sort by

43 publications mentioning ath-MIR164b

Open access articles that are associated with the species Arabidopsis thaliana and mention the gene name MIR164b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 183
These four plant lines with either wild-type miR164 and target gene levels (Figure S4A; Col-0 and drb35), or reduced miR164 accumulation and up-regulated target gene expression (Figure S4B; drb1 and drb12), all develop rosette leaves with smooth margins and inflorescence stems that are not fused. [score:10]
Although DRB2 was expressed at low levels in Col-0 seedlings and floral tissues, no change in miR164 accumulation or target gene expression was observed in the corresponding tissue of drb235 plants. [score:7]
MiR164 accumulation and target gene expression are also reduced and up-regulated respectively in drb12 plants, however these changes are not as severe as those detected in drb1 plants. [score:7]
Our analyses suggest that loss of CUC1 expression and reduced CUC2 levels in the specific tissues where miR164 accumulation is elevated in the absence of DRB2 activity, namely the SAM region, directs the rosette leaf margin serration phenotype expressed by drb2, drb23, drb25 and drb235 plants. [score:6]
Taken together, these results suggest that these two closely related targets have different DRB requirements for regulation of their wild-type expression by miR164. [score:6]
Unlike CUC1 and CUC2, CUC3 does not contain a miR164 target sequence, however, CUC3 expression has been shown to be regulated by these two closely related family members [33], [34]. [score:6]
0035933.g004 Figure 4. (A) miR164 accumulation, MIR164 precursor transcript processing and target gene expression in the SAM region of drb1, drb2 and drb12 plants. [score:5]
In addition to Col-0, the drb35 double mutant was also included in these analyses as a wild-type control for miR164 accumulation, target gene expression (Figure 2A), leaf margin serration and inflorescence stem architecture (Figures 1A and 1B). [score:5]
RT-PCR analysis revealed that DRB2, together with the miR164 targets CUC1 and CUC2 showed high levels of overlapping expression in the Col-0 SAM region sample (Figure 3A). [score:5]
Changes to miR164 accumulation and/or the expression of two of its target genes, CUC1 and CUC2 are associated with alterations to rosette leaf margin serration as well as defects in SAM formation and cotyledon, sepal and stamen separation [31], [37], [38]. [score:5]
Furthermore, RT-PCR analysis revealed that in accordance with enhanced precursor transcript processing and mature miRNA accumulation, the expression levels of two of the targets of miR164, namely CUC1 and CUC2 were reduced. [score:5]
Northern blotting showed that miR164 accumulation was highly elevated in the corresponding tissue of drb235 plants and in accordance RT-PCR revealed a corresponding loss of target gene expression. [score:5]
The observed reduction in CUC3 levels in all four of the analyzed drb2-containing backgrounds suggested that miR164 target gene expression was indeed reduced in the same tissues where miR164 levels were shown to be elevated by northern blotting. [score:5]
To further assess the influence of the miRNA precursor transcript on DRB1- and DRB2 -mediated miRNA-directed silencing, the endogenous miRNA sequences of PRI-MIR164B and PRI-MIR169A were replaced with an identical artificial miRNA (amiRNA) sequence targeting PHYTOENE DESATURASE (PDS; amiR-PDS) for amiRNA-directed RNA silencing. [score:5]
The analyses presented in Figure 3B show that in the SAM region of drb1 plants, miR164 accumulation is significantly reduced and that the expression of its target genes, CUC1 and CUC2 is proportionately elevated. [score:5]
RT-PCR revealed a direct correlation between precursor transcript processing efficiency, PRI-MIR164A and PRI-MIR164B expression, and miRNA accumulation in these three drb mutant lines. [score:4]
MiR164 accumulation, along with DRB2, CUC1 and CUC2 expression was therefore assessed in specific tissues of Col-0 and drb235 plants to correlate these expression changes with the drb235 phenotype. [score:4]
Taken together, these results again associated the loss of DRB2 activity with enhanced PRI-MIR164B processing, mature miR164 (amiR-PDS) accumulation and sRNA-directed target gene (PDS) silencing (Figure 5B). [score:4]
