ライフサイエンスコーパス: PTGS

1 PTGS could be initiated in both nrpd1a and nrpd1b mutant

2 PTGS in this system was associated with both small RNA m

3 quired for high levels of transcription in a PTGS-independent manner.

4 ame genes were also required for spread of a PTGS silencing signal out of the veins of Arabidopsis [7

5 Our observations further support a PTGS mechanism for meiotic silencing and offer insight i

6 These results suggest that HC-Pro targets a PTGS maintenance (as opposed to an initiation or signali

7 o enter cytoplasmic siRNA bodies to activate PTGS.

8 n small RNA production and (ii) do not alter PTGS triggered by inverted-repeat transgenes directly pr

9 Although PTGS has proven effective against a variety of target ge

10 nes, cytokines, matrix metalloproteases, and PTGS/COX2, consistent with a core inflammatory response.

11 on transgenes under 35S or 19S promoters and PTGS on the endogenous nitrite reductase gene (Nii).

12 that SmD1 interplays with splicing, RQC, and PTGS.

13 relationship between short RNA sequences and PTGS.

14 of cassava geminiviruses in regulating anti-PTGS activity and their relation to synergism are discus

15 porting an antagonistic relationship between PTGS and TGS.

16 STZ metabolism was unaffected by PTGS deficiency.

17 ting posttranscriptional gene-silencing (cis-PTGS) pathway operated by the RNAi machinery at heteroch

18 In saddle cultivars, PTGS is spatially inhibited in the central region around

19 ic component, as a new player in cytoplasmic PTGS.

20 coat by region-specific inhibition of DCL4 (PTGS).

21 cribe a reporter system where RDR6-dependent PTGS is initiated by restricted expression of an inverte

22 ied as a specific inhibitor in two different PTGS systems, constitutive and inducible.

23 ACA-targeting miRNAs in Poaceae also direct PTGS for calmodulin-like proteins which are putative Ca(

24 n determining the efficiency of AON-directed PTGS.

25 -of-function mutants, due to miR391-directed PTGS of ACA10.

26 k of off-target gene silencing exists during PTGS in plants.

27 can to identify potential off-targets during PTGS.

28 extensive production of siRNAs and efficient PTGS of CER3.

29 onidase (GUS) transgene was shown to exhibit PTGS.

30 is not essential for but rather facilitates PTGS.

31 We propose that SmD1 facilitates PTGS by protecting transgene-derived aberrant RNAs from

32 ditis elegans and, in the case of SMG-2, for PTGS.

33 ol is useful to design better constructs for PTGS by minimizing off-target gene silencing in both pla

34 p between Dicer-like 4 (DCL4), essential for PTGS, and flavonoid aglycons, which can inhibit DCL4.

35 sequence specificity were also explored for PTGS-associated transgene methylation and for the target

36 ce with targeted disruption of the genes for PTGS and PGE receptors (PTGERs).

37 smd1b was identified in a genetic screen for PTGS deficiency, revealing the involvement of SmD1, a co

38 nts have potential off-targets when used for PTGS that could obscure experimental results.

39 silencing through a mechanism distinct from PTGS and TGS.

40 However, PTGS mediated by tobacco rattle virus (TRV) was not affe

41 This identifies PTGS as a general mechanism for eliminating highly abund

42 nvisioned for amplicons could be achieved if PTGS could be overcome and if the resulting plants did n

43 Because jmj14 mutations impair PTGS of transgenes expressed under various plant or vira

44 e taken into consideration when implementing PTGS-based strategies to control plant virus accumulatio

45 In PTGS, the transgene is transcribed but the transcripts f

46 1, a component of the Smith (Sm) complex, in PTGS.

47 ne silencing 3 (SGS3), a master component in PTGS.

48 mutations at the SDE3 locus are defective in PTGS mediated by a green fluorescent protein transgene.

49 study revealed a noncanonical role of FVE in PTGS.

50 dopsis, we find that two enzymes involved in PTGS, Dicer-like 4 and RNA-dependent RNA polymerase 6, a

51 A-dependent RNA polymerase and a nuclease in PTGS systems and the close relationship between methylat

52 onsilenced ones, indicating a direct role in PTGS.

53 hat P1/HC-Pro and 2b interfere at step(s) in PTGS that are downstream of any common components in the

54 HC-Pro inactivated PTGS in plants containing a preexisting silenced beta-gl

55 ith intrinsic direct repeats can also induce PTGS at a very high frequency (80-100%).

