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44 publications mentioning ath-MIR165b

Open access articles that are associated with the species Arabidopsis thaliana and mention the gene name MIR165b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 201
miR165/166 targets directly regulate the expression of BG1Since the expression of BG1 was enhanced in STTM165/166, we next investigated its expression in PHB: PHB G202G-YFP lines to determine whether higher expression of PHB could also affect the expression of BG1. [score:13]
Targets of miR165/166 directly regulate the expression of ABI4Since the expression of ABA-responsive genes was upregulated in STTM165/166 under normal conditions, we speculated that ABA signaling may be activated or endogenous ABA level is altered. [score:12]
Once miR165/166 is repressed, its repression on target genes will be released, and the upregulated expression of miR165/166 targets will directly promote the accumulation of ABI4, which in turn activates downstream ABA responsive genes. [score:11]
Unlike some miRNAs, such as miR160, miR167 and miR393, which directly target and regulate the expression of key components of the auxin response pathway, the miR165/166 targets themselves are not major components of hormone response pathways but they regulate the transcription of important components of hormone pathways. [score:10]
Therefore, upregulation of the miR165/166 target gene expression caused by compromised miR165/166 function results in the increased expression of BG1, which in turn further modulates ABA homeostasis. [score:10]
We examined the expression of miR165/166 and its targets in STTM165/166 at this early developmental stage with or without by qRT-PCR analysis, and found that the levels of mature miR165/166 were indeed dramatically reduced (Fig 3D and S2 Fig), and all the five target RNAs examined were elevated to different extents (Fig 3E and S2 Fig). [score:8]
In this study, we found that HD-ZIPIII transcription factors, which are the direct targets of miR165/166, could directly bind to the ABI4 gene promoter and regulate its expression. [score:8]
Meanwhile, the increased miR165/166 targets could also upregulate the expression of the BG1 gene, which at least in part contributes to the elevation of ABA content in STTM165/166. [score:8]
Targets of miR165/166 directly regulate the expression of ABI4. [score:7]
miR165/166 targets directly regulate the expression of BG1. [score:7]
Given that miR165/166 is an important regulator in plant growth and development, the miR165/166 meditated regulatory module might help coordinate developmental programs with environmental cues to optimize plant growth and developmental processes under stress. [score:6]
We also discovered that miR165/166 -mediated negative regulation of its targets is essential for maintaining ABA homeostasis at least partly through modulating the expression of BG1, which converts inactive ABA to active ABA. [score:6]
This indicates that a miR165/166 target can directly modulate ABI4 expression. [score:6]
Since the expression level of miR165/166 can be reduced to different extents using short tandem target mimicry (STTM), in the present work, we used STTM165/166 transformants with moderate developmental phenotype to examine its potential role in abiotic stress responses. [score:6]
We found that ABI4 acts downstream of a miR165/166 -mediated pathway and could be directly regulated by a miR165/166 target. [score:5]
Since ABI3, ABI4 and ABI5 are central regulators in the control of ABA- responsive genes, we determined the effect of knockdown miR165/166 on the expression of these genes. [score:5]
Bioinformatic analysis revealed that a typical HD-ZIPIII binding consensus sequence exists in the ABI4 promoter region (Fig 5C), and this prompted us to determine whether ABI4 could be directly regulated by a miR165/166 targeted HD-ZIPIII. [score:5]
Quantitative RT-PCR analysis of the expression of both mature miR165/166 and its targets of 2-day-old seedlings grown on the MS medium containing 1.0 μM ABA. [score:5]
We show that disruption of miR165/166 -mediated repression of its targets through reducing miR165/166 expression levels leads to a drought and cold resistance phenotype and ABA hypersensitivity during and after seed germination. [score:5]
Regulation of miR165/166 expression may help plants to cope with environmental stresses. [score:4]
To establish the molecular link between a miR165/166 mediated regulatory module and an ABA mediated regulatory network, we first compared expression of ABA-responsive genes, such as RESPONSIVE TO DESSICATION 29A (RD29A), RD29B, RAB18, EM1 and EM6 in wild type and STTM165/166 plants. [score:4]
Given that CBF genes play critical roles in freezing tolerance, we analyzed the expression of these genes to test whether miR165/166 mediated regulation of freezing tolerance occurs through modulating CBF factors. [score:4]
The miR165/166 mediated regulatory module affects the expression of ABA- responsive genes. [score:4]
Our study links the miR165/166 -mediated regulatory module to the ABA regulatory network and demonstrates a critical role for the miRNA in ABA responses and homeostasis. [score:3]
To determine whether the miR165/166 mediated network plays important roles in response to abiotic stress, the previously reported stable transgenic Arabidopsis STTM165/166-31nt plants [65], in which the expression of miR165/166 is dramatically reduced, were used in stress resistance tests. [score:3]
We also tested the ABA response of mutants of miR165/166 target genes, but did not observe a significant difference with that of the wild type (S3 Fig). [score:3]
It has been observed that the expression of miR165/166 was altered under different abiotic stress conditions, such as cold, heat, salt and oxidative stress [66– 70]. [score:3]
miR165/166 targets the Class III homeodomain leucine zipper family of transcription factor genes, including PHBULOSA (PHB), PHVOLUTA (PHV), REVOLUTA (REV), ATHB-8 and ATHB-15, which are required for the promotion of adaxial identity of lateral organs [59– 62]. [score:3]
This indicates that regulation of the BG1 gene mediated by the miR165/166 regulatory module contributes to changes in ABA content. [score:3]
miR165/166 is one of the most extensively studied miRNAs, which have been shown to be involved in plant development. [score:2]
Here we provide evidence that the miR165/166- PHB module is involved in regulating ABA homeostasis. [score:2]
Our work reveals that miR165/166 -mediated regulatory module is linked with ABA responses and homeostasis through ABI4 and BG1. [score:2]
Deregulation of miR165/166 results in an ABA response phenotype. [score:2]
Future studies will determine whether the role of miR165/166 mediated regulatory module in ABA response and homeostasis is conserved in other plant species. [score:2]
Here we present evidence for an important role for miR165/166 in the regulation of ABA and abiotic stress responses and the maintenance of ABA homeostasis. [score:2]
The ABA-related phenotype that results from the compromised miR165/166 function indicates that a miR165/166 mediated regulatory module may affect ABA responses. [score:2]
miR165/166 is evolutionarily conserved in a wide range of plant species and its function in plant development is also very conserved. [score:2]
