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31 publications mentioning ath-MIR398a

Open access articles that are associated with the species Arabidopsis thaliana and mention the gene name MIR398a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 88
Expression Changes of Drought Associated miRNAs Target Genes under PEG8000 Stress and NaHS Treatment in Arabidopsis We selected ARF8 (target gene of miR167); TIR1, AFB2 and AFB3 (target genes of miR393); GRF1, GRF2 and GRF3 (target genes of miR396); CSD1 and CSD2 (target genes of miR398) to determine possible transcriptional changes of drought -associated miRNA target genes. [score:15]
We selected ARF8 (target gene of miR167); TIR1, AFB2 and AFB3 (target genes of miR393); GRF1, GRF2 and GRF3 (target genes of miR396); CSD1 and CSD2 (target genes of miR398) to determine possible transcriptional changes of drought -associated miRNA target genes. [score:11]
In comparison, MIR398a and MIR398b were first downregulated and then upregulated; MIR398c was downregulated during the 12 h period. [score:10]
Under drought stress, miR167, miR393 and miR396 are upregulated, miR169 is downregulated and miR398 is differentially regulated [17]. [score:8]
On the other hand, H [2]S is involved in regulating the expression of drought associated miRNAs such as miR167, miR393, miR396 and miR398 and can therefore affect their target gene expressions and so to improve the tolerance of Arabidopsis to drought. [score:8]
Expression of MIR167a, MIR167c, MIR167d, MIR398a, MIR398b and MIR398c transcripts in lcd are significantly lower than WT under PEG8000 treatment while that of MIR393a and MIR396a are higher (Figure 4), which did not match the expression pattern of the miRNA target genes. [score:7]
miR398 target genes that code for the free radical scavenger SOD and these genes have been shown to be down-regulated during times of oxidative stress [36]. [score:6]
from qRT-PCR showed elevated expression levels of MIR167a, MIR167c, MIR167d, MIR393a and MIR396a (Figure 4A) and decreased expression levels of MIR398a, MIR398b and MIR398c (Figure 4B) in both lcd and WT under PEG8000 treatment compared with non -treated plants. [score:4]
When PEG8000 treated lcd mutants were compared with PEG8000 treated WT, lcd showed a lower expression level of MIR167a, MIR167c, MIR167d, MIR398a, MIR398b and MIR398c and a higher expression level of MIR393a and MIR396a. [score:4]
miR398 targets superoxide dismutase (SOD) coding genes. [score:3]
In this paper we have shown that the expression of MIR398a and MIR398c/MIR398b first increased as PEG8000 concentration went up from 0 to 0.05 g ml [−1]/0.2 g ml [−1] and then decreased (Figure 2B). [score:3]
Therefore decreased miR398 expression of plants exposed to higher PEG8000 concentrations might suggest that severe drought induced stress was created by an oxidative environment inside the Arabidopsis cells. [score:3]
lcd was pre -treated with 50 µmol L [−1] NaHS for 12 h and 0.2 g ml [−1] PEG8000 for 2 h; (B) MIR398a, MIR398b and MIR398c expression in WT and lcd treated with 50 µmol L [−1] NaHS and 0.2 g ml [−1] PEG8000. [score:3]
CSD1and CSD2 (targets of miR398) play an important role in scavenging activity of ROS (results shown in Figure 8) [23]; SOD enzyme activity increased in both WT and lcd under PEG8000 (Figure 8A); Similarly, H [2]O [2] and MDA contents increased in both WT and lcd under PEG8000 and it is notable that MDA content increased to a greater extent in lcd compared with WT (Figure 8B and 8C). [score:2]
MIR398a and MIR398c transcripts decreased as time progressed, While MIR398b transcripts increased as time progressed, until they reached a maximum at 2 h into the treatment, after which started decreasing (Figure 2A); transcripts first increased and then decreased as PEG8000 concentration increased (Figure 2B). [score:1]
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2
[+] score: 62
Similarly, the gene expression levels of the miR395 target SULTR2;1 and the miR398 targets CSD1 and CSD2 decreased in the leaves after 72 h Cd exposure (Table  2), while the expression of their regulating miRNAs increased (Table  1). [score:10]