56 ingle-stranded DNA (ssDNA) viruses to induce PTGS in infected plants irrespective of the severity of

57 re the primary targets for ACMV-[CM]-induced PTGS, whereas the C terminus of BC1 was targeted for the

58 of PTGS referred to as direct repeat-induced PTGS (driPTGS).

59 transgene with three or four repeats induced PTGS in almost 100% of the primary transformants, regard

60 Here, three types of transgene-induced PTGS and one example of virus-induced PTGS were analyzed

61 oderately higher levels during virus-induced PTGS at higher temperatures, and there was no change in

62 However, the efficacy of virus-induced PTGS varied depending on the intrinsic features of the v

63 nduced PTGS and one example of virus-induced PTGS were analyzed in plants.

64 , but not toxic, levels of cadmium inhibited PTGS, suggesting induction of a pathway that interferes

65 Short sequences were able to initiate PTGS of an endogenous gene, phyotene desaturase, althoug

66 s may be a component of the RNA interference/PTGS machinery.

67 bition of PTGS allowed several insights into PTGS development.

68 peat transgenes directly producing dsRNA (IR-PTGS), PRP39a, and SmD1b appear to synergistically promo

69 y transgenes containing inverted repeats (IR-PTGS), and SGS2/SDE1 is dispensable for RNA VIGS.

70 migration, such as AREG, CD24, EPHB2, ITGAX, PTGS, SCT1, SERPINB2, SERPINE1, SLPI, SNAI2, and TWIST,

71 demonstrate that TCV CP suppressed the local PTGS as strongly as several previously reported virus-co

72 The amplicon-mediated PTGS mechanism can target transiently expressed RNAs tha

73 ins might significantly improve AON-mediated PTGS in vivo.

74 The current consensus is that siRNA-mediated PTGS occurs primarily in the cytoplasm where target mRNA

75 structure imposes on AON- vs. siRNA-mediated PTGS, AON- and siRNA-mediated cleavage of defined mRNA s

76 lyses revealed a hidden conservation for miR-PTGS of ACA10 homologs in spermatophytes.

77 cted posttranscriptional gene silencing (miR-PTGS) is an integral component of gene regulatory networ

78 el approach for the consistent activation of PTGS that can be used to specifically target and suppres

79 recruiting RDR6 for further amplification of PTGS, DCL2 is crucial for RDR6-dependent systemic PTGS.

80 view of the subcellular compartmentation of PTGS in plants.

81 Contrarily to PTGS-1, deficiency of PTGS-2 activity significantly amplified STZ effect, caus

82 The data suggest that the degree of PTGS signal movement correlates with the degree of PD ap

83 ransgene may act as a primary determinant of PTGS referred to as direct repeat-induced PTGS (driPTGS)

84 may represent the specificity determinant of PTGS.

85 ne sequences influenced the effectiveness of PTGS.

86 Diminished efficiency of PTGS in ski mutants compared with cer7, as evidenced by

87 showed no major changes in the expression of PTGS or RQC components or in small RNA production and (i

88 s, ego-1 mutants were resistant to a form of PTGS called RNA interference.

89 viruses act as both targets and inducers of PTGS has led to the idea that PTGS may have evolved as a

90 Induction of PTGS using RNA viruses as vectors or as transgenes provi

91 The pattern of cadmium-induced inhibition of PTGS allowed several insights into PTGS development.

92 hanism of this region-specific inhibition of PTGS remains unclear.

93 HC-Pro into these plants resulted in loss of PTGS, loss of small RNAs, and partial loss of methylatio

94 he HCPro acts by blocking the maintenance of PTGS in tissues where silencing had already been set, wh

95 Maintenance of PTGS requires RNA-dependent RNA polymerase 6 (RDR6), and

96 maintain TGS are required for maintenance of PTGS, and that RDR6 uses distinct templates in the initi

97 transitive RNA silencing and maintenance of PTGS.

98 PTGS, uncoupling between these two modes of PTGS.

99 ype and showed enhanced systemic movement of PTGS to grafted shoots.

100 unt virus (TBSV), that prevents the onset of PTGS in the infiltrated tissues and allows high level of

101 evented only systemic but not local onset of PTGS, uncoupling between these two modes of PTGS.