One well-known miRNA, miR165/166, has critical roles in plant development. [score:2]
Proper regulation of miR165/166 is important for normal ABA responses. [score:2]
Thus, miR165/166 is relevant to ABI4 in ABA responses. [score:1]
Our results show that miR165/166 plays critical roles in drought and cold stress resistance as well as in ABA responses. [score:1]
These results indicate that miR165/166 may modulate freezing tolerance through CBF-independent factors. [score:1]
These results indicate that blocking the full function of miR165/166 disturbs ABA responses. [score:1]
[1 to 20 of 43 sentences]
2
[+] score: 127
Other miRNAs from this paper: ath-MIR165a
Here we characterized in detail how FIL -expression and miR165/166-free (presumptively PHB-like genes expression) domains change during leaf development by careful observations of the gene expression markers and by lineage analysis of FIL -expressing cells. [score:8]
However, during the early developmental stages, the FIL -expressing and miR165/166-active cells switch the nuclear gene expression state to that expressing PHB-like genes, thus FMB shifts. [score:8]
However, it was difficult to determine whether the FIL -expressing and miR165/166-active cells are all leaf founder cells because of the absence of a marker to distinguish those cells from the remaining meristem cells in which FIL expression and miR165/166-activity were not detected. [score:5]
It has been described previously that the FIL -expression domain is separated from the expression domain of PHB-like genes, or the miR165/166-free domain, with no or a little overlap in primordia of leaves [29], flowers [30], cotyledons [31] and sepals [25]. [score:5]
Furthermore, we found that this restriction of FIL expression and miR165/166 activity is retarded and lamina becomes narrow when the plastid function is inhibited in leaf primordia. [score:5]
During the later stages, though the expansion of the miR165/166-free domain and restriction of the FIL -expression domain continued to some extent, FIL expression was kept in the elongating margin cells, whole abaxial epidermis and most of the abaxial-most mesophyll even after the leaves exceed 1 mm in length and the round lamina morphology is developed (Figure S2K–P). [score:5]
The results showed that all leaf founder cells express FIL and have miR165/166 activity, but the FIL -expressing cells become miR165/166-free cells sequentially from the adaxial to the abaxial side after leaf initiation. [score:5]
1003655.g002 Figure 2The boundary between the FIL -expression and miR165/166-free domains shifts during leaf development. [score:4]
The boundary between the FIL -expression and miR165/166-free domains shifts during leaf development. [score:4]
One possible scenario is that ABI4 and GLK1 also affect the expression levels of FIL, miR165/166 and other adaxial- and abaxial-specific genes through the transcriptional regulation. [score:4]
The boundary between FIL expression and miR165/166-free domains shifts from adaxial side to the abaxial side during leaf primordial development. [score:4]
PHB-like genes repress miR165/166 activity by positively regulating AGO10/ PINHEAD [77], [78], by decreasing miR165/166 expression level via cytokinin signal [79] and possibly by activating tasiR-ARFs [25]. [score:4]
Therefore, our results strongly suggest that the GUN1 -dependent plastid retrograde signal regulates leaf morphogenesis by affecting the dynamic change in the FIL -expression and miR165/166-free domains in leaf primordia. [score:4]
When FILpro:GFP 35Spro:miYFP-W markers were introduced into phb-1d/+, the FIL -expression and miR165/166-free domains were separated as in the wild type (Figure 4A–E). [score:3]
Most leaf cells express FIL and have miR165/166 activity just after leaf initiation. [score:3]
Before leaf initiation (around P0 stages), FIL was likely expressed in all the leaf founder cells (Figure S2C, S2D), as previously reported [13], [14], and miR165/166 activity was higher in these cells than in the surrounding cells (Figure S2C, S2D). [score:3]
The FMB position changes suggest that leaf cells switch from the FIL -expressing state to the miR165/166-free state, and the switch occurs sequentially from the adaxial to the abaxial cell layers and also from the central to the marginal cells within a layer. [score:3]
In other words, the boundary between FIL -expression and miR165/166-free domains shifts from the adaxial to the abaxial side similarly to the above computer simulation. [score:3]
The activity of miR165/166 in turn represses the expression of PHB-like genes through mRNA cleavage [80] and DNA methylation [81]. [score:3]
The microRNA miR165/166 represses the expression of PHB-like genes through mRNA cleavage in the abaxial region [21]. [score:3]
The Boundary between FIL -expression and mir165/166-free Domains ShiftsThe almost exclusive relationship between the abaxial FIL -expression domain and the adaxial miR165/166-free domain has been characterized well [25], [29]– [31]. [score:3]
The Boundary between FIL -expression and mir165/166-free Domains Shifts. [score:3]
Just after a leaf primordium initiated but before the six cell layers become obvious (P1 stage, approximately 20-µm-long), most leaf cells appeared to express FIL and have miR165/166 activity with the exception of only a few adaxial epidermal cells (Figure S2E, S2F). [score:3]
We hereafter refer to the boundary between FIL -expression and miR165/166-free domains as the FMB. [score:3]
To characterize in detail the spatio-temporal patterns of the FIL -expression and miR165/166-free domains during leaf development, we observed these domains at a series of leaf developmental stages. [score:3]
1003655.g008 Figure 8Most leaf cells express FIL and have miR165/166 activity just after leaf initiation. [score:3]
The FIL -expression and miR165/166-free domains were visualized by two fluorescent markers, FILpro:GFP (green fluorescent protein driven by the FIL promoter) and 35Spro:miYFP-W (miR165/166-sensor yellow fluorescent protein driven by the Cauliflower Mosaic Virus 35S promoter), respectively, as previously described [29]. [score:3]
In 50-µm-long primordia (P1–P2 stages), the FIL -expression and miR165/166-free domains occupied four to five abaxial cell layers and one to two adaxial cell layers, respectively, within the six cell layers (Figure 2A). [score:3]
Accordingly, a mutual repressive relationship is known at least between PHB-like genes and miR165/166 whereas the regulatory relationship between PHB-like genes and FIL is yet to be elucidated. [score:2]
If the domain separation is due to mutual repression between miR165/166 and PHB-like genes, FIL and PHB-like genes and between upstream regulators for these genes, the domain boundary might not be necessarily maintained. [score:2]
To characterize the dynamics of FIL -expression and miR165/166-free domains, the markers FILpro:GFP and 35Spro:miYFP-W were observed in various developmental stages of enf2 leaf primordia. [score:2]
It has been characterized well that the functions of FIL, PHB-like genes and miR165/166 are required for the lamina growth because their loss-of-function mutations and overexpression lead to narrow lamina or needle-like leaf formation [10], [13], [14], [44]– [48]. [score:2]