Three miRNAs had an altered expression at the earliest time-point of 2 h: in roots and leaves an upregulation of pri-miR395c after Cu exposure and of pri-miR398a after Cd and Cu exposure was observed, while a downregulation of pri-miR826 in Cu- and Cd-exposed roots was noticed. [score:9]
On the one hand, the expression of miR398 is downregulated by copper (Cu) and iron (Fe), causing increased copper/zinc superoxide dismutase (CSD) expression [21, 22]. [score:8]
Gayomba et al. [41] demonstrated that SPL7 is involved in the Cd -induced increase of miR398, as well as in the upregulated expression of FSD1 and COPT1/2/6. [score:6]
Concerning the expression levels of the miR398 targets CSD1 and CSD2, no genotype effect was noticed in the roots under control conditions (Table  5). [score:5]
However, Cd exposure resulted in the leaves in induced expression levels of miR395, miR397 and miR398 and this led to reduced transcript levels of their targets SULTR2;1, LAC2, LAC4 and LAC17, and CSD1 and CSD2 (Tables  1 and 2). [score:5]
The induction of the miR398 expression under Cu deprivation is regulated by the active transcription factor SQUAMOSA promoter binding protein-like7 (SPL7) assumed to be a central regulator in Cu homeostasis [24]. [score:5]
Previous studies also demonstrated the downregulation of miR398 after Cu exposure in A. thaliana [21, 22]. [score:4]
The induced expression of pri-miR398a in the Cd- and Cu-exposed roots and in the Cu-exposed leaves diminished over time and even disappeared after 72 h (Table  1). [score:3]
The Cd and Cu responsive pri-miRNAs that we identified in our experimental setup (Table  1), showed no altered expression in their study, except for pri-miR398a/b/c after Cu exposure, which could be due to the different experimental setups. [score:3]
This is conform with the findings of Gayomba et al. [41] where transcript levels of other genes with a GTAC-containing promoter (COPT2, COPT6, FSD1 and miR398) were reduced in the spl7 mutant. [score:1]
Until lately, miR398 was the only miRNA family that was known to be involved in Cu and Cd stress in A. thaliana [21, 22]. [score:1]
On the other hand, excess cadmium (Cd) induces miR398 and this response is also seen under low Cu availability [22, 23]. [score:1]
Therefore, the putatively SPL7 -dependent miR398 -mediated maintenance of CSD transcript levels can be a first-line defence against Cu -induced oxidative stress. [score:1]
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3
[+] score: 50
We found that miR398, proposed to be directly linked to the plant stress regulatory network, was up-regulated in both tissues as shown by the H-T sequencing (Tables  1 and 2) and the expression pattern was validated by the qPCR which revealed a significant up-regulation in both tissues (Figure  5A, B). [score:11]
The sequencing analysis showed that in both callus and leaf tissues, various stress regulated-miRNAs were differentially expressed and real time PCR validated the expression profile of miR156, miR158, miR159, miR169, miR393, miR398, miR399 and miR408 along with their target genes. [score:8]
In both callus and leaf tissues, four miRNAs (miR156, miR169, miR398 and miR408) were up-regulated, two miRNAs (miR158, and miR393) were down-regulated with two other miRNAs (miR159 and miR396) only found in the callus tissue (Figure  5A, B). [score:7]
The significant down-regulation of CSD revealed by the qPCR in both tissues (Figure  6A, B) indicated a role for miR398 -mediated gene regulation in response to LPS. [score:5]
The expression data was then compared against the H-T sequencing data analysis which revealed that five (miR156, miR169, miR398, miR399 and miR408) of the nine miRNAs in callus tissue and six (miR158, miR159, miR169, miR393, miR396 and miR408) of the nine miRNAs in leaf tissue showed expression patterns that were similar to those observed with the H-T sequencing data. [score:4]
To validate the sequencing results with the bioinformatics -based analysis and based on their key function in gene regulation, the following mature miRNA were selected for expression profile analysis: miR156, mi158, miR159, miR169, miR393, miR396, miR398, miR399 and miR408. [score:4]
