the Bunyaviridae. Infection with TSWV resulted
in complete reactivation of GFP expression, similar to the case for
Potato virus Y, but distinct from that for Cucumber mosaic virus, two
viruses known to carry genes encoding silencing suppressor proteins.
Agrobacterium-based leaf injections with individual TSWV genes
identified the NSs gene to be responsible for the RNA silencing-
suppressing activity displayed by this virus. The absence of short
interfering RNAs in NSs-expressing leaf sectors suggests that the
tospoviral NSs protein interferes with the intrinsic RNA silencing
present in plants. Suppression of RNA silencing was also observed when
the NS3 protein of the Rice hoja blanca tenuivirus, a nonenveloped
negative-strand virus, was expressed. These results indicate that plant-
infecting negative-strand RNA viruses carry a gene for a suppressor of
RNA silencing.

Title: RNA interference: Listening to the sound of silence.
Author, Editor, Inventor: Zamore-Phillip-D {a}
Source: Nature-Structural-Biology. [print] September 2001 2001; 8 (9):
746-750.
Abstract: The term RNA interference (RNAi) describes the use of
double-stranded RNA to target specific mRNAs for degradation, thereby
silencing their expression. RNAi is one manifestation of a broad class
of RNA silencing phenomena that are found in plants, animals and fungi.
The discovery of RNAi has changed our understanding of how cells guard
their genomes, led to the development of new strategies for blocking
gene function, and may yet yield RNA-based drugs to treat human disease.

Title: The coat protein of turnip crinkle virus suppresses
posttranscriptional gene silencing at an early initiation step.
Author, Editor, Inventor: Qu-Feng; Ren-Tao; Morris-T-Jack {a}
Source: Journal-of-Virology. [print] January 2003 2003; 77 (1):511-522.
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 i
nterfering 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.

Title: Long-distance movement, virulence, and RNA silencing suppression
controlled by a single protein in hordei- and potyviruses:
Complementary functions between virus families.
Author, Editor, Inventor: Yelina-Natalia-E; Savenkov-Eugene-I;
Solovyev-Andrey-G; Morozov-Sergey-Y; Valkonen-Jari-P-T {a}
Source: Journal-of-Virology. [print] December 2002 2002; 76 (24):
12981-12991.
Abstract: RNA silencing is a natural defense mechanism against genetic
stress factors, including viruses. A mutant hordeivirus (Barley stripe
mosaic virus (BSMV)) lacking the gammab gene was confined to
inoculated leaves in Nicotiana benthamiana, but systemic infection was
observed in transgenic N. benthamiana expressing the potyviral
silencing suppressor protein HCpro, suggesting that the gammab protein
may be a long-distance movement factor and have antisilencing
activity. This was shown for gammab proteins of both BSMV and Poa
semilatent virus (PSLV), a related hordeivirus. Besides the functions
in RNA silencing suppression, gammab and HCpro had analogous effects
on symptoms induced by the hordeiviruses. Severe BSMV-induced symptoms
were correlated with high HCpro concentrations in the HCpro-transgenic
plants, and substitution of the gammab cistron of BSMV with that of
PSLV led to greatly increased symptom severity and an altered pattern
of viral gene expression. The efficient systemic infection with the
chimera was followed by the development of dark green islands
(localized recovery from infection) in leaves and exemption of new
developing leaves from infection. Recovery and the accumulation of
short RNAs diagnostic of RNA silencing in the recovered tissues in
wild-type N. benthamiana were suppressed in HCpro-transgenic plants.
These results provide evidence that potyviral HCpro and hordeivirus
gammab proteins contribute to systemic viral infection, symptom
severity, and RNA silencing suppression. HCpro's ability to suppress
the recovery of plants from viral infection emphasizes recovery as a
manifestation of RNA silencing.

Title: Identification of a novel RNA silencing suppressor, NSs protein
of Tomato spotted wilt virus.
Author, Editor, Inventor: Takeda-Atsushi; Sugiyama-Kazuhiko;
Nagano-Hideaki; Mori-Masashi; Kaido-Masanori; Mise-Kazuyuki {a};
Tsuda-Shinya; Okuno-Tetsuro
Source: FEBS-Letters. [print] 4 December 2002 2002; 532 (1-2): 75-79.
Publication Year: 2002
Abstract: RNA silencing or post-transcriptional gene silencing (PTGS)
in plants is known as a defense system against virus infection. Several
plant viruses have been shown to encode an RNA silencing suppressor.
Using a green fluorescent protein-based transient suppression assay, we
show that NSs protein of Tomato spotted wilt virus (TSWV) has RNA
silencing suppressor activity. TSWV NSs protein suppressed sense
transgene-induced PTGS but did not suppress inverted repeat
transgene-induced PTGS. TSWV NSs protein is the first RNA silencing
suppressor identified in negative-strand RNA viruses.