These narrow and needle-like morphologies are similar to those of abaxialized leaves, including the leaves of 35Spro:FIL plants [13], [14], rev recessive mutants harboring another enhancer mutations [10], [44], [45] and 35Spro:MIR165 plants [46]– [48]. [score:2]
On the other hand, the miR165/166-free domain in this stage was expanded compared to those in the early stages keeping the slight overlap with the FIL -expression domain. [score:2]
In this context, the candidates of the mobile factors are miR165/166, cytokinin and possibly tasiR-ARFs. [score:1]
The almost exclusive relationship between the abaxial FIL -expression domain and the adaxial miR165/166-free domain has been characterized well [25], [29]– [31]. [score:1]
Such situation roughly corresponds to phb-1d/+ mutant in which the cleavage efficiency for PHB mRNA by miR165/166 is reduced [80] and the speed of FMB shifting is faster than in the wild type. [score:1]
Such abaxial-specific genes include FIL and miR165/166. [score:1]
In this study, we characterized that the expression of FIL and the activity of miR165/166 are induced in all cells of initiating leaf primordia, and then repressed sequentially from the adaxial cells, thus gradually restricted to the abaxial cells. [score:1]
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3
[+] score: 60
Other miRNAs from this paper: ath-MIR165a
The allele phb-1d that expresses miRNA165/6-resistant PHB transcripts has ectopic PHB transcripts expressionZhou et al. (2007), Miyashima et al. (2011) PHB -| WOX5 In se mutants, which fail to repress PHB expression, embryonic WOX5 expression is absentGrigg et al. (2009) PHB → JKD jkd transcripts levels are reduced in the phb-1d miRNA-resistant PHB alleleMiyashima et al. (2011) CLE40 →  ACRCLE40p treatment strongly increased ACR expressionStahl et al. (2009) CLE40 -|  WOX5In cle40 mutants the WOX5 expression domain is expanded, and CLE40p treatment reduced WOX5 expression in the QCStahl et al. (2009) SHR → MGP The expression of MGP is severely reduced in the shr background. [score:17]
A CHIP-chip analysis detected JKD as a direct target gene of SHRWelch et al. (2007), Cui et al. (2011) SCR → JKD The post-embryionic expression of JKD is reduced in scr rootsWelch et al. (2007) SCR →  WOX5 WOX5 expression is reduced in shr mutantsSarkar et al. (2007) SHR →  WOX5 WOX5 expression is undetectable in scr mutantsSarkar et al. (2007) Auxin signalin pathway → WOX5 In mp or bdl mutants background WOX5 expression is rarely detectedSarkar et al. (2007) Auxin signalin pathway -|  WOX5In iaa17 mutants background WOX5 expression is decreasedDing and Friml (2010) SCR →  miRNA165/6In scr single mutants, miRNA165/6 expression is greatly reduced. [score:16]
Moreover, SHR and SCR promote miRNA165/6 expression, while miRNA165/6 represses PHB mRNA translation (Carlsbecker et al., 2010). [score:5]
Because our mo del does not incorporate space explicitly, we replaced molecular diffusion and movement by including a positive self-regulatory edge in nodes that move among cells (i. e., SHR, CLE, and miRNA165/6) to allow expression of these nodes where they move and no node positively regulates them. [score:5]
The miRNA165/6 moves from its transcription domain and negatively regulates the expression of HD-ZIP III genes in the stele (Carlsbecker et al., 2010). [score:4]
Overexpression of miR165 affects apical meristem formation, organ polarity establishment and vascular development in Arabidopsis. [score:4]
Their targets include the transcription factors JKD and MGP, as well as miRNA165/6 (Sozzani et al., 2010). [score:3]
A ChIP-PCR assay confirmed that SHR binds to miRNA165/6 promoterCarlsbecker et al. (2010), Miyashima et al. (2011) miRNA165/6 -|  PHBOver expression of miRNA165/6 causes a decrease in the transcript levels of PHB. [score:2]
A ChIP-PCR assay confirmed that SCR binds to miRNA165/6 promoterCarlsbecker et al. (2010), Miyashima et al. (2011) SHR →  miRNA165/6In shr single mutants, miRNA165/6 expression is greatly reduced. [score:2]
Cell signalling by microRNA165/6 directs gene dose -dependent root cell fate. [score:1]
Non-cell-autonomous microRNA165 acts in a dose -dependent manner to regulate multiple differentiation status in the Arabidopsis root. [score:1]
[1 to 20 of 11 sentences]
4
[+] score: 44
It is worth noting that at the chosen threshold, the false discovery rate is quite high (153/221), however, false positives (i. e. enriched regions not close to the targeted loci) are not a major concern for downstream analysis, because false positives, when later assembled into contigs during de novo assembly, will lack the sequence targeted by the probe (i. e. mature miR165/166). [score:5]
Successful enrichment at all MIR166 and MIR165 lociAn Arabidopsis genomic DNA sample prepared with the optimized targeted enrichment protocol was fragmented to an approximate mean size of 400 bp and sequenced on one lane of an Illumina GAIIx sequencer. [score:3]
Specifically, at the lower extreme of five reads per nt, the two MIR165 loci, whose enrichment level were the lowest among all targets due to one mismatch to the capture probe, were missing in the assembled contigs. [score:3]
Blue dots indicate targeted MIR165/166 loci. [score:3]
A targeted enrichment experiment, using the protocol optimized in Arabidopsis, was performed to enrich MIR165/166 loci in Zea mays (maize), whose genome is highly repetitive and 17 times the size of Arabidopsis genome [31]. [score:3]
At the intermediate coverage levels, for example, ten reads per nt, all targets but MIR165b (lowest enrichment, Fig. S2, 2 [nd] panel) were recovered (Table S4). [score:3]
With this threshold, seven out of the eight enriched regions flanking MIR165/166 loci were recovered (Fig. 4E–F, Fig. S2), the only exception being the MIR166e locus (Fig. 4B), possibly due to the secondary non-specific peak near the targeted locus confounding the linear dependence pattern. [score:3]
Alternatively, the failure of enrichment may be due to the fact that the maize genome is 20 times as large as Arabidopsis genome, and 11 distinct MIR165/166 loci are present in Z. mays compared to eight in Arabidopsis, so the potential targeted sites are diluted to one fifteenth in Z. mays. [score:2]
Seven out of the eight MIR165/166 loci were recovered in the assembled contigs, missing only MIR166c/MIR166d. [score:1]
Table S4 Quality of assembled MIR165/166 contigs. [score:1]
A peak enrichment of 100-fold or more was evident for the seven MIR166 loci in the genome with full complementarity to the capture probe, while a slightly lower peak of enrichment was evident for both MIR165 loci in the genome which have one mismatch to the probe (Fig. 2A–B). [score:1]
Analysis of repetitiveness of MIR165/166 flanking sequences in maize and Arabidopsis The maize reference genome was retrieved from http://ftp. [score:1]
All the loci with zero or one mismatches are MIR165 or MIR166 loci, and Student's t test revealed that the mean normalized coverage of loci with perfect complementarity and with one mismatch were both significantly different from the null hypothesis of one with p-values <0.01 and <0.05, respectively (Fig. 5A). [score:1]
Next, the enrichment pattern was assessed across the genome, focusing on all “enriched” regions regardless of whether or not they were MIR166 or MIR165 loci. [score:1]