Experimental studies in Arabidopsis and other plants have shown that abiotic and biotic stresses induce differential expression of a set of miRNAs such as: miR156, miR159, miR165, miR167, miR168, miR169, miR319, miR393, miR395, miR396, miR398, miR399, and miR402 [7, 18- 23]. [score:3]
The repression of the CSD by the overexpression of miR398 might thus be required to enhance A. thaliana’s response to LPS perception. [score:3]
In Arabidopsis, prior studies demonstrated that miR398 is involved in responses to abiotic - and biotic stresses and it targets at least four mRNAs which include the cytosolic copper/zinc superoxide dismutase1 (CSD1), the chloroplastic CSD2, a subunit of the mitochondrial cytochrome C oxidase, COX5b-1, and the copper chaperone for superoxide dismutase [63, 64]. [score:3]
The regulation of genes encoding copper proteins by miR398 and miR408 suggests a link between copper homeostasis and its contribution to the activation of the A. thaliana response to LPS through mechanisms that are as yet unknown. [score:2]
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4
[+] score: 27
The miR398 family have been validated to be up-regulated in Arabidopsis (Guan et al., 2013) and wheat (Kumar et al., 2014), but down-regulated in rice (Sailaja et al., 2014) and Brassica rapa (Yu et al., 2012b). [score:7]
However, in Brassica rapa, heat stress reduced the expression of the conserved miRNAs bra-miR398a and bra-miR398b, which guides heat response of their target gene BracCSD1 (Yu et al., 2012b). [score:5]
Transgenic plants overexpressing miR398-resistant versions of CSD1, CSD2, or CCS under the control of their native promoters were hypersensitive to heat stress, and the expression of many HSF and HSP genes under heat stress was reduced in these plants. [score:5]
Thus, HSFs, miR398 and its target genes CSD1, CSD2, and CCS form an essential regulatory loop for thermotolerance in Arabidopsis (Guan et al., 2013). [score:4]
Heat stress rapidly induced ath-miR398 and reduced transcripts of its target genes COPPER/ZINC SUPEROXIDE DISMUTASE 1(CSD1), CSD2 and COPPER CHAPERONE FOR SOD 1 (CCS) that control ROS accumulation (Guan et al., 2013). [score:3]
Heat stress induction of miR398 triggers a regulatory loop that is critical for thermotolerance in Arabidopsis. [score:2]
Moreover, HSFA1b and HSFA7b were found to be responsible for heat induction of miR398. [score:1]
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5
[+] score: 26
Other targets of miR398, CSD1 and CSD2, however, were down-regulated during senescence in siliques. [score:6]
Surprisingly, the expression of COX5B-1 was relatively unchanged in leaves or siliques during senescence despite regulation of miR398 itself (Fig.   6e). [score:4]
Other targets of miR398, SUPEROXIDE DISMUTASE 1(CSD1) and SUPEROXIDE DISMUTASE 2 (CSD2), which are responsible for reducing reactive oxygen species (ROS) during oxidative stress, were unchanged in leaves but declined in senescing siliques (Fig.   6e). [score:3]
miR398 has been reported to respond to a host of nutrients including phosphate, nitrate and sucrose and targets genes involved in glucose metabolism and the response to oxidative stress (Sunkar et al. 2006; Dugas & Bartel 2008; Pant et al. 2009). [score:3]
Surprisingly COX5b-1, a target of miR398, was unchanged during senescence (Fig.   6e) despite its reported responses to sucrose levels (Comelli et al. 2009). [score:3]
miR398 targets a host of genes involved in a variety of different processes ranging from glucose metabolism to the oxidative stress response. [score:3]
In keeping with the nutrient remobilization hypothesis, five out of the seven miRNAs (miR408, miR399, miR827, miR447 and miR398), which were senescence regulated, have been previously reported to be nutrient responsive (Fujii et al. 2005; Ab del-Ghany & Pilon 2008; Dugas & Bartel 2008; Pant et al. 2009; Kant et al. 2011), indicating that they may play a currently underappreciated role in controlling the flow of nutrients from vegetative to reproductive tissue. [score:2]
