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 Although PTGS has proven effective against a variety of target ge

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

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

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

12 relationship between short RNA sequences and PTGS.

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

14 porting an antagonistic relationship between PTGS and TGS.

15 STZ metabolism was unaffected by PTGS deficiency.

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

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

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

19 n determining the efficiency of AON-directed PTGS.

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

21 can to identify potential off-targets during PTGS.

22 extensive production of siRNAs and efficient PTGS of CER3.

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

24 is not essential for but rather facilitates PTGS.

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

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

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

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

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

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

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

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

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

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

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

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

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

38 1, a component of the Smith (Sm) complex, in PTGS.

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

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

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

42 onsilenced ones, indicating a direct role in PTGS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 bition of PTGS allowed several insights into PTGS development.

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

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

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

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

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

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

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

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

66 view of the subcellular compartmentation of PTGS in plants.

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

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

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

70 may represent the specificity determinant of PTGS.

71 ne sequences influenced the effectiveness of PTGS.

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

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

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

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

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

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

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

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

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

81 transitive RNA silencing and maintenance of PTGS.

82 PTGS, uncoupling between these two modes of PTGS.

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

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

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

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

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

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

89 report identifying a cellular suppressor of PTGS.

90 acco etch virus functions as a suppressor of PTGS.

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

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

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

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

95 rather than cytosolic mRNA as the target of PTGS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 nsgene posttranscriptional gene silencing (S-PTGS).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 RNAi) or posttranscriptional gene silencing (PTGS).

163 RNAs via posttranscriptional gene silencing (PTGS).

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

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

166 ading to posttranscriptional gene silencing (PTGS).

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

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

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

170 plant viruses encode proteins that suppress PTGS.

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

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

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

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

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

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

177 rnip crinkle virus (TCV) strongly suppresses PTGS.

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

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

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

181 DCL2 is crucial for RDR6-dependent systemic PTGS.

182 mutants impaired in RDR6-dependent systemic PTGS.

183 tissue for efficient RDR6-dependent systemic PTGS.

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

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

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

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

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

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

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

191 The PTGS-competent short sequences resulted in similar patte

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

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

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

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

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

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

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

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

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

201 transmissible gene silencing associated with PTGS [6].

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

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

204 d the small interfering RNAs associated with PTGS.

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

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

207 saic virus have been shown to interfere with PTGS.

208 induction of a pathway that interferes with PTGS.

209 hat mobile silencing is associated only with PTGS.