Indeed, an analysis of the 20 kb flanking regions of 12 maize MIR166 loci showed an average 20mer frequency of 317 (Fig. S3A), while the average 20mer frequency of the 20 kb flanking regions was 6.6 for the nine Arabidopsis MIR165/166 loci (Fig. S3B). [score:1]
de novo assembly of enriched MIR166 and MIR165 loci. [score:1]
Indeed, the number of MIR165/166 loci recovered in the assembled contigs changed with varying read coverage. [score:1]
The same analysis was performed for the 9 Arabidopsis MIR165/166 loci and was shown in Fig. S3B. [score:1]
0083721.g006 Figure 6 de novo assembly of enriched MIR166 and MIR165 loci. [score:1]
After merging and extending, a total of 64 highly enriched regions were generated (Fig. S2), including all eight MIR165/166 loci (MIR166c and MIR166d are closely linked on chromosome five, and as such were merged into a single locus in this analysis). [score:1]
All contigs greater than one kb in length and having sequence complementary to the capture probe (identified by BLASTn against the miR166 sequence) were indeed MIR165/166 flanking regions (identified by BLASTn against the genome) (Fig. 6). [score:1]
This enriched locus had no sequence similarity to the MIR165/166 flanking regions (+/− 5 kb), nor did it exhibit similarity to rRNA sequences, thus ruling out simple explanations for its enrichment. [score:1]
Analysis of repetitiveness of MIR165/166 flanking sequences in maize and Arabidopsis. [score:1]
Shaded panels are regions surrounding the eight MIR165/166 loci (MIR166c and MIR166d are two bins apart, therefore are shown in the same panel). [score:1]
There are seven MIR166 loci with perfect matches to the probe, and two MIR165 loci with a single mismatch to the probe (miR165 and miR166 are highly similar miRNA families; Fig. 2A). [score:1]
Successful enrichment at all MIR166 and MIR165 loci. [score:1]
When observing the landscape of adjacent bins centered on a highly enriched bin, MIR165/166 flanking regions all exhibited a bell shape, reflecting lower enrichment further away from the probe binding site (Fig. 4A–B, Fig. S2, shaded panels), while other enriched regions generally showed only one or two highly enriched bins flanked by regions with a coverage close to the background level, possibly due to random amplification during sequencing or unannotated copy number variation relative to the reference genome assembly (Fig. 4C, Fig. S2, unshaded panels). [score:1]
[1 to 20 of 27 sentences]
5
[+] score: 41
Expression of a miR165/166 target mimic sequence (MIM165/166) in LS-CMV remarkably alters phenotypes of solanaceous species. [score:5]
We selected the miR165/166 TM sequence (MIM165/166) since, when expressed from LS-CMV, it efficiently inhibited miR165/166 activity in wild-type Arabidopsis plants 19. [score:5]
Leaves were also distorted in shape with reduced lamina area and production of enations from vein tissue on the abaxial surface (Fig. 3) indicative of disruption of adaxial/abaxial and medial/lateral features of leaf development that occur in plants when miR165/166 activity is inhibited 24. [score:4]
Importantly, the genes encoding miR165/166 and its target transcript HD-ZIP III have been evolutionarily conserved 24, making this system a good mo del for testing the efficacy of TM technology across multiple plant species. [score:3]
A pLS309 variant, pLS309-MIM165/166 carrying a miR165/166 target mimic sequence (MIM165/166) was described previously 19. [score:3]
In addition, a STTM sequence for miR165/166 expressed by a TRV variant launched by agroinfection induced phenotypic changes in N. benthamiana 16. [score:3]
Consistent with the effects seen on plant phenotype, we found that steady-state accumulation of miR165/166 was depressed in leaves of plants infected with LS-MIM165/166 (Fig. 4b), whilst in these tissues the accumulation of the target mRNA HD-ZIP III was elevated (Fig. 4c). [score:3]
It is worth noting that in N. benthamiana plants the expression of an STTM for miR165/166 from a TRV-derived vector did not cause such a strong phenotype as seen here. [score:3]
Using the protocol, we constructed pCB301-LS309-MIM165/166 and pCB301-LS309-MIM-CK by inserting the miR165/166 target mimic sequence (MIM165/166) and the microRNA-unrelated TM sequence (MIM-CK) adapted from the previous reports 13 19. [score:3]
Small leaves grew from the petioles of tobacco plants infected with LS-MIM165/166 (Fig. 3b), consistent with known roles of miR165/166 in regulation of meristematic activity 24. [score:2]
Quantitative analysis of tomato miR165/166 target HD-ZIP III transcript steady-state accumulation was carried out using reverse transcription-quantitative PCR as described previously 10 using primers for the tomato HD-ZIP III transcript described previously 27. [score:2]
Accumulation of viral RNA, miR165/166 and HD-ZIP III in tomato plants. [score:1]
We agroinfected leaves of plants of N. benthamiana, tobacco and tomato with mixtures of A. tumefaciens cells transformed with either pCB301-LS109 or pCB301-LS209, together with cells carrying either pCB301-LS309 (containing the wild-type LS -RNA3 sequence) or pCB301-LS309-MIM165/166 (containing the LS -RNA3 sequence modified to carry the miR165/166 TM sequence), or pCB301-LS309-MIM-CK (harboring the dummy TM). [score:1]
UC82) by LS-CMV and that no alteration in accumulation of miR165/166 or its star strand occurs during infection with this strain 22. [score:1]
Using TRV-STTM165/166 Sha and colleagues 16 noted evidence for some loss of apical dominance and production of enations but not the same drastic effects seen with the CMV- delivered TM for miR165/166 (Fig. 3a). [score:1]
However, by 28 dpi tomato plants agroinfected with LS-MIM165/166 showed stunting (Fig. 3c, upper panel), remarkable deformation of upper compound leaves (Fig. 3c, middle panel), and leaflets exhibited growth of enations from the veins on the abaxial surface (Fig. 3c, lower panel) which, as discussed above, is a hallmark of disrupted miR165/166 activity 24. [score:1]
[1 to 20 of 16 sentences]
6
[+] score: 40
Ectopic Expression of the HD-ZIPIII Genes PHB or PHV Is Sufficient for Seed Gene Expression in SeedlingsIt has been well established that the miR165/166 family miRNAs target the transcripts of the HD-ZIPIII genes, controlling their expression level and domain, to fulfill their roles in plant development including leaf polarity determination [42]– [45]. [score:10]
To demonstrate that the specific loss of miR166 can cause the ectopic expression of seed maturation genes, we obtained the recently developed transgenic lines that exhibit a dramatic reduction in miR165/166 accumulation achieved by the expression of a short tandem target mimic (STTM165/166) [41]. [score:7]
It has been well established that the miR165/166 family miRNAs target the transcripts of the HD-ZIPIII genes, controlling their expression level and domain, to fulfill their roles in plant development including leaf polarity determination [42]– [45]. [score:6]
Previous studies have shown that PHB and PHV promote embryonic development, and that the expression of these genes must be repressed by miR165/166 for embryonic development to proceed normally. [score:5]
Therefore, this work has added miR165/166 to the documented repertoire of postgermination repressors of the embryonic program (reviewed in [2]), and more importantly, established PHB, and possibly PHV, as direct positive regulators of the master regulator of seed maturation LEC2. [score:4]