Title: Silencing of a viral RNA silencing suppressor in transgenic
plants.
Author, Editor, Inventor: Savenkov-Eugene-I {a}; Valkonen-Jari-P-T
Source: Journal-of-General-Virology. [print] September, 2002; 83 (9):
2325-2335.
Abstract: High expression levels of the helper component proteinase
(HCpro), a known virus suppressor of RNA silencing, were attained in
Nicotiana benthamiana transformed with the HCpro cistron of Potato
virus A (PVA, genus Potyvirus). No spontaneous silencing of the HCpro
transgene was observed, in contrast to the PVA coat protein (CP)-
encoding transgene in other transgenic lines. HCpro-transgenic plants
were initially susceptible to PVA and were systemically infected by 14
days post-inoculation (p.i.) but, 1 to 2 weeks later, the new expanding
leaves at positions +6 and +7 above the inoculated leaf showed a
peculiar recovery phenotype. Leaf tips (the oldest part of the leaf)
were chlorotic and contained high titres of PVA, whereas the rest of
the leaf was symptomless and contained greatly reduced or non-
detectable levels of viral RNA, CP and transgene mRNA. The spatial
recovery phenotype suggests that RNA silencing is initiated in close
proximity to meristematic tissues. Leaves at position +8 and higher
were symptomless and virus-free but not completely resistant to
mechanical inoculation with PVA. However, they were not infected with
the virus systemically transported from the lower infected leaves,
suggesting a vascular tissue-based resistance mechanism. Recovery of
the HCpro-transgenic plants from infection with different PVA isolates
was dependent on the level of sequence homology with the transgene.
Methylation of the HCpro transgene followed recovery. These data show
that the transgene mRNA for a silencing suppressor can be silenced
by a presumably 'strong' silencing inducer (replicating homologous
virus).

Title: Viral suppression of systemic silencing.
Author, Editor, Inventor: Baulcombe-David {a}
Source: Trends-in-Microbiology. [print] July, 2002; 10 (7): 306-308.
Abstract: RNA silencing in plants is a form of antiviral defense that
was originally discovered from the anomalous effects of transgenes.
The process is associated with a systemic signal, presumed to be RNA,
and is suppressed by plant virus-encoded proteins. One of these
proteins, the 2b protein of cucumber mosaic virus, prevents systemic
spread of the signal molecule but, curiously, is located in the nucleus
of infected cells. The antiviral role of silencing might also apply in
animals because a suppressor of silencing encoded by an insect virus
was identified recently.

Title: A viral protein suppresses RNA silencing and binds silencing-
generated, 21- to 25-nucleotide double-stranded RNAs.
Author, Editor, Inventor: Silhavy-Daniel {a}; Molnar-Attila;
Lucioli-Alessandra; Szittya-Gyorgy; Hornyik-Csaba; Tavazza-Mario;
Burgyan-Jozsef
Source: EMBO-European-Molecular-Biology-Organization-Journal. [print]
June 17, 2002; 21 (12): 3070-3080.
Abstract: Posttranscriptional gene silencing (PTGS) processes double-
stranded (ds) RNAs into 21-25 nucleotide (nt) RNA fragments that direct
ribonucleases to target cognate mRNAs. In higher plants, PTGS also
generates mobile signals conferring sequence-specific silencing in
distant organs. Since PTGS acts as an antiviral system in plants,
successful virus infection requires evasion or suppression of gene
silencing. Here we report that the 19 kDa protein (p19) of
tombusviruses is a potent silencing suppressor that prevents the spread
of mobile silencing signal. In vitro, p19 binds PTGS-generated, 21-25
nt dsRNAs and 21-nt synthetic dsRNAs with 2-nt 3' overhanging end(s),
while it barely interacts with single-stranded (ss) RNAs, long dsRNAs
or blunt-ended 21-nt dsRNAs. We propose that p19 mediates silencing
suppression by sequestering the PTGS-generated 21-25 nt dsRNAs, thus
depleting the specificity determinants of PTGS effector complexes.
Moreover, the observation that p19-expressing transgenic plants show
altered leaf morphology might indicate that the p19-targeted PTGS
pathway is also important in the regulation of plant development.