To further test the association between tissue-specific elevation of miR164 accumulation with the drb235 developmental phenotype, miR164, CUC1 and CUC2 levels were assessed in additional drb mutants that also have altered miR164 accumulation but do not express the rosette leaf margin serration or inflorescence stem fusion defects of drb235 plants. [score:4]
In addition, T-DNA insertion knockouts of the MIR164A locus or plants engineered to express a miR164-resistant version of CUC2 (CUC2g-m4 plants), develop highly serrated rosette leaves [31], [34], [45]. [score:4]
In contrast, miR164 -mediated CUC1 and CUC2 expression is deregulated in drb1 and drb12 plants where miR164 levels are reduced and both of these mutant lines display rosette leaves with smooth margins (Figures 3B and S4B). [score:4]
These tissue-specific alterations to miR164 accumulation and target transcript expression could account for the phenotypic differences displayed by our drb mutant lines and those previously characterized for plants lines where miR164, CUC1 and CUC2 levels are altered in all tissues and throughout all stages of development. [score:4]
The leaf margins of cuc1-13 plants are indistinguishable from those of Col-0 plants and rosette leaves with smooth margins are displayed by the cuc2-3 mutant or by plants ectopically over -expressing miR164 precursor transcripts [30], [31], [33]. [score:3]
PRI-MIR164A and PRI-MIR164B expression was reduced in drb2, but the level of each precursor transcript was increased in drb1 and drb12 plants. [score:3]
This indicates that the inflorescence stem fusions observed in drb235 plants result from tissue-specific elevation of miR164 accumulation and a corresponding loss of CUC1 and CUC2 expression. [score:3]
In our series of drb mutants, including drb2, drb23, drb25 and drb235 plants, all of which were shown to have elevated miR164 levels and corresponding reductions or complete loss of CUC1 and CUC2 expression, developed rosette leaves with serrated margins (Figures 1A, 3B and S4). [score:3]
In the same tissues in the drb235 triple mutant however, enhanced miR164 accumulation results in the complete loss of both CUC1 and CUC2 expression. [score:3]
These analyses also revealed that enhanced mature miR164 accumulation in the absence of DRB2 expression is tissue-specific. [score:3]
Modification of PRI-MIR164B and PRI-MIR169A to replace their endogenous sRNA silencing signals with the same PDS -targeting amiRNA confirmed that the antagonistic and synergistic action of DRB2 on DRB1 function in miRNA biogenesis occurs at the pri-miRNA level. [score:3]
RT-PCR analysis of pri-miRNA expression suggested that the enhanced accumulation of miR164 observed in the drb2, drb23, drb25 and drb235 mutant backgrounds resulted from more efficient processing of the precursor transcripts, PRI-MIR164A and PRI-MIR164B in the absence of DRB2 activity (Figure 2A). [score:3]
A similar trend was also observed for the drb235 inflorescence stem sample where the loss of DRB2 activity was demonstrated to result in enhanced miR164 accumulation and a corresponding loss of CUC1 and CUC2 expression (Figure 3A). [score:3]
Elevated miR164 accumulation in the SAM region of drb2 plants leads to the loss of CUC1 expression and significantly reduced levels of CUC2 (Figure 3B). [score:3]
In this tissue (Figure 3A), and in the SAM region of drb235 plants (Figures 2A and 3A), the elevated levels of miR164 completely represses CUC1 and CUC2 expression. [score:3]
Previous genetic analyses have shown that CUC1 and CUC2 are functionally redundant and that plants defective for CUC1 and CUC2 activity, including the cuc1 cuc2 double mutant, or plants engineered to constitutively and ubiquitously express either the MIR164A or MIR164B precursor transcript, display vegetative and floral organ fusion defects [30], [33], [37], [38], [44]. [score:3]
The tissue-specific over -expression of miR164. [score:3]
As demonstrated for miR164 and miR169, Figure S3B shows that the levels of two additional miRNAs, specifically miR841 and miR170 (Table 1), are elevated and reduced respectively in the absence of DRB2 expression (Figure S3A). [score:3]
0035933.g003 Figure 3(A) Northern blot assessment of miR164 accumulation and RT-PCR analysis of DRB2, CUC1 and CUC2 expression in specific tissues collected from Col-0 and drb235 plants. [score:3]
Plants lacking miR164c accumulation or ectopically expressing either the MIR164A or MIR164B precursor transcript produce abnormal floral organs as a consequence of altered CUC1 and CUC2 activities [30], [31], [39]. [score:3]