miR398 showed a mild induction as senescence progressed in leaves and a much larger reduction in siliques (Fig.   2). [score:1]
While sucrose, phosphate and nitrate deficiencies have been reported to repress miR398 (Dugas & Bartel 2008; Pant et al. 2009), its levels were actually increased during aging in leaves. [score:1]
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6
[+] score: 24
As previously mentioned, disease resistant transgenic rice have been produced by overexpressing either miR160, miR398 or miR7695 (Campo et al. 2013; Li et al. 2013), thus supporting the potential of MIR genes to prevent rice disease. [score:7]
miR160 targets Auxin Response Factors (ARFs) whereas miR398 targets Cu/Zn superoxide dismutase genes. [score:5]
It is also known that miR160a functions as a positive regulator of PAMP -induced callose deposition, whereas miR398 and miR773 negatively regulate PAMP -induced callose deposition and hence disease resistance to P. syringae (Fig.   1). [score:5]
Accordingly, transgenic Arabidopsis lines overexpressing miR398 are compromised in resistance to the bacterial pathogen P. syringae (Li et al. 2010). [score:3]
MiR398 is involved in PTI responses through the control of ROS production, this miRNA targeting two Cu/Zn superoxide dismutase genes (CSD1 and CSD2) and a copper chaperone for superoxide dismutase (Fig.   1). [score:3]
In rice, the involvement of miR160, miR398 and miR7695 (in bold) in PTI responses is documented (Campo et al. 2013; Li et al. 2013). [score:1]
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7
[+] score: 22
Among these targets, it can be mentioned members of the SOD family (targets of miR398), ARF8 an auxin response factor (target of miR167), DCL1 (target of miR162), AGO1 (target of miR168) and AGO2 (target of miR403). [score:13]
Although miRNAs in plants predominantly operate through transcript cleavage, several studies on miRNAs such as miR156, miR172, miR398, miR164 and miR165/6 show that transcript cleavage as well as translation repression may act upon the same targets [53, 54]. [score:5]
Among the 30 miRNA families detected at 2dpi, 10 (miR160, miR161, miR167, miR171, miR172, miR390, miR394, miR396, miR398 and miR408) displayed contrasting expression levels between viruses. [score:3]
Slight discrepancies were observed at 2dpi in relation to miR398 and miR472 of ORMV-infected plants. [score:1]
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8
[+] score: 15
Other miRNAs from this paper: ath-MIR398b, ath-MIR398c
Genes: γ-glutamylcysteine synthetase (GSH1), glutathione synthetase (GSH2), phytochelatin synthase (PCS1), iron superoxide dismutase (FSD1), copper/zinc superoxide dismutase (CSD1-2), primary microRNA398 transcripts (pri-MIR398a-c), catalase (CAT1-3), ascorbate peroxidase (APX1-2), dehydroascorbate reductase (DHAR1-3), glutathione reductase (GR), Toll-Interleukin-1 class (TIR), upregulated by oxidative stress (UPOX). [score:4]
The SOD pathway was activated but to a smaller extent than in roots: CSD1/2 transcripts were decreased and pri-MIR398a-c was significantly up-regulated in some conditions, but no significant induction of FSD1 was present. [score:4]
Genes: γ-glutamylcysteine synthetase (GSH1), glutathione synthetase (GSH2), phytochelatin synthase (PCS1), iron superoxide dismutase (FSD1), copper/zinc superoxide dismutase (CSD1-2), primary microRNA398 transcripts (pri-MIR398a-c), catalase (CAT1-3), ascorbate peroxidase (APX1-2), dehydroascorbate reductase (DHAR1-3), glutathione reductase (GR1-2), Toll-Interleukin-1 class (TIR), upregulated by oxidative stress (UPOX). [score:4]
However, all genotypes activated the SOD pathway in a dose -dependent manner, i. e. increasing FeSOD (FSD1) and microRNA398 [primary microRNA398 transcripts (pri-MIR398a-c)] expression, resulting in decreasing CuZnSOD (CSD1/2) transcript levels. [score:3]
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9
[+] score: 13