Title: Barley stripe mosaic virus-induced gene silencing in a monocot
plant.
Author, Editor, Inventor: Holzberg-Steve; Brosio-Paul; Gross-Cynthia;
Pogue-Gregory-P {a}
Source: Plant-Journal. [print] May, 2002; 30 (3): 315-327.
Abstract: RNA silencing of endogenous plant genes can be achieved by
virus-mediated, transient expression of homologous gene fragments.
This powerful, reverse genetic approach, known as virus-induced gene
silencing (VIGS), has been demonstrated only in dicot plant species,
where it has become an important tool for functional genomics. Barley
stripe mosaic virus (BSMV) is a tripartite, positive-sense RNA virus
that infects many agriculturally important monocot species including
barley, oats, wheat and maize. To demonstrate VIGS in a monocot host,
we modified BSMV to express untranslatable foreign inserts downstream
of the gammab gene,in either sense or antisense orientations. Phytoene
desaturase (PDS) is required for synthesizing carotenoids, compounds
that protect chlorophyll from photo-bleaching. A partial PDS cDNA
amplified from barley was 90, 88 and 74% identical to PDS cDNAs from
rice, maize and Nicotiana benthamiana, respectively. Barley infected
with BSMV expressing barley, rice or maize PDS fragments became photo-
bleached and accumulated phytoene (the substrate for PDS) in a manner
similar to plants treated with the chemical inhibitor of PDS,
norflurazon. In contrast, barley infected with wild-type BSMV, or
BSMV expressing either N.benthamiana PDS or antisense green fluorescent
protein (GFP), did not photo-bleach or accumulate phytoene. Thus BSMV
silencing of the endogenous PDS was homology-dependent. Deletion of the
coat protein enhanced the ability of BSMV to silence PDS. This is the
first demonstration of VIGS in a monocot, and suggests that BSMV can
be used for functional genomics and studies of RNA-silencing mechanisms
in monocot plant species.

Title: Post-transcriptional gene silencing in plants.
Author, Editor, Inventor: Vaucheret-Herve {a}; Beclin-Christophe;
Fagard-Mathilde
Source: Journal-of-Cell-Science. [print] September, 2001; 114 (17):
3083-3091.
Abstract: Post-transcriptional gene silencing (PTGS) in plants is an
RNA-degradation mechanism that shows similarities to RNA interference
(RNAi) in animals. Indeed, both involve double-stranded RNA (dsRNA),
spread within the organism from a localised initiating area, correlate
with the accumulation of small interfering RNA (siRNA) and require
putative RNA-dependent RNA polymerases, RNA helicases and proteins of
unknown functions containing PAZ and Piwi domains. However, some
differences are evident. First, PTGS in plants requires at least two
genes - SGS3 (which encodes a protein of unknown function containing
a coil-coiled domain) and MET1 (which encodes a DNA-methyltransferase)
- that are absent in C. elegans and thus are not required for RNAi.
Second, all Arabidopsis mutants that exhibit impaired PTGS are
hypersusceptible to infection by the cucumovirus CMV, indicating that
PTGS participates in a mechanism for plant resistance to viruses.
Interestingly, many viruses have developed strategies to counteract
PTGS and successfully infect plants - for example, by potentiating
endogenous suppressors of PTGS. Whether viruses can counteract RNAi
in animals and whether endogenoussuppressors of RNAi exist in animals
is still unknown.

Title: RNA silencing as a plant immune system against viruses.
Author, Editor, Inventor: Voinnet-Olivier {a}
Source: Trends-in-Genetics. [print] August, 2001; 17 (8): 449-459.
Abstract: 'RNA silencing' refers to related processes of post-
trancriptional control of gene expression found in plants, animals and
fungi. A unifying feature of RNA silencing is that it mediates
sequence-specific degradation of target transcripts, recruiting RNA
molecules of 21-23 nucleotides as specificity determinants. In higher
plants, RNA silencing serves as an adaptive, antiviral defence system,
which is transmitted systemically in response to localized virus
challenge. Plant viruses have elaborated a variety of counter-defensive
measures to overcome the host silencing response. One of these
strategies is to produce proteins that target the cell autonomous or
signalling steps of RNA silencing. It is not known whether a similar
antiviral mechanism also operates in animal cells.