The moderate increase in PRI-MIR164A and PRI-MIR164B levels in drb12 plants compared to their higher levels of expression in drb1 plants correlated with elevated miR164 accumulation in the double mutant (Figure 4A). [score:2]
However, molecular analyses, as demonstrated by northern blotting and RT-PCR, showed that the over-accumulation of the PRI-MIR164B- delivered sRNA in the absence of DRB2 activity, resulted in additional severe reductions to overall plant growth and development in drb2/amiR [164B]-PDS and drb235/amiR [164B]-PDS plants. [score:2]
Curiously, the phenotypic consequences of altered miR164, CUC1 and CUC2 levels on rosette leaf margin development reported here contrast with those described previously. [score:2]
Northern blotting showed that in wild-type plants, miR164 levels are spatiotemporally regulated. [score:2]
The data presented in Figure 4A suggests that in the absence of DRB2 activity in drb12 plants, miR164 precursor transcripts are more freely available to enter the canonical miRNA biogenesis pathway mediated by the DCL1/DRB1 partnership, but in this double mutant plant DCL1 cannot efficiently process the increased levels of available substrate as it is also defective in DRB1 activity. [score:1]
Figure S4 Leaf margin phenotypes displayed by drb mutants with altered miR164, CUC1 and CUC2 levels in the SAM region. [score:1]
This suggests that other tissues collected as part of the seedling sample, including cotyledons, young leaves and roots are masking the observed changes in miR164, CUC1 and CUC2 levels in the SAM region of drb235 seedlings. [score:1]
This suggests that in wild-type plants, DRB2 does not interact with the PRI-MIR164C transcript and that the tissue-specific elevation of miR164 accumulation observed in plants lacking the activity of DRB2 results from a loss of the repressive effects of DRB2 on DCL1/DRB1 -mediated, PRI-MIR164A and PRI-MIR164B processing (Figure 2A). [score:1]
The modified PRI-MIR164B and PRI-MIR169A sequences were cloned into pART7 using the introduced XhoI/ EcoRI and XbaI/ HindIII restriction sites. [score:1]
The accumulation of the elevated miRNA class representative, miR164, was enhanced in all plant lines lacking DRB2 activity (Figures 2A and S3A). [score:1]
Northern blotting revealed a clear association between the loss of DRB2 activity (Figure S3A) and enhanced mature sRNA accumulation for the elevated miRNA class representative, miR164 (Figure 2A). [score:1]
Unlike drb1 and drb12 plants, altered miR164 accumulation correlates with the observed changes to rosette leaf margin serration and/or inflorescence stem architecture in drb2 and drb235 plants. [score:1]
The drb235 phenotype results from the tissue-specific elevation of miR164 accumulation. [score:1]
Genomic fragments containing the PRI-MIR164B (AT5G01747) and PRI-MIR169A (AT3G13405) sequences and flanking regulatory regions were amplified by PCR with primer pairs pMIR164B-F1/R1 and pMIR169A-F1/R1 and cloned into the pGEM-T Easy cloning vector to produce pGEM-T: MIR164B and pGEM-T: MIR169A respectively. [score:1]
We and others have previously shown that DRB1 is required for the biogenesis and wild-type accumulation of the miR164 sRNA [7], [40]. [score:1]
RT-PCR analysis of drb1, drb2 and drb12 plants revealed that the observed changes to miR164 and miR169 levels in these three mutant lines was a result of alterations to precursor transcript processing efficiency (Figure 4). [score:1]
[1 to 20 of 54 sentences]
2
[+] score: 159
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c
These data show that a mutation in the regulatory binding domain of the MIR164 target site of the CUC2 mRNA is also able to suppress the hws fused sepal phenotype. [score:7]
We propose that HWS regulates a target that directly or indirectly modulates MIR164B and MIR164C which, in turn, negatively regulates CUC1 and CUC2 to control formation of sepal boundaries and floral organ number. [score:7]
Overexpressing HWS results in a decreased transcript level of MIR164, suggesting that the target of HWS play an important role in regulating MIR164, either in their production, function or degradation; indeed, our own work and that of [42] propose a role for HWS in the microRNA pathway. [score:6]
[46] reported that RBE regulates the expression of all three MIR164 genes, and that RBE interacts with the promoter of MIR164C, a gene that has been reported to be involved in the regulation of petal number in Arabidopsis [20]. [score:5]