While the expressions of 14 families (miR156/miR157, miR158, miR160, miR162, miR165/miR166, miR168, miR169, miR171, miR390, miR393, miR394, miR396, miR398, and miR399) were dramatically reduced, 3 families (miR159, miR167, and miR172) were up-regulated in CsCl -treated seedlings. [score:6]
Posttranscriptional induction of two Cu/Zn superoxide dismutase genes in Arabidopsis is mediated by downregulation of miR398 and important for oxidative stress tolerance. [score:4]
The expression of MiR398 is dramatically decreased in response to excessive Cu, resulting in accumulation of CSD1 and CSD2 genes for Cu/Zn superoxide dismutases [22, 23]. [score:2]
miR167, miR168, miR172, miR396, and miR398) were notably increased (Fig 3B, S2 Fig). [score:1]
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10
[+] score: 13
With superoxide dismutases (SODs), substituting the Cu form (Cu/ZnSOD) with the Fe counterpart (FeSOD) is done by SPL7 under Cu-limited conditions by expressing FeSOD mRNA (FSD1) and miR398, since miR398 targets Cu/ZnSOD mRNAs (CSD1 and CSD2) for degradation (Ab del-Ghany et al., 2005; Ravet and Pilon, 2013). [score:5]
Dynamic miR398 expression regulation under drought stress remains a controversial matter as it hinders assigning a clear role for ABA during the process (Ding et al., 2013). [score:4]
Since miR398 controls antioxidant activities, in addition to Cu-deficiency, other processes involving enhanced ROS regulate its expression (Zhu et al., 2011). [score:4]
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11
[+] score: 11
For miR156, miR160, miR169, miR171, miR172, miR395, miR397, miR398, miR399, miR408, miR775, miR780.1, miR827, miR842, miR846, miR857, and miR2111, their targets have been predicted and most of them were validated previously (Table 2). [score:3]
The homeostasis of another essential nutrient, copper, is regulated by miR398, which directs the degradation of Copper/zinc Superoxide Dismutase mRNA when copper is limited [14]. [score:3]
Deep sequencing analyses also suggested that miR169, miR395, and miR398 were expressed at low levels under P -deficient conditions [12]. [score:3]
Recently, several miRNAs were identified to be responsive to N limitation in Arabidopsis, which includes miR156, miR167, miR169, and miR398 [13], [17]. [score:1]
When plants were deprived of Cu, the abundance of miR397, miR398, miR408, and miR857 increased significantly. [score:1]
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12
[+] score: 10
In addition to miR398, three microRNAs, namely, miR397, miR408, and miR857, target genes that encode Cu-containing proteins (Ab del-Ghany and Pilon, 2008). [score:3]
miR398 can directly regulate CSD mRNA degradation under -Cu (Yamasaki et al., 2007). [score:3]
SPL7 can bind directly to GATC motifs in miR398 promoter (Yamasaki et al., 2009). [score:2]
miR398 regulates the mRNA stability of major Cu-containing proteins, such as CSD1, CSD2, and COX5b-1, under Cu-limited conditions. [score:2]
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13
[+] score: 8
Other repressed families were miR397, miR398 and miR408, known to be involved in copper regulation and to be differentially expressed in response to biotic stress [34, 46, 47]. [score:4]
The miR397, miR398 and miR408 families were also repressed (log [2]fold < -1.4); they are involved in copper regulation by targeting laccases, copper superoxide dismutases and plantacyanins, respectively [34]. [score:4]
[1 to 20 of 2 sentences]
14
[+] score: 8
Moreover, the down-regulation of the MiR398 gene was inversely correlated with the 3.5-fold increase in the expression levels of cytochrome C oxidase subunit V, one of its known target genes (Jones-Rhoades and Bartel, 2004; Figure S10B in Supplementary Materials). [score:7]
Diurnal oscillation in the accumulation of Arabidopsis microRNAs, miR167, miR168, miR171 and miR398. [score:1]
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15
[+] score: 8