miR165/166 is concentrated in the abaxial domain to restrict the expression of the HD-ZIPIII transcription factor genes to the adaxial domain in the lateral organs in Arabidopsis [42]– [44] and maize [45]. [score:3]
While our studies have established miR165/166 and implicated miR156 as players in the repression of the seed maturation program in vegetative development, two recent studies have also revealed important roles of miRNAs in regulating the morphogenesis-to-maturation phase transition [53], [54]. [score:3]
These studies focused on the roles of the miR165/166- PHB/PHV module in early embryo patterning. [score:1]
An obvious question is whether miR165/166 also acts similarly in early embryogenesis to control the morphogenesis-to-maturation phase transition. [score:1]
[1 to 20 of 9 sentences]
7
[+] score: 37
The expression of target PHB was downregulated at 12 h/RT (Fig.   4a), where as it was upregulated at 24 h/RT and 48 h/RT (Fig.   4a), indicating their post-transcriptional regulation by miR165/166 in these conditions. [score:12]
At 48 h/4 °C, miR165 expression was upregulated compared to DS but the expression of PHB was severely decreased in 48 h/4 °C (Fig.   4a). [score:7]
We validated the expression of  PHB (PHABULOSA) (Fig.   4a), PHV (PHAVOLUTA) (Fig.   4b), ATHB8 (Arabidopsis thaliana HOMEOBOX GENE8) (Fig.   4c) and ATHB15 (Arabidopsis thaliana HOMEOBOX GENE15) (Fig.   4d), which are targets of miR165/166. [score:5]
In cold imbibition (4 °C) condition at 12 h, miR165 expression was less compared to DS, where as PHB (Fig.   4a) expression was high. [score:4]
We observed significant upregulaion of miR165/166 in 12 h/RT and downregulation at 24 h/RT and 48 h/RT (Fig.   2a). [score:4]
The highest expression of miR165/166 was observed in case of 12 h/RT (Fig.   2a), which drastically changed in case of 12 h/4 °C. [score:3]
Previous reports implicated miR165/166 module in leaf, shoot, root vascular patterning (Zhou et al., 2007) and also in seed germination in maize [20] and rice [21]. [score:1]
The other miRNAs for validation were miR165/166 (Fig.   2a), miR172a (Fig.   2b), miR390b (Fig.   2c), miR160a (Fig.   2d), miR156h (Fig.   2e), miR164a (Fig.   3a), miR169b (Fig.   3b), miR161.1 (Fig.   3c), miR399a (Fig.   3d), miR824 (Fig.   3f), miR834 (Fig.   3g), miR854 (Fig.   3h) and miR2112-5p (Fig.   3i). [score:1]
[1 to 20 of 8 sentences]
8
[+] score: 36
Other miRNAs from this paper: ath-MIR165a
Additionally, the mo del points to some testable interactions that could occur either directly or indirectly and that may feed back to experimental work: that CKs upregulate APL, that KAN and ATHB-8 downregulate each other via MIR165/6, that ATHB-8 self-upregulates, and that AHP6 is regulated in the shoot as it is regulated in the root (positively by IAA and negatively by CKs). [score:14]
This set includes the HD-ZIP III gene ATHB-8, which is expressed in preprocambial and procambial cells [19], [20], and KANADI (KAN), which has been shown to downregulate HD-ZIP III genes in other contexts and has been suggested to downregulate ATHB-8 via miRNA165/6 (MIR) [10]. [score:9]
According to experimental evidence for the system under study (see Table 1 in File S1 for data supporting regulatory interactions and Table 2 in File S1 for a summary of expression and localization patterns), the hormone IAA, the peptide TDIF, and the microRNA MIR165/6 are able to move among the cells. [score:4]
It is not yet understood how the presence of KAN is confined to the phloem, but when we consider this mutual downregulation (mediated by MIR165/6, see Figure 2), the mo del can reproduce the expected cellular profiles, including that of the phloem. [score:4]
It has been shown, for example, that MIR165/6 is important for determining the different types of xylem cells (metaxylem and protoxylem) in the root [62], and future developments of this mo del could help in understanding the dynamics of such sub-differentiation. [score:2]
Importantly, TDIF and miRNA165/6 are able to diffuse between neighboring cells [7], [25]– [27]. [score:1]
The molecular details of such interaction have not been revealed, but it is proposed to be mediated by MIR165/6 [10]. [score:1]
In the case of TDIF and MIR165/6, the mobility is defined as diffusion and is given by the following equation: (2)where is the total amount of TDIF or MIR165 in cell. [score:1]
[1 to 20 of 8 sentences]
9
[+] score: 30
Other miRNAs from this paper: ath-MIR165a
We modified PHB so that it was not efficiently targeted for degradation by miR165/6, and then expressed it under the WOODEN LEG (WOL) promoter, which drives gene expression in stele cells in the root meristem [31] (S5 Fig. ). [score:7]
Previously, we reported that SHR -dependent expression of miR165/6 in the ground tissue layer quantitatively and spatially restricts HD-ZIP III expression within the stele, which is necessary for normal xylem tissue patterning [24]. [score:5]
We also observed that the short root phenotype of shr mutants could be partially recovered when miR165/6 was miss-expressed in the ground tissue or stele, suggesting that ectopic HD-ZIP III expression reduced root growth in this mutant. [score:5]
SCR regulates miR165/6 expression together with SHR [24]. [score:4]
Two types of modified PHB were used: one with a single silent mutation that partially interferes with miR165/6 binding (PHB-m) [24], and the other with four silent mutations that strongly block miR165/6 binding (PHB-em) (S4A Fig. ). [score:3]
In the root meristem of shr mutants, PHB is observed throughout the stele (S4B Fig. ), which results in the short root phenotype that can be rescued by the misexpression of miR165/6 in the ground tissue. [score:3]
In shr mutant plants, PHB, which in the meristem is actively restricted to the central region of the stele by SHORTROOT (SHR) via miR165/6, suppresses root meristem activity leading to root growth arrest. [score:3]
[1 to 20 of 7 sentences]
10
[+] score: 25
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-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-MIR398a, 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
miR165 affects shoot apical meristem development via the regulation of HD-ZIP III genes 51 52; miR172 mediates juvenile-to-adult transition by the suppression of several AP2 transcription factors 53; and miR773 targets a gene that encodes a DNA methyltransferase 36. [score:7]
miR163, miR169b/c, miR170, miR391, miR447, miR843 and miR848 were specifically upregulated, whereas miR159, miR162, miR164a/b, miR165, miR169d–g, miR172c/d, miR173, miR319, miR773, and miR864-3p were specifically downregulated by –C conditions. [score:7]
Under N limitation conditions, miR165, miR172c/d/e and miR773 were upregulated whereas under C starvation conditions, they were downregulated. [score:7]
Under –N conditions, miR165, miR167c, miR171b/c, miR172c–e, miR773, miR823, miR824, miR826, miR829.1, and miR842 were induced specifically, whereas miR157d, miR158a, miR161.2, miR400, miR447, miR822, miR833-5p, miR843, and miR852 were suppressed. [score:3]
In addition, the responses of miR165, miR172c/d/e, and miR773 to C starvation were opposite to that to N starvation. [score:1]