In our material, we could not detect changes of expression of MIR164A, suggesting that regulation for each MIR164 gene may be different and MIR164B and MIR164C are regulated by HWS. [score:5]
cuc2-1D carries a transversion mutation (G→T) in the CUC2 mRNA regulatory binding domain of the MIR164 target site ([24]; Fig 2D). [score:5]
These results suggest that the sepal fusion phenotype observed in the hws-1 mutant, which phenocopies the sepal fusion of a MIR164B overexpressing line [21, 22], is due to an increase of MIR164B and MIR164C levels, while overexpressing the HWS gene results in a decrease of transcript levels of MIR164C. [score:5]
Mutation of the MIR164 target domain in CUC1 or CUC2 results in an over-accumulation of MIRNA164B and MIRNA164C transcripts, suggesting a feedback loop mechanism where higher levels of CUC1 or CUC2 mRNA trigger the accumulation of MIRNA164B and MIRNA164C to reduce the higher levels of CUC transcript. [score:4]
The cuc1-1D mutation introduces a substitution (G→A) in the CUC1 MIR164 target site (nucleotide 9/21 from the 5’ end; Fig 2B). [score:4]
Schematic diagram of MIR164, MIR164 complementary binding sites in CUC1 and CUC2 mRNAs and CUC1, CUC2 proteins or their equivalent in generated constructs; (A), wild type (B), cuc1-1D mutation; (C), cuc1-1D mutation and MIR164 modified site introduced for complementation analyses; (D), cuc2-1D mutation (modified from [24]); (E), cuc1-1D silent version (cuc1-1D-SV). [score:4]
Our results suggest that CUC1 regulates MIR164 directly or indirectly via a feedback loop mechanism. [score:4]
The mutant shs1 in hws-1 suppresses the sepal fusion phenotype and carries a transition in the MIR164 binding domain of CUC1To further understand the molecular mechanism of HWS in plant development, we mutagenized hws-1 seeds (Columbia background) with ethylmethylsulphonate (EMS) and screened for revertants of the hws-1 floral sepal fusion phenotype. [score:4]
These data support the assertion that the single point mutation in the binding domain of MIR164 is sufficient to suppress the floral fusion phenotype of hws mutants. [score:4]
Introgression of the cuc2-1D mutation into hws-1 suppresses the sepal fusion phenotypeThe MIR164 binding sites are identical in CUC1 and CUC2 (Fig 2A). [score:4]
A feedback loop mechanism between MIR164 and CUC is present in flowersThe cuc1-1D mutation introduces a substitution (G→A) in the CUC1 MIR164 target site (nucleotide 9/21 from the 5’ end; Fig 2B). [score:4]
This mutation is located in the binding domain of the MIR164 target site of CUC1 [21, 25] and introduces the amino-acid substitution cysteine→ tyrosine in CUC1 (Fig 2A and 2B). [score:4]
The sepal fusion phenotype observed in the hws-1 mutant, which phenocopies the sepal fusion of a MIR164B overexpression line [21, 22], is likely due to an increase of MIR164B and MIR164BC levels. [score:3]
The mutant shs1 in hws-1 suppresses the sepal fusion phenotype and carries a transition in the MIR164 binding domain of CUC1. [score:3]
We hypothesize that HWS contributes to boundary formation and regulation of organ number by indirectly altering transcripts of MIR164, CUC1 and CUC2. [score:3]
Constitutively expressing the MIR164B gene results in plants showing partial fusion of cotyledons and floral organs comparable to double mutant cuc1/ cuc2 plants. [score:3]
Interestingly, in a cuc1-1D mutant a seven-fold increase in expression of CUC2 can be observed, suggesting that in this particular mutant insufficient MIR164 is produced to maintain normal transcript levels of the CUC1 and CUC2 genes, or there can be a sequestration of MIR164 by the mutated CUC1 gene. [score:3]
It was reported that expression of MIR164A, MIR164B and MIR164C in inflorescences of wild type, single, double and triple MIR mutants show partial overlap [35]. [score:3]
Our RT-PCR results in the Pro [35S]: HWS indicate that the target of HWS likely affects accumulation of MIR164. [score:3]
cuc1-1D is mutated in the MIR164 target site of CUC1 mRNA. [score:3]
This modification does not change the amino-acid sequence, but likely weakens the binding affinity of the MIR164 (Fig 2E) to its target sequence of CUC1. [score:3]
Alternatively, the target for HWS might modulate CUC1 and CUC2 levels, which subsequently alter MIR164B and MIR164C levels. [score:3]
These data suggest that the mutation in cuc1-1D is enough to disrupt the binding of the mature MIR164 molecule to the mRNA of CUC1 and it generates a version of CUC1 mRNA resistant to microRNA directed degradation. [score:3]