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157d, ath-MIR158a, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR161, ath-MIR162a, ath-MIR162b, ath-MIR163, ath-MIR164a, ath-MIR164b, ath-MIR165a, ath-MIR165b, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR169a, ath-MIR170, ath-MIR172a, ath-MIR172b, ath-MIR173, ath-MIR159b, ath-MIR319a, ath-MIR319b, ath-MIR167d, ath-MIR169b, ath-MIR169c, ath-MIR169d, ath-MIR169e, ath-MIR169f, ath-MIR169g, ath-MIR169h, ath-MIR169i, ath-MIR169j, ath-MIR169k, ath-MIR169l, ath-MIR169m, ath-MIR169n, ath-MIR171b, ath-MIR172c, ath-MIR172d, ath-MIR391, ath-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, ath-MIR397a, ath-MIR397b, ath-MIR398b, ath-MIR398c, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, ath-MIR400, ath-MIR408, ath-MIR156g, ath-MIR156h, ath-MIR158b, ath-MIR159c, ath-MIR319c, ath-MIR164c, ath-MIR167c, ath-MIR172e, ath-MIR447a, ath-MIR447b, ath-MIR447c, ath-MIR773a, ath-MIR775, ath-MIR822, ath-MIR823, ath-MIR826a, ath-MIR827, ath-MIR829, ath-MIR833a, ath-MIR837, ath-MIR841a, ath-MIR842, ath-MIR843, ath-MIR845a, ath-MIR848, ath-MIR852, ath-MIR824, ath-MIR854a, ath-MIR854b, ath-MIR854c, ath-MIR854d, ath-MIR857, ath-MIR864, ath-MIR2111a, ath-MIR2111b, ath-MIR773b, ath-MIR841b, ath-MIR854e, ath-MIR833b, ath-MIR156i, ath-MIR156j, ath-MIR826b
Although the miR826 sequence was not found because of low expression abundance in –P, we found that –C -induced miR169b/c, –S -induced miR395, and –Cu -induced miRNAs (miR397, miR398, miR408, and miR857) were significantly suppressed in roots grown in –P conditions (Supplemental Table 5). [score:5]
For example, –Cu induced miRNAs (miR397, miR398, miR408, and miR857) that were suppressed by –C, –N, –S, and –P. [score:3]
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16
[+] score: 7
Recently we described the up-regulation of miR398a/b and miR408 under water deficit and the corresponding down regulation of their respective targets, COX5b and plantacyanin [4]. [score:7]
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17
[+] score: 6
In three cases—miR402 targeting of the transcription factor DML3 (UniProt: O49498) (Fig 5A), miR398 regulation of free radical metabolism (Fig 5B), and miR395 regulation of sulfur metabolism (Fig 5C), there was no evidence of co-regulation by kinases. [score:6]
[1 to 20 of 1 sentences]
18
[+] score: 6
The question arises whether these adjacent genes are involved in the regulation of miR398–mediated thermotolerance. [score:2]
Heat stress induction of miR398 triggers a regulatory loop that is critical for thermotolerance in Arabidopsis[35]. [score:2]
Eight cis-NATs were coincidently the precursors of miR162, miR167, miR171, miR172, miR398 and miR408 (Table  3). [score:1]
Among them, miR398a and miR398b were very sensitive to heat stress, and MIR398b precursor was also decreased under heat stress in B. rapa. [score:1]
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19
[+] score: 6
Other miRNAs from this paper: ath-MIR398b, ath-MIR398c, ath-MIR408
Moreover, and as expected since it was mediated by miR398 degradation, Cu excess induced the expression of the CSD1 and the CCS marker genes under LDHC conditions at both 0h and 12h, and expression was greater at 0h than at 12h in both cases (Supplementary Fig. S3 at JXB online). [score:5]
This substitution is mediated by the GTAC motifs present in the FSD1 and MIR398 promoter regions, where this latter miRNA mediates the degradation of CSD genes and their chaperone CCS mRNAs (Ab del-Ghany et al., 2005; Pilon et al., 2006). [score:1]
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20
[+] score: 5
In the transgenic lines drb1/DRB-C1, drb1/DRB-C2, drb1/DRB-C4, and drb1/DRB-C9, which displayed wild-type-like phenotypes, accumulation of miR164, miR165/166, miR398 and miR408 and target gene expression of CUP SHAPED COTLEDONS2 (CUC2; miR164), ARABIDOPSIS THALIANA HOMEOBOX PROTEIN14 (ATHB-14; miR165/166), REVOLUTA (REV; miR165/166), COPPER/ZINC SUPEROXIDE DISMUTASE2 (CSD2; miR398), and PLANTACYANIN (ARPN; miR408) were at approximately wild-type levels (Figures 3A,B). [score:5]
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21
[+] score: 5
Other miRNAs from this paper: ath-MIR398b, ath-MIR398c
For example, the superoxide dismutase CSD2 mRNA is targeted by the miR398 to repress translation under “low Cu [+] [+]” conditions, this mechanism requires VCS (Brodersen et al., 2008). [score:5]