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11
[+] score: 21
Considering the wide range of downstream target genes (e. g. HD-ZIP III proteins), for the development of shoots and roots, the reduction of miR165/166 and subsequent accumulation of the target genes might account for the developmental and growth defects under Cs-toxicity (Fig 1). [score:7]
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]
Among the down-regulated miRNAs, it is worthwhile to take note of the miR165/166 family—consisting of seven individual MIR166 and two MIR165 genes—which specifically responded to CsCl-treatment. [score:4]
As shown in the radial chart in Fig 4C, expression of the miR157, miR160, miR165, miR168, miR171, miR319, and miR403 families was decreased by around 80% to 140% in CsCl -treated seedlings. [score:3]
In the case of KCl treatment, the miRNA counts of 4 families (miR156/miR157, miR169, miR394, and miR399) were reduced, whereas 9 families (miR159, miR164, miR165/miR166. [score:1]
[1 to 20 of 5 sentences]
12
[+] score: 14
In total about 86 targets genes were predicted among which most of them encode transcription factors (TFs) targeted by miR156, miR159, miR165, miR166, miR169, miR319, miR408, miR829, miR2934, miR5029 and miR5642. [score:5]
In addition, the sequencing results also revealed that various other stress-regulated miRNAs were expressed in response to LPS which include: miR161, miR165, miR166, miR167, miR168 miR401, miR403, miR405 and miR5635. [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]
are regulated by the identified miR156, miR159, miR165, miR166, miR169, miR319, miR408, miR829, miR2934, miR5029 and miR5642 (Tables  3 and 4). [score:2]
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13
[+] score: 14
ARGONAUTE1 (AGO1) affects the regulation of miR165/166, which stimulates the cleavage of HD-ZIPIIIs transcripts in cells located on the adaxial side (Kidner and Martienssen, 2004) whereas, AGO7/ZIPPY (ZIP) stabilizes ta-siR-ARF, which further targets the degradation of auxin-related transcription factors, ETTIN (ETT)/ARF3 and ARF4 on the abaxial side (Adenot et al., 2006; Hunter et al., 2006). [score:4]
AGO1 regulates miR165/66 which inhibits HD-ZIP III whereas AGO7 stabilizes ta-siR-ARF which causes the degradation of ARF3/4, which itself is controlled by auxin. [score:4]
Transcription factors, SHR (SHORT ROOT) and SCR (SCARECROW) activate miR165/166, which further inhibits HD-ZIP III. [score:3]
HD ZIP-III transcription factors are regulated by two members of GARS family of transcription factors, SHR (SHORT ROOT) and SCARECROW (SCR) which activate the genes encoding miR165/166 (Miyashima et al., 2013). [score:2]
Two small RNAs, the 21-nucleotide microRNA (miR165/166) and the 24-nucleotide transacting small interfering RNA (ta-siRNA), ta-siR-ARF, are also involved in determining leaf polarity (Chitwood et al., 2007, 2009; Nogueira et al., 2007). [score:1]
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14
[+] score: 14
In turn, the miR165/166 targets, the homeodomain-leucine zipper class III (HD-zip III) genes, have complicated overlapping and antagonistic roles in many aspects of meristem development [46– 49]. [score:4]
Thus, genetic manipulation of AGO10 or miRNA165/166 function would have a mixed effect by simultaneously promoting and inhibiting stem cell specification. [score:3]
Unlike AGO1, which has a broad ranging function in miRNA action [38– 42], AGO10 appears to be fairly specific for the miR165/166 family, where AGO10 paradoxically prevents these miRNAs from repressing their targets [35, 43– 45]. [score:3]
The failure to clearly identify AGO10, miR165/166 and the HD-zip III genes as representing a CLV/WUS-independent stem cell pathway despite intense study likely rests on two features of these regulators [34– 36, 43, 49]. [score:2]
Genetic alteration of miR165/166 function results in meristem defects [34, 43]. [score:1]
The ARGONAUTE10 gene modulates shoot apical meristem maintenance and establishment of leaf polarity by repressing miR165/166 in Arabidopsis. [score:1]
[1 to 20 of 6 sentences]
15
[+] score: 12
miRNA Position of Target Sites Arabidopsis Genes AtD27 MAX3 MAX4 MAX1 ath-miR156g - - - 302–323 ath-miR165a - - 950–971 842–861 ath-miR165b - 1469–1493 950–971 842–861 ath-miR166a-g - 1469–1493 951–971 842–861 1280–1301 ath-miR395b,c,f - - - 336–357 ath-miR401 - 1701–1725 - - - Rice Genes D27 D17/ HTD1 D10 OsMAX1 osa-miR444 47–70 557–581 172–154 458–478 1055–1076 363–380 221–239 1292–1318 osa-miR528 14–33 363–380 1192–1214 331–351 864–885 1113–1138 The effect of different hormone treatments on gene expression was checked for all of the Arabidopsis genes that are responsible for the strigolactone biosynthesis pathway. [score:5]
Moreover, some of the miRNAs that were identified regulate the activity of not only the MAX1, -3 and - 4 genes, but also TFs, which induces the expression of some of the genes that were investigated, such as miR165b whose target gene is ATHB9 [78]. [score:4]
The target sequences for seven different miRNAs (ath-miR165b; ath-miR166a-g) were found in the mRNA of all three MAX genes. [score:3]
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16
[+] score: 12
In addition, HD-ZIPIII genes are the targets of miR165/166 -mediated gene regulation, and its expression is repressed at the adaxial side. [score:6]
Leaf ad-ab patterning is regulated by several distinct transcription factor (TF) families, of which some are regulated by two kinds of small RNAs, namely, microRNAs (miR165/166) and trans-acting short interfering RNAs (TAS3-derived tasiR-ARF). [score:3]
Identification of leaf Ad-Ab patterning genes in B. rapaA total of 26 genes involved in leaf ad-ab patterning have been identified in A. thaliana, which include 17 genes encoding for seven TF families of leaf polarity determinants, namely, 6 adaxial determinants, 6 middle domain determinants, and 5 abaxial determinants; the remaining 9 genes are involved in the production and activity of small RNA determinants (miR165/166 and ta-siRNA) (Table 1). [score:1]
A total of 26 genes involved in leaf ad-ab patterning have been identified in A. thaliana, which include 17 genes encoding for seven TF families of leaf polarity determinants, namely, 6 adaxial determinants, 6 middle domain determinants, and 5 abaxial determinants; the remaining 9 genes are involved in the production and activity of small RNA determinants (miR165/166 and ta-siRNA) (Table 1). [score:1]
On the other hand, KANADI family genes (KAN1–3) (Eshed et al., 2001, 2004; Kerstetter et al., 2001), AUXIN RESPONSE FACTORS (ARF) ETTIN (ETT/ARF3) and ARF4 (Pekker et al., 2005), and miR165/166 small RNAs (Kidner and Martienssen, 2004) are abaxial-specific. [score:1]
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17
[+] score: 9
Other miRNAs from this paper: ath-MIR165a, ath-MIR394a, ath-MIR394b
In the absence of ZLL function, AGO1 is proposed to bind miR165/6 and down-regulate Class III HD-ZIP transcription factors within the embryonic SAM, thereby inducing stem cell differentiation [17]. [score:4]
In combination with a zll mutation, which allows AGO1 greater access to miR165/166, increased levels of SQN in Ler-0 enhance repression of AGO1 targets, such as the Class III HD-ZIPs, and lead to a high frequency of terminal stem cell differentiation. [score:4]