102 Surprisingly, we also found that reversal of PTGS and TGS by ADK inactivation depended on whether exp

103 a previously unrecognized protective role of PTGS-2-derived PGE(2) in STZ-induced diabetes mediated b

104 support a mechanism in which suppression of PTGS by PVCV causes blotched flowers.

105 because this virus may have a suppressor of PTGS (VSR).

106 proach with the use of a viral suppressor of PTGS, tobacco etch virus (TEV) helper component proteina

107 at protein, which is the viral suppressor of PTGS.

108 report identifying a cellular suppressor of PTGS.

109 acco etch virus functions as a suppressor of PTGS.

110 ses have been shown to encode suppressors of PTGS in order to survive this host defense.

111 The ability of these viral suppressors of PTGS to interfere with TGS was tested using the 271 locu

112 ndian cassava mosaic virus as suppressors of PTGS, indicating that geminiviruses evolved differently

113 rather than cytosolic mRNA as the target of PTGS.

114 t viruses are both activators and targets of PTGS, these data provide compelling evidence that PTGS r

115 Treatment of PTGS-2(-/-) and wild-type mice with PTGER2/PTGER4 agonis

116 Third, cadmium effects on PTGS closely paralleled those on the movement of tobamov

117 In plants, PTGS can be triggered locally and then spread throughout

118 l cytosines were less efficient at promoting PTGS of the transgene mRNA.

119 of an ER-associated AGO1 turnover and proper PTGS maintenance and further show how the VSR P0 manipul

120 of the mechanisms by which viruses regulate PTGS may well lead to better ways to control gene expres

121 factors play an important role in regulating PTGS efficiency in vivo.

122 RNAs mediate posttranscriptional regulation (PTGS) via mRNA cleavage [4] whereas the 24 nt sRNAs are

123 RIBONUCLEASE2 (XRN2), XRN3, and XRN4 restore PTGS in smd1b, indicating that SmD1 is not essential for

124 Both P1/HC-Pro and 2b reversed PTGS of Nii genes in 271-containing tobacco plants, but

125 es, suggesting nonredundant roles in the RQC/PTGS interplay.

126 tions appear distinct in both splicing and S-PTGS.

127 reactivates various transgenes silenced by S-PTGS and shows reduced Histone3 Lysine9 Lysine14 acetyla

128 to-5' RNA degradation generally counteract S-PTGS, likely by reducing the amount of transgene aberran

129 lenced transgenes into S-PTGS and enhanced S-PTGS on partially silenced transgenes, indicating that c

130 rocessing factor 39)a also plays a role in S-PTGS in Arabidopsis thaliana.

131 into double-stranded RNA (dsRNA) initiates S-PTGS.

132 d the entry of nonsilenced transgenes into S-PTGS and enhanced S-PTGS on partially silenced transgene

133 e mutant exhibited enhanced suppression of S-PTGS compared to the single mutants.

134 levels, thus preventing the triggering of S-PTGS.

135 sated AGO1 partial deficiency and restored S-PTGS with 100% efficiency.

136 e-mediated post-transcriptional silencing (S-PTGS).

137 nsgene posttranscriptional gene silencing (S-PTGS).

138 ansgene aberrant RNAs that are used by the S-PTGS pathway to build up small interfering RNAs that gui

139 voke the entry of endogenous mRNA into the S-PTGS pathway, suggest poor RNA quality upon the transcri

140 rovoke the entry of transgene RNA into the S-PTGS pathway, whereas simultaneous impairment of both pa

141 synergistically promote a step specific to S-PTGS.

142 scriptional silencing of sense transgenes (S-PTGS [post-transcriptional genesilencing]).

143 ncing (PTGS) mediated by sense transgenes (S-PTGS) results in RNA degradation and DNA methylation of

144 s of transcription are required to trigger S-PTGS.

145 pression of transgenes that do not trigger S-PTGS.

146 ver, expression of transgenes that undergo S-PTGS in a wild-type background is reduced in jmj14 sgs3

147 iptional and transcriptional gene silencing (PTGS and TGS, respectively) participate in defense again

148 rease in posttranscriptional gene silencing (PTGS) activity.

149 promote post-transcriptional gene silencing (PTGS) and transgene methylation.

150 cluding post-transcriptional gene silencing (PTGS) and/or rapid turnover of the transgenic proteins.