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22
[+] score: 4
Certain mutations in the miR398 complementary motif site reduced the effects of miR398 on CSD mRNA, but not on protein levels [3]. [score:2]
Support for the existence of miRNA binding sites with reduced complementarity in plants comes from an analysis of miR398, which regulates COPPER SUPEROXIDE DISMUTASE (CSD) genes. [score:2]
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23
[+] score: 3
Other miRNAs from this paper: ath-MIR398b, ath-MIR398c
Yamasaki et al. [41] proposed that miRNA398 is involved in the regulation of Cu homeostasis since MIR398b/c contains Cu-sensitive GTAC motifs in its promoter region. [score:2]
Zhu C. Ding Y. F. Liu H. L. miR398 and plant stress responses Physiol. [score:1]
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24
[+] score: 3
These miRNAs are reported to function in regulation of genes related to growth (miR157/171/824) [59], Brassica-specific stomatal organization (miR824), pollen development (miR824) [60], abiotic stress tolerance, and plant–pathogen interactions (miR398) [61]. [score:3]
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25
[+] score: 3
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR164a, ath-MIR164b, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR168a, ath-MIR168b, ath-MIR171a, ath-MIR172a, ath-MIR172b, ath-MIR159b, ath-MIR319a, osa-MIR156a, osa-MIR156b, osa-MIR156c, osa-MIR156d, osa-MIR156e, osa-MIR156f, osa-MIR156g, osa-MIR156h, osa-MIR156i, osa-MIR156j, osa-MIR160a, osa-MIR160b, osa-MIR160c, osa-MIR160d, osa-MIR164a, osa-MIR164b, osa-MIR166a, osa-MIR166b, osa-MIR166c, osa-MIR166d, osa-MIR166e, osa-MIR166f, osa-MIR167a, osa-MIR167b, osa-MIR167c, osa-MIR171a, ath-MIR167d, ath-MIR172c, ath-MIR172d, ath-MIR393a, ath-MIR393b, ath-MIR396a, ath-MIR396b, osa-MIR393a, osa-MIR396a, osa-MIR396b, osa-MIR396c, osa-MIR398a, ath-MIR156g, ath-MIR156h, ath-MIR159c, ath-MIR164c, ath-MIR167c, ath-MIR172e, osa-MIR156k, osa-MIR156l, osa-MIR159a, osa-MIR159b, osa-MIR159c, osa-MIR159d, osa-MIR159e, osa-MIR159f, osa-MIR319a, osa-MIR160e, osa-MIR160f, osa-MIR164c, osa-MIR166k, osa-MIR166l, osa-MIR167d, osa-MIR167e, osa-MIR167f, osa-MIR167g, osa-MIR167h, osa-MIR167i, osa-MIR168a, osa-MIR168b, osa-MIR172a, osa-MIR172b, osa-MIR172c, osa-MIR166g, osa-MIR166h, osa-MIR166i, osa-MIR393b, osa-MIR172d, osa-MIR167j, osa-MIR166m, osa-MIR166j, osa-MIR437, osa-MIR396e, osa-MIR444a, osa-MIR528, osa-MIR531a, osa-MIR1425, osa-MIR444b, osa-MIR444c, osa-MIR444d, osa-MIR444e, osa-MIR444f, osa-MIR531b, osa-MIR1862a, osa-MIR1862b, osa-MIR1862c, osa-MIR1873, osa-MIR1862d, osa-MIR1862e, osa-MIR396f, osa-MIR396g, osa-MIR396h, osa-MIR396d, osa-MIR1862f, osa-MIR1862g, ath-MIR5021, osa-MIR5072, osa-MIR5077, ath-MIR156i, ath-MIR156j, osa-MIR531c
Maximum variation was observed in the expression of miR172c-5p and miR398a-3p. [score:3]
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26
[+] score: 2
Similarly, miRNAs responsive to bacterial (miR160, miR167, miR393, miR396, miR398 and miR825) and viral infections (miR156 and miR164) were not altered in the OE lines [33- 35]. [score:1]
For miRNAs that are induced by nutritional stresses, such as phosphate deficiency (miR399) copper deficiency (miR398), and sulfate deficiency (miR395), their abundance were low in all lines and were not significantly changed in our OE lines [22, 30- 32]. [score:1]
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27
[+] score: 2
miR171, miR398, miR168, and miR167 oscillate diurnally but are not under clock-control (Sire et al., 2009). [score:1]
Diurnal oscillation in the accumulation of Arabidopsis, miR167 miR168 miR171 and miR398. [score:1]
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28
[+] score: 2
mir398 [97], [101] CSD and CytC oxidase family members. [score:1]
Mir319c At2g28190 mir398a, mir398b, mir398c At1g63360 mir472a At1g24880 mir859a Data retrieved from searches of the published literature and databases. [score:1]
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29
[+] score: 1