Recent biochemical and genetic evidence suggests that in the embryo, ZLL acts as a miRNA “locker” to sequester microRNA165/6, thereby limiting its incorporation into the active AGO1 RNA-Induced Silencing Complex (RISC) [12, 16]. [score:1]
[1 to 20 of 3 sentences]
18
[+] score: 9
Other miRNAs from this paper: ath-MIR165a, ath-MIR166g, ath-MIR394a, ath-MIR394b
miRNA165/166, are mobile signaling molecules that suppress CK signaling via inhibition of CK production [58, 59]. [score:5]
Overexpression of miR165 affects apical meristem formation, organ polarity establishment and vascular development in Arabidopsis. [score:4]
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19
[+] score: 8
It was possible to confirm predicted target downregulation for other induced conserved miRNA families, including miR394, miR165 and miR171 which target an F-box family protein, an ATHB transcription factor and a scarecrow-like transcription factor, respectively (Figure 3). [score:8]
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20
[+] score: 7
Targets of miR165/166, including the transcription factor-encoding genes PHAVOLUTA and PHABULOSA, control leaf polarity, and dominant mutations that disrupt the miRNA target site in these genes cause severe alterations in leaf morphology [47]– [49]. [score:6]
NAC1, CUC1, CUC2, ANAC079, ANAC092, ANAC100, AT3G12977 1 MIM165/166 miR165/miR166 Rounder leaves. [score:1]
[1 to 20 of 2 sentences]
21
[+] score: 6
For example, miR159, miR165, miR166, and miR168 are usually incorporated into AGO1 -based RISCs, but associate with other AGOs in AGO1 -deficient Arabidopsis mutants, where this redirection is supposed to be mediated by stabilizing proteins (Vaucheret, 2009; Zhu et al., 2011). [score:2]
For example, the miR165 and miR166 families were surmised to be bound by AGO10 as opposed to AGO1 because of the higher number of unpaired bases than can be tolerated by AGO1 (Zhu et al., 2011). [score:1]
The members of the miR165/166 families contain a 5′-uridine, but are specifically associated with AGO10 instead of AGO1 (Zhu et al., 2011). [score:1]
AGO10 predominantly associates with members of miR165/166 family containing a 5′-uridine (Zhu et al., 2011). [score:1]
By contrast, AGO10 (also referred to as ZWILLE or PINHEAD) specifically associates with members of the miR165 and miR166 families (Mallory et al., 2009; Zhu et al., 2011). [score:1]
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22
[+] score: 6
The five miRNA targets examined, AtAGO1 (miR168), DCL1 (miR162), PHABULOSA (PHB) (miR165/166), MYB33 (miR159), and CUP-SHAPED COTYLEDONS 2 (CUC2) (miR164), all showed elevated un-cleaved mRNA abundances in ago1–27 plants relative to wild type (Figure 2B), consistent with what has previously been reported (Morel et al., 2002). [score:3]
While AtAGO10 associates with miRNAs and is capable of cleaving target transcripts in vitro, it is not an efficient gene-silencer in vivo and instead attenuates AtAGO1 -associated miRNA activity by sequestering miRNAs, having a particular preference for miR165/166 (Zhu et al., 2011). [score:3]
[1 to 20 of 2 sentences]
23
[+] score: 5
miR165 and miR166 are the two miRNAs that differ by only one nucleotide in their mature sequence and both target transcripts of same HD-ZIP III gene family members [13]. [score:3]
Carlsbecker A Cell signalling by microRNA165/6 directs gene dose -dependent root cell fateNature. [score:1]
Arabidopsis genome encodes seven MIR166 (MIR166A– G) and two MIR165 (MIR165A-B), which finally produce same mature miR166 and miR165, respectively. [score:1]
[1 to 20 of 3 sentences]
24
[+] score: 5
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]
[1 to 20 of 1 sentences]
25
[+] score: 5
Other miRNAs from this paper: ath-MIR165a
In the SAM, HD-ZIPIII genes are negatively regulated by miRNA165/6, which, in turn, are direct targets of the dimer SHR/SCR [55]. [score:5]
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26
[+] 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]
[1 to 20 of 1 sentences]
27
[+] score: 4
On the contrary, miR156, miR158, miR164, miR165, miR400, miR5654, miR775, miR829, miR838 and miR852 were down-regulated by TCV infection. [score:4]
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28
[+] score: 4
[50] CK-|MIR166 Cytokinin treatment strongly represses the expression of MIR165 in the RAM. [score:3]
[30]PHB– | MIR166 In computational simulations, the mutual degradation between MIR165/6 and PHB create sharp boundaries between the MIR165/6 and PHB activity domains. [score:1]
[1 to 20 of 2 sentences]
29
[+] score: 4
Other miRNAs from this paper: ath-MIR165a
PHABULOSA, which is a microRNA target, is methylated in a short region located downstream of the ath-miR165/166 recognition site, which lies, quite unusually, at a splice junction [38]. [score:3]
Further support for this idea comes from the observation that, ATHB8, a Chromosome 4 homolog of PHABULOSA, which also matches ath-miR165/166, does not have detectable methylation in either Ler or Col. [score:1]
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30
[+] score: 4
During early seedling development the regulation mediated by the presence of miR165, miR166, miR164, and miR319 is of special importance for germination and developmental phase transitions (Wang and Li, 2007; Rubio-Somoza and Weigel, 2011). [score:4]
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31
[+] score: 3
Prigge and Clark [73], and Floyd and Bowman [75] have previously suggested that HD-Zip III sequences across all land plants produce transcripts that could be targeted by miRNA165 and miRNA166. [score:3]
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32
[+] score: 3
Based on A. thaliana annotation, miRNA target genes were found for several conserved miRNAs in hybrid yellow poplar (Table S4): ARF10 (miR160), CYP96A1 (miR162), NAC (miR164), PHB and DNA -binding factor (miR165/166), NF-YA8 (miR169), SCARECROW transcription factor family protein (miR170/171), SNZ (miR172), MYB (miR319), GRF (miR396), copper ion binding (miR408), SPL11 (miR529) etc. [score:3]
[1 to 20 of 1 sentences]
33
[+] score: 2
Other miRNAs from this paper: ath-MIR165a, ath-MIR166b
Cell signalling by microRNA165/6 directs gene dose -dependent root cell fate. [score:1]
Non-cell-autonomous microRNA165 acts in a dose -dependent manner to regulate multiple differentiation status in the Arabidopsis root. [score:1]
[1 to 20 of 2 sentences]
34
[+] score: 2
Other miRNAs from this paper: ath-MIR165a, ath-MIR394a, ath-MIR394b
For example, the endogenous miRNAs miR165/6, tasiRNA (tasiR-ARF), and miR394 serve as morphogen-like signals, forming gradients to determine cell fate during leaf and root development (Chitwood et al., 2009; Carlsbecker et al., 2010; Skopelitis, Husbands & Timmermans, 2012; Knauer et al., 2013). [score:2]
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35
[+] score: 2
Gene ID microRNA At1g30490 mir165a, mir165b, mir166a, mir166b, mir166c, mir166d, mir166e, mir166f, mir166g At1g30210 mir319a, mir319b. [score:1]
mir165 [97] HD-ZIPIII family members including PHV, PHB, REV, ATHB-8, and ATHB-15 mir166 [97] HD-ZIPIII family members including PHV, PHB, REV, ATHB-8, and ATHB-15 mir167 [93] ARF family members ARF6 and ARF8. [score:1]
[1 to 20 of 2 sentences]