151 ) effect posttranscriptional gene silencing (PTGS) by hybridizing to an mRNA and then directing its c

152 GS) and post-transcriptional gene silencing (PTGS) can be self-reinforcing, and this allows maintenan

153 whereas posttranscriptional gene silencing (PTGS) eliminates both aberrant and functional RNAs throu

154 ation of posttranscriptional gene silencing (PTGS) for gene function study in both plants and animals

155 tivates post-transcriptional gene silencing (PTGS) in every plant.

156 Posttranscriptional gene silencing (PTGS) in plants inactivates some aberrant or highly expr

157 Posttranscriptional gene silencing (PTGS) in plants is a natural defense mechanism against v

158 nal and post-transcriptional gene silencing (PTGS) in plants, aiming at highlighting new modes of act

159 some and posttranscriptional gene silencing (PTGS) in regulating CER3 transcript levels, we investiga

160 ated to post-transcriptional gene silencing (PTGS) in transgenic plants.

161 Post-transcriptional gene silencing (PTGS) is a fundamental regulatory mechanism operating in

162 ow that post-transcriptional gene silencing (PTGS) is a major cause for this lack of efficiency.

163 Posttranscriptional gene silencing (PTGS) is a nucleotide sequence-specific defense mechanis

164 Posttranscriptional gene silencing (PTGS) is a regulatory mechanism to suppress undesired tr

165 Post-transcriptional gene silencing (PTGS) is a sequence-specific RNA degradation mechanism t

166 Post-transcriptional gene silencing (PTGS) is a sequence-specific RNA degradation process con

167 Posttranscriptional gene silencing (PTGS) is an ancient eukaryotic regulatory mechanism in w

168 Post-transcriptional gene silencing (PTGS) is an important mechanism for regulation of plant

169 plants, post-transcriptional gene silencing (PTGS) is mediated by DICER-LIKE 1 (DCL1)-dependent micro

170 izes the posttranscriptional gene silencing (PTGS) machinery of plants to restrain viral infections s

171 to be a post-transcriptional gene silencing (PTGS) mechanism.

172 Posttranscriptional gene silencing (PTGS) mediated by sense transgenes (S-PTGS) results in R

173 Posttranscriptional gene silencing (PTGS) mediated by siRNAs is an evolutionarily conserved

174 Post-transcriptional gene silencing (PTGS) of a green fluorescent protein (GFP) transgene is

175 o elicit posttranscriptional gene silencing (PTGS) of iaaM and ipt.

176 used by post-transcriptional gene silencing (PTGS) of the key enzyme of anthocyanin biosynthesis.

177 Posttranscriptional gene silencing (PTGS) of transgenes involves abundant 21-nucleotide smal

178 Post-transcriptional gene silencing (PTGS) provides protection in plants against virus infect

179 ssor of post-transcriptional gene silencing (PTGS) with a PVX amplicon carrying a gene encoding L1, a

180 In posttranscriptional gene silencing (PTGS), "quelling," and RNA interference (RNAi), 21-25 nu

181 rgets of posttranscriptional gene silencing (PTGS), a natural defense mechanism in plants.

182 ssors of posttranscriptional gene silencing (PTGS), an adaptive antiviral defense response that limit

183 rkers of posttranscriptional gene silencing (PTGS), are powerful tools that interfere with gene expre

184 inhibit post-transcriptional gene silencing (PTGS), but with little or no effect on miRNA functions.

185 Posttranscriptional gene silencing (PTGS), or RNA silencing, is a sequence-specific RNA degr

186 trigger post-transcriptional gene silencing (PTGS), presumably via a double stranded RNA induced by c

187 induce post-transcriptional gene silencing (PTGS), the TRV2 genome is genetically modified to carry

188 ays for post-transcriptional gene silencing (PTGS), whereas AGO4 regulates transcriptional gene silen

189 ed into post-transcriptional gene silencing (PTGS), which involves the cleavage of target messenger R

190 ement of posttranscriptional gene silencing (PTGS), which is an antiviral defense mechanism in plants

191 ired for posttranscriptional gene silencing (PTGS)--SUPPRESSOR OF GENE SILENCING3 (SGS3) and SUPPRESS

192 m using post-transcriptional gene silencing (PTGS).

193 ject to post-transcriptional gene silencing (PTGS).

194 RNAi) or posttranscriptional gene silencing (PTGS).

195 ated in post-transcriptional gene silencing (PTGS).