Title: RNA silencing in plants: Defense and counterdefense.
Author, Editor, Inventor: Vance-Vicki {a}; Vaucheret-Herve
Source: Science-Washington-D-C. [print] 22 June, 2001; 292 (5525):
2277-2280.
Abstract: RNA silencing is a remarkable type of gene regulation based
on sequence-specific targeting and degradation of RNA. The term
encompasses related pathways found in a broad range of eukaryotic
organisms, including fungi, plants, and animals. In plants, it serves
as an antiviral defense, and many plant viruses encode suppressors of
silencing. The emerging view is that RNA silencing is part of a
sophisticated network of interconnected pathways for cellular defense,
RNA surveillance, and development and that it may become a powerful
tool to manipulate gene expression experimentally.

Title: Activation and suppression of RNA silencing by plant viruses.
Author, Editor, Inventor: Carrington-James-C {a}; Kasschau-Kristin-D;
Johansen-Lisa-K
Source: Virology-. [print] March 1, 2001; 281 (1): 1-5.

Title: A model for RNA-mediated gene silencing in higher plants.
Author, Editor, Inventor: Wassenegger-Michael; Pelissier-Thiery
Source: Plant-Molecular-Biology. May, 1998; 37 (2) 349-362.
Abstract: Homology-dependent gene silencing (HdGS) which is the generic
term for transcriptional gene silencing (TGS), post-transcriptional
gene silencing (PTGS) and RNA-mediated virus-resistance (RmVR) has been
shown to frequently occur in transgenic plants. The role of RNA as a
target and initiator of PTGS and RmVR is more and more manifested.
Because TGS is assumed to be induced by a DNA-DNA interaction-mediated
promoter methylation, a possible involvement of RNA in TGS was not
really considered up to now. In this review we attempt to demonstrate
that all three types of HdGS could be triggered by one RNA-based
mechanism. A model proposing TGS as a consequence of RNA-directed DNA
methylation (RdDM) and a refined mRNA threshold mechanism are presented.
In contrast to the view that high amounts of mRNA are required we
assume that the concentration of RNAs that can serve as efficient
templates for a plant-encoded RNA-directed RNA polymerase (RdRP) plays
a key role in HdGS and possibly also in natural gene regulation of
non-transformed cells. According to this idea a particular information
must be encoded to render mRNA turn-over products a suitable RdRP
substrate. It will be discussed that such a mechanism could account
for the silencing phenomena of poorly transcribed transgenes. Finally,
an explanation for the coherency between PTGS and DNA methylation
is documented.

cheers

If this is a school or uni question you should have access to bids/web
of science/ science direct and be able to find the current articles if
not try scirus.

if memory serves the current hypothesis is that plants are able to take
advantage of the fact that a lot of plant viral pathogens have a double
stranded RNA genome.
The double stranded RNA is cut up in to ~23bp bits by a DICER (?)
enzyme, these bits are used to prime binding of another RNAse so and
single stranded RNA is also rendered untranslatable.

This silencing ability is able to spread from the site of initial
activation thus protecting the new plant growth (i don't remember if it
spreads to existing tissue).

look up: PTGS - post transcription gene silencing, siRNA short
interfering RNAs

i've just found a useful article - Waterhouse et al TRENDS in plant
science vol 6 no 7 2001 p297


depends on the plant and it's uses. in theory you could have a varetiy
of conserved viral sequences constitutively expressed as hair pins (will
make a double stranded RNA on their own) so the virus can't get a 'foot
hold' and do damage with infection. however this would cost the plant.
If you happen to be a faceless multinational who wants to generate some
transgenic monoclonal crop plant then some version of this would
probably be what your looking for as it would be easy to make (depend on
transformation efficiency of the plant of course). there would be more
elegant methods - inducible systems linked to a transcriptional
activator (gal4 ?) and kicking out a variety of hairpins then shutting
down when not in use. although being a thing of beauty such system would
probably never get funding because it would take at least twice as long
to make then you should do lengthy trails as any transgene could affect
the metabolic profile of the plant in an unpredictable way.
grrr.
ops. time for me to have a little sit down.

craig