In agreement with previously reported data [35], our results also show that in floral buds and flowers of our lines studied, CUC1 and CUC2 transcripts are regulated by MIR164B and MIR164C. [score:2]
To investigate if mutation in the MIR164 binding site of CUC2 could also suppress the sepal fusion in hws-1, the hws-1 and cuc2-1D mutants were crossed (Figs 1B, 1J, 1R, 3B, 3G and 3L) [24]. [score:2]
The binding affinity of MIR164 to the CUC1 mRNA and the presence of HWS are crucial for sepal fusion rescue and for regulating floral organ number and identity. [score:2]
Mutations are underlined, the amino acid substitutions are identified in red/blue font, and changes in binding affinity from the MIR164 are indicated with a red dot. [score:2]
Mutations and constructs in CUC1, CUC2 and MIR164. [score:2]
These findings support the hypothesis that correct binding of MIR164 to the CUC1 mRNA is important for sepal boundary formation and regulation of floral organ number. [score:2]
0185106.g002 Fig 2Mutations and constructs in CUC1, CUC2 and MIR164. [score:2]
Redundancy and specialization among plant microRNAs: role of the MIR164 family in developmental robustness. [score:2]
Plants containing mRNAs resistant versions of CUC1 or CUC2 to MIR164 display alterations in development including increased petal numbers and reduced sepal numbers [22], increased formation of carpel margin meristems [23], alterations in location and size of boundaries [21] and enlarged vegetative and reproductive lateral organs [24]. [score:2]
The observed phenotypes in hws-1, cuc1-1D and hws-1/ cuc1-1D with either a mutated MIR164 or a silent mutation of CUC1 introgressed into them demonstrate that the efficacy in generating a MIR164 resistant allele of the CUC1 gene lies in the nucleotide change rather than the amino-acid substitution. [score:2]
Transformation of either cuc1-1D or hws-1/ cuc1-1D with this modified MIR164 transgene confirmed that this point mutation was enough to restore the wild-type and hws-1 phenotypes of the cuc1-1D and hws-1/cuc1-1D mutants, respectively (Fig 2F, 2G, 2H, 2I, 2J and 2K); twenty-four independent transformants were analysed, all plants reverted to wild-type in cuc1-1D or hws-1 in hws-1/cuc1-1D mutants. [score:2]
We have shown that the regulatory domain of MIR164 is crucial for this event to take place. [score:2]
Moreover, the data indicate that the nucleotide changed in cuc1-1D is crucial for the regulation of transcript levels of the CUC1 mRNA by MIR164. [score:2]
The cuc1-1D mutation has two major effects: (1) a single nucleotide change in the binding domain of MIR164 of the CUC1 mRNA transcript and (2) an amino-acid substitution in the CUC1 protein. [score:2]
MIR164 regulate boundary formation and floral organ number by establishing and maintaining the boundary domain by controlling post-transcriptional degradation of the CUC1 and CUC2 mRNAs [20– 22]. [score:2]
Our work here has demonstrated that HWS contributes to the co-ordination of floral organ number and boundary formation by altering MIR164 and CUC1 transcript levels. [score:1]
Our results show that the sepal fusion rescue is a consequence of changing the binding affinity of MIR164. [score:1]
These results support the hypothesis that the rescued sepal fusion and increased number of floral organs in the hws-1/cuc1-1D line are due to the change in the binding affinity of MIR164 to the mRNA of CUC1 and not to the amino-acid substitution in the CUC1 protein. [score:1]
The binding affinity of MIR164 to the CUC1 mRNA and the presence of HWS are crucial for sepal fusion rescue and for regulating floral organ number and identityTo investigate if the sepal fusion rescue and the extra floral organs phenotypes observed in the cuc1-1D/ hws-1 mutant is due to altering the binding affinity of MIR164 to the mRNA of CUC1; or to the amino-acid substitution (Fig 2B) in the CUC1 protein; a silent mutation C→T was introduced 1.236kb downstream from the ATG of CUC1 where MIR164 binds. [score:1]
However, transcript levels of MIR164B and MIR164C were significantly increased by about 8 and 2, 6 and 4, 4 and 7 and 5 fold in the hws-1, cuc1-1D, hws-1/cuc1-1D and cuc2-1D mutants, respectively (p<0.001), while in the, Pro [35S]: HWS they were similar or lower than in the wild-type (Fig 6E and 6F). [score:1]
Our results suggest a feedback loop mechanism where higher levels of CUC1 or CUC2 mRNA trigger the accumulation of MIR164B and MIR164C to reduce the higher levels of CUC1 transcript. [score:1]