Other miRNAs from this paper: ath-MIR159a, ath-MIR162a, ath-MIR162b, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR169a, ath-MIR171a, ath-MIR159b, ath-MIR319a, ath-MIR319b, osa-MIR162a, osa-MIR166a, osa-MIR166b, osa-MIR166c, osa-MIR166d, osa-MIR166e, osa-MIR166f, osa-MIR169a, osa-MIR171a, ath-MIR169b, ath-MIR169c, ath-MIR169d, ath-MIR169e, ath-MIR169f, ath-MIR169g, ath-MIR169h, ath-MIR169i, ath-MIR169j, ath-MIR169k, ath-MIR169l, ath-MIR169m, ath-MIR169n, ath-MIR171b, ath-MIR171c, ath-MIR390a, ath-MIR390b, ath-MIR396a, ath-MIR396b, ath-MIR398b, ath-MIR398c, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, osa-MIR396a, osa-MIR396b, osa-MIR396c, osa-MIR398a, osa-MIR398b, osa-MIR399a, osa-MIR399b, osa-MIR399c, osa-MIR399d, osa-MIR399e, osa-MIR399f, osa-MIR399g, osa-MIR399h, osa-MIR399i, osa-MIR399j, osa-MIR399k, ath-MIR408, ath-MIR159c, ath-MIR319c, osa-MIR156k, osa-MIR159a, osa-MIR159b, osa-MIR159c, osa-MIR159d, osa-MIR159e, osa-MIR159f, osa-MIR319a, osa-MIR319b, osa-MIR162b, osa-MIR166k, osa-MIR166l, osa-MIR169b, osa-MIR169c, osa-MIR169d, osa-MIR169e, osa-MIR169f, osa-MIR169g, osa-MIR169h, osa-MIR169i, osa-MIR169j, osa-MIR169k, osa-MIR169l, osa-MIR169m, osa-MIR169n, osa-MIR169o, osa-MIR169p, osa-MIR169q, osa-MIR171b, osa-MIR171c, osa-MIR171d, osa-MIR171e, osa-MIR171f, osa-MIR171g, osa-MIR166g, osa-MIR166h, osa-MIR166i, osa-MIR171h, osa-MIR408, osa-MIR171i, osa-MIR166m, osa-MIR166j, ath-MIR414, osa-MIR414, osa-MIR390, osa-MIR396e, ptc-MIR156k, ptc-MIR159a, ptc-MIR159b, ptc-MIR159d, ptc-MIR159e, ptc-MIR159c, ptc-MIR162a, ptc-MIR162b, ptc-MIR166a, ptc-MIR166b, ptc-MIR166c, ptc-MIR166d, ptc-MIR166e, ptc-MIR166f, ptc-MIR166g, ptc-MIR166h, ptc-MIR166i, ptc-MIR166j, ptc-MIR166k, ptc-MIR166l, ptc-MIR166m, ptc-MIR166n, ptc-MIR166o, ptc-MIR166p, ptc-MIR166q, ptc-MIR169a, ptc-MIR169aa, ptc-MIR169ab, ptc-MIR169ac, ptc-MIR169ad, ptc-MIR169ae, ptc-MIR169af, ptc-MIR169b, ptc-MIR169c, ptc-MIR169d, ptc-MIR169e, ptc-MIR169f, ptc-MIR169g, ptc-MIR169h, ptc-MIR169i, ptc-MIR169j, ptc-MIR169k, ptc-MIR169l, ptc-MIR169m, ptc-MIR169n, ptc-MIR169o, ptc-MIR169p, ptc-MIR169q, ptc-MIR169r, ptc-MIR169s, ptc-MIR169t, ptc-MIR169u, ptc-MIR169v, ptc-MIR169w, ptc-MIR169x, ptc-MIR169y, ptc-MIR169z, ptc-MIR171a, ptc-MIR171b, ptc-MIR171c, ptc-MIR171d, ptc-MIR171e, ptc-MIR171f, ptc-MIR171g, ptc-MIR171h, ptc-MIR171i, ptc-MIR319a, ptc-MIR319b, ptc-MIR319c, ptc-MIR319d, ptc-MIR319e, ptc-MIR319f, ptc-MIR319g, ptc-MIR319h, ptc-MIR319i, ptc-MIR390a, ptc-MIR390b, ptc-MIR390c, ptc-MIR390d, ptc-MIR396a, ptc-MIR396b, ptc-MIR396c, ptc-MIR396d, ptc-MIR396e, ptc-MIR396f, ptc-MIR396g, ptc-MIR398a, ptc-MIR398b, ptc-MIR398c, ptc-MIR399a, ptc-MIR399b, ptc-MIR399d, ptc-MIR399f, ptc-MIR399g, ptc-MIR399h, ptc-MIR399i, ptc-MIR399j, ptc-MIR399c, ptc-MIR399e, ptc-MIR408, ptc-MIR482a, ptc-MIR171k, osa-MIR169r, ptc-MIR171l, ptc-MIR171m, ptc-MIR171j, ptc-MIR1448, osa-MIR396f, osa-MIR2118a, osa-MIR2118b, osa-MIR2118c, osa-MIR2118d, osa-MIR2118e, osa-MIR2118f, osa-MIR2118g, osa-MIR2118h, osa-MIR2118i, osa-MIR2118j, osa-MIR2118k, osa-MIR2118l, osa-MIR2118m, osa-MIR2118n, osa-MIR2118o, osa-MIR2118p, osa-MIR2118q, osa-MIR2118r, osa-MIR396g, osa-MIR396h, osa-MIR396d, ptc-MIR482d, ptc-MIR169ag, ptc-MIR482b, ptc-MIR482c, pde-MIR159, pde-MIR162, pde-MIR166a, pde-MIR166b, pde-MIR169, pde-MIR171, pde-MIR390, pde-MIR396, pde-MIR482a, pde-MIR482b, pde-MIR482c, pde-MIR482d, pde-MIR946, pde-MIR947, pde-MIR949a, pde-MIR950, pde-MIR951, pde-MIR952a, pde-MIR952b, pde-MIR952c, pde-MIR1311, pde-MIR1312, pde-MIR1313, pde-MIR1314, pde-MIR3701, pde-MIR3704a, pde-MIR3704b, pde-MIR3712
Three P. taeda miRNA families, including pta-MIR319, pta-MIR398 and pta-MIR408, were not found in P. densata. [score:1]
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30
[+] score: 1
Other miRNAs from this paper: ath-MIR398b, ath-MIR398c
The strength of the miR398-Csd2-CCS1 regulon is subject to natural variation in Arabidopsis thaliana. [score:1]
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31
[+] score: 1
Failure to identify miR398a, miR399a, miR399d, miR399e, miR399f and miR447c was due to a lack of sequence reads. [score:1]
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