196 ited by post-transcriptional gene silencing (PTGS).

197 RNAs via posttranscriptional gene silencing (PTGS).

198 fect on post-transcriptional gene silencing (PTGS).

199 ading to posttranscriptional gene silencing (PTGS).

200 s using post-transcriptional gene silencing (PTGS).

201 plants, post-transcriptional RNA silencing (PTGS) signals move beyond their sites of synthesis using

202 rocess (post-transcriptional gene silencing, PTGS).

203 n (i.e. post-transcriptional gene silencing, PTGS).

204 plant viruses encode proteins that suppress PTGS.

205 ive synergistic genes, were able to suppress PTGS induced by green fluorescent protein (GFP) and elim

206 TCV CP was able to suppress PTGS induced by sense, antisense, and double-stranded RN

207 ealed that a P1/ HC-Pro transgene suppressed PTGS of the GUS sequence.

208 ase (HC-Pro) of plant potyviruses suppresses PTGS in plants.

209 ase (HC-Pro) of plant potyviruses suppresses PTGS.

210 er component-proteinase (HC-Pro), suppresses PTGS of silenced transgenes.

211 rnip crinkle virus (TCV) strongly suppresses PTGS.

212 rachidonic acid by PG-endoperoxide synthase (PTGS)-1 and PTGS2.

213 e of cyclooxygenase (prostaglandin synthase [PTGS]) enzymes and prostaglandin (PG) E(2) signaling pat

214 Prostaglandin endoperoxide synthases (PTGS), commonly referred to as cyclooxygenases (COX-1 an

215 mutants impaired in RDR6-dependent systemic PTGS.

216 tissue for efficient RDR6-dependent systemic PTGS.

217 DCL2 is crucial for RDR6-dependent systemic PTGS.

218 nd post-transcriptional gene silencing (TGS, PTGS) in perspective to the rapidly burgeoning knowledge

219 these data provide compelling evidence that PTGS represents a natural mechanism for plant protection

220 nd inducers of PTGS has led to the idea that PTGS may have evolved as an anti-viral defense mechanism

221 These results indicate that PTGS and TGS operate through unlinked pathways or that P

222 silencing in plants and the indications that PTGS is an ancient mechanism in eukaryotic organisms, un

223 ulation of gene expression, and suggest that PTGS plays a central role in the temporal control of sho

224 The PTGS induced by three or four repeats is consistently in

225 The PTGS of ACA10 homologs is therefore directed by a miRNA

226 The PTGS-competent short sequences resulted in similar patte

227 TE-overlapping/proximal genes, load into the PTGS effector ARGONAUTE1 (AGO1), and display a subtle ef

228 h low dose of probenecid as well as with the PTGS inhibitor indomethacin or Meloxicam synergistically

229 virus-based VIGS, its inherent connection to PTGS, and what is known about the systemic spread of sil

230 Contrarily to PTGS-1, deficiency of PTGS-2 activity significantly ampl

231 A silencing mechanism similar to PTGS appears to function as an adaptive antiviral respon

232 plains in part how these viruses can trigger PTGS in plants.

233 ing geminiviruses were capable of triggering PTGS by producing two classes of virus-specific short in

234 geting reporter transgene mRNA de novo using PTGS was 23 nucleotides (nt) of complete identity, a siz

235 We propose that, via PTGS, disiRNAs could help to tighten the expression of e

236 e in the mechanism that is circumvented when PTGS is mediated by TRV.

237 Here, we report that plants in which PTGS has been suppressed by HC-Pro fail to accumulate th

238 ning revealed robust evidence for widespread PTGS of ACA10 homologs directed by a superfamily of rela

239 transmissible gene silencing associated with PTGS [6].

240 onding to that of small RNAs associated with PTGS in plants and RNA interference (RNAi) in animals.

241 d the short interfering RNAs associated with PTGS, with a correlated increase in GFP mRNA accumulatio

242 d the small interfering RNAs associated with PTGS.

243 d in jmj14 sgs3 double mutants compared with PTGS-deficient sgs3 mutants, indicating that JMJ14 is re

244 is zinc and aluminum, did not interfere with PTGS and viral systemic movement.

245 saic virus have been shown to interfere with PTGS.

246 induction of a pathway that interferes with PTGS.

247 hat mobile silencing is associated only with PTGS.