36
[+] score: 2
The partial results are shown in Table  5, and the complete results are available in Additional file 5. Table 5 Top 5 prediction results for miRNAs responding to high-salt conditions and TMV-Cg stress Stress miRNA Score High-salt ath-miR418 0.932 ath-miR166 0.929 ath-miR160 0.908 ath-miR841 0.892 ath-miR169 0.816 TMV-Cg ath-miR165 1.000 ath-miR156 0.939 ath-miR418 0.932 ath-miR160 0.908 ath-miR8177 0.899 To our knowledge, most of the existing methods mentioned previously have not been implemented as publicly available software packages. [score:1]
We also predicted several new miRNAs that are likely to respond to the TMV-Cg virus, including miR165 [36, 37], miR156 [34, 38], miR418, miR160 [36, 38], and miR393 [36, 37, 39]. [score:1]
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37
[+] score: 2
Our data indicate that 3 microRNAs, miR159, miR165, miR171b,c are enriched in the sporophyte while the remaining 14 microRNAs were pollen enriched. [score:1]
We performed qRT-PCR on a subset of 17 microRNAs, ranging from those frequently detected (miR156 and miR161, with respectively 59 and 45 reads) to singletons (miR162, miR171a, miR171bc, and miR773), and including those showing 1 or 2 sequence mismatches (miR162, miR165, miR173 and miR773, see Additional file 1: Table S1). [score:1]
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38
[+] score: 1
Accumulations of miR159, miR168 and miR165 are insensitive to decreased DCL1 activity unlike other miRNAs such as miR173, indicative of alternative dicer activity for the processing of these miRNAs [51]. [score:1]
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39
[+] score: 1
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157a, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR165a, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR169a, ath-MIR172a, ath-MIR172b, ath-MIR159b, ath-MIR319a, ath-MIR319b, 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-MIR166a, osa-MIR166b, osa-MIR166c, osa-MIR166d, osa-MIR166e, osa-MIR166f, osa-MIR167a, osa-MIR167b, osa-MIR167c, osa-MIR169a, 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-MIR172c, ath-MIR172d, ath-MIR394a, ath-MIR394b, ath-MIR396a, ath-MIR396b, osa-MIR394, osa-MIR396a, osa-MIR396b, osa-MIR396c, ath-MIR403, ath-MIR408, ath-MIR156g, ath-MIR156h, ath-MIR159c, ath-MIR319c, ath-MIR167c, ath-MIR172e, osa-MIR156k, osa-MIR156l, osa-MIR159a, osa-MIR159b, osa-MIR159c, osa-MIR159d, osa-MIR159e, osa-MIR159f, osa-MIR319a, osa-MIR319b, osa-MIR160e, osa-MIR160f, osa-MIR166k, osa-MIR166l, osa-MIR167d, osa-MIR167e, osa-MIR167f, osa-MIR167g, osa-MIR167h, osa-MIR167i, 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-MIR172a, osa-MIR172b, osa-MIR172c, osa-MIR166g, osa-MIR166h, osa-MIR166i, osa-MIR408, osa-MIR172d, osa-MIR167j, osa-MIR166m, osa-MIR166j, ath-MIR414, osa-MIR414, osa-MIR396e, ath-MIR856, ath-MIR858a, osa-MIR169r, osa-MIR396f, ath-MIR2111a, ath-MIR2111b, osa-MIR396g, osa-MIR396h, osa-MIR396d, ath-MIR858b, ath-MIR156i, ath-MIR156j
Most of the miRNA families were found to be conserved in a variety of plant species e. g. using a comparative genomics based strategy homologs of miR319, miR156/157, miR169, miR165/166, miR394 and miR159 were found in 51,45,41,40,40 and 30 diverse plant species respectively [38]. [score:1]
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[+] score: 1
Other miRNAs from this paper: ath-MIR165a
In accordance with this hypothesis, the microRNA 165/166 is absent in shr and scr mutants [38], and HD-ZIP III mRNA is not degradated, but ectopic metaxylem is formed, in the miR165/166-resistant phb-7d mutant [2]. [score:1]
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[+] score: 1
This pattern was specific to the MIR166g precursor and was not observed in any of the other eight MIR165 or MIR166 genes. [score:1]
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[+] score: 1
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157a, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR165a, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR169a, ath-MIR170, ath-MIR171a, ath-MIR172a, ath-MIR172b, ath-MIR159b, ath-MIR319a, ath-MIR319b, osa-MIR156a, osa-MIR156b, osa-MIR156c, osa-MIR156d, osa-MIR156e, osa-MIR156f, osa-MIR156g, osa-MIR156h, osa-MIR156i, osa-MIR156j, 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-MIR172c, ath-MIR172d, ath-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, osa-MIR395b, osa-MIR395d, osa-MIR395e, osa-MIR395g, osa-MIR395h, osa-MIR395i, osa-MIR395j, osa-MIR395k, osa-MIR395l, osa-MIR395s, osa-MIR395t, osa-MIR395c, osa-MIR395a, osa-MIR395f, osa-MIR395u, osa-MIR399a, osa-MIR399b, osa-MIR399c, osa-MIR399d, osa-MIR399e, osa-MIR399f, osa-MIR399g, osa-MIR399h, osa-MIR399i, osa-MIR399j, osa-MIR399k, ath-MIR401, ath-MIR156g, ath-MIR156h, ath-MIR159c, ath-MIR319c, ath-MIR172e, osa-MIR156k, osa-MIR156l, osa-MIR159a, osa-MIR159b, osa-MIR159c, osa-MIR159d, osa-MIR159e, osa-MIR159f, osa-MIR319a, osa-MIR319b, 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-MIR172a, osa-MIR172b, osa-MIR172c, osa-MIR166g, osa-MIR166h, osa-MIR166i, osa-MIR171h, osa-MIR172d, osa-MIR171i, osa-MIR166m, osa-MIR166j, ath-MIR413, ath-MIR414, ath-MIR415, ath-MIR416, ath-MIR417, osa-MIR413, osa-MIR414, osa-MIR415, osa-MIR416, osa-MIR417, ath-MIR426, osa-MIR426, osa-MIR438, osa-MIR444a, ptc-MIR156a, ptc-MIR156b, ptc-MIR156c, ptc-MIR156d, ptc-MIR156e, ptc-MIR156f, ptc-MIR156g, ptc-MIR156h, ptc-MIR156i, ptc-MIR156j, ptc-MIR156k, ptc-MIR159a, ptc-MIR159b, ptc-MIR159d, ptc-MIR159e, ptc-MIR159c, 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-MIR172a, ptc-MIR172b, ptc-MIR172c, ptc-MIR172d, ptc-MIR172e, ptc-MIR172f, ptc-MIR172g, ptc-MIR172h, ptc-MIR172i, ptc-MIR319a, ptc-MIR319b, ptc-MIR319c, ptc-MIR319d, ptc-MIR319e, ptc-MIR319f, ptc-MIR319g, ptc-MIR319h, ptc-MIR319i, ptc-MIR395a, ptc-MIR395b, ptc-MIR395c, ptc-MIR395d, ptc-MIR395e, ptc-MIR395f, ptc-MIR395g, ptc-MIR395h, ptc-MIR395i, ptc-MIR395j, ptc-MIR399a, ptc-MIR399b, ptc-MIR399d, ptc-MIR399f, ptc-MIR399g, ptc-MIR399h, ptc-MIR399i, ptc-MIR399j, ptc-MIR399c, ptc-MIR399e, ptc-MIR481a, ptc-MIR482a, osa-MIR395m, osa-MIR395n, osa-MIR395o, osa-MIR395p, osa-MIR395q, osa-MIR395v, osa-MIR395w, osa-MIR395r, ptc-MIR171k, osa-MIR169r, osa-MIR444b, osa-MIR444c, osa-MIR444d, osa-MIR444e, osa-MIR444f, ptc-MIR171l, ptc-MIR171m, ptc-MIR171j, osa-MIR395x, osa-MIR395y, ath-MIR156i, ath-MIR156j, ptc-MIR482d, ptc-MIR156l, ptc-MIR169ag, ptc-MIR482b, ptc-MIR395k, ptc-MIR482c
In Arabidopsis, only the miR171 family is divided in two families, and the following miRBase families are pairwise grouped together: MIR319–MIR159, MIR156–MIR157, MIR165–MIR166, and MIR170–MIR171. [score:1]
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In Arabidopsis, miR156, miR158, miR159, miR165, miR167, miR168, miR169, miR171, miR319, miR393, miR394 and miR396 are drought-responsive. [score:1]
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The regulators of abaxial identity are microRNA165/166 and LITTLE ZIPPER (ZPR), which both repress HD-ZIP (Mallory et al., 2004; Wenkel et al., 2007); KANADI (KAN), which is repressed by AS2 (Wu et al., 2008); ETTIN/ARF3, which is repressed by AS2 and tasiRNA (Garcia et al., 2006; Iwasaki et al., 2013; Takahashi et al., 2013). [score:1]
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