0185106.g006 Fig 6Transcript levels of CUC1 CUC2, MIR164A, MIR164B and MIR164C genes are affected in single and double mutants and in the Pro [35]: HWS lines. [score:1]
A mutated version of the MIR164B gene reverts the floral phenotypes in cuc1-1D and hws-1/cuc1-1D backgrounds. [score:1]
A feedback loop mechanism between MIR164 and CUC is present in flowers. [score:1]
A mutated version of the MIR164B gene reverts the floral phenotypes in cuc1-1D and hws-1/cuc1-1D backgroundsTo investigate if the phenotypes observed in the cuc1-1D and hws-1/cuc1-1D mutants result from altering the binding affinity of MIR164 to the mRNA of CUC1, we generated a construct containing a 1.340kb genomic region of MIR164B gene expressed under the control of the CaMV 35S promoter. [score:1]
The amino-acid substitution in the CUC1 protein could change the conformation of the protein affecting its functionality, or alternatively, the nucleotide change could affect the binding affinity of the MIR164 to the CUC1 mRNA. [score:1]
To investigate if the phenotypes observed in the cuc1-1D and hws-1/cuc1-1D mutants result from altering the binding affinity of MIR164 to the mRNA of CUC1, we generated a construct containing a 1.340kb genomic region of MIR164B gene expressed under the control of the CaMV 35S promoter. [score:1]
In the hws-1 mutant, MIR164B and MIR164C levels are elevated, while levels MIR164A are unchanged. [score:1]
It has been demonstrated that cleavage of CUC1 mRNA occurs between nucleotides pairing to residue10 of the MIR164 [36]. [score:1]
If the extra floral organs are the consequence of changing the binding affinity of MIR164 to the mRNA of CUC1, an increase in floral organ numbers in the hws-1 background and an equal or more extreme phenotype in the cuc1-1D and hws-1/cuc1-1D lines are expected. [score:1]
Transcript levels of CUC1 CUC2, MIR164A, MIR164B and MIR164C genes are affected in single and double mutants and in the Pro [35]: HWS lines. [score:1]
Our data reveal that HWS controls floral organ number by modulating transcript accumulation levels of MIR164, CUC1 and CUC2 genes. [score:1]
The MIR164 binding sites are identical in CUC1 and CUC2 (Fig 2A). [score:1]
It has been proposed that MIR164 limit the expansion of the boundary domain by degrading CUC1 and CUC2 mRNAs [21] and NAC genes repressing growth [38]. [score:1]
Sequence data can be found in the Arabidopsis Genome Initiative or GenBank/EMBL databases under the following accession numbers: HWS, At3g61590; CUC1, At3g15170; CUC2, AT5G53950; MIR164A, At2g47585; MIR164B, At5g01747; and MIR164C, At5g27807. [score:1]
[1 to 20 of 62 sentences]
3
[+] score: 132
Expression of a miR164-Resistant form of MtNAM Leads to a Breakdown in Carpel Margin Fusion and Other Developmental Fusion Events in Medicago truncatula FlowersTo test the role of the NAM/miR164 developmental module on carpel closure in M. truncatula, we produced transgenic plants expressing genomic constructs of MtNAM (MtNAMg-m4 and MtNAMg-wt), respectively, with or without four point mutations in their predicted miR164 -binding sites, identical to those present in the CUC2g-m4 construct (Nikovics et al., 2006). [score:8]
These transcription factors are expressed at organ margins and tissue boundaries, and their down-regulation by miR164 consequently facilitates organ outgrowth and/or developmental fusion. [score:7]
These expression data reveal several underlying similarities in the expression of miR164-regulated NAM orthologs between A. thaliana and M. truncatula. [score:6]
Given the role of the NAM/miR164 module in carpel closure in both A. thaliana and M. truncatula (Figures 2 and 4), and the gene expression differences we have noted between the congenitally and post-genitally fused carpel margins of these two respective species, it would be interesting to compare the expression of NAM orthologs in a range of Fabales that show different spatial and temporal patterns of carpel closure. [score:5]
To test the role of the NAM/miR164 developmental module on carpel closure in M. truncatula, we produced transgenic plants expressing genomic constructs of MtNAM (MtNAMg-m4 and MtNAMg-wt), respectively, with or without four point mutations in their predicted miR164 -binding sites, identical to those present in the CUC2g-m4 construct (Nikovics et al., 2006). [score:5]
Accordingly, we furthermore hypothesize, based on our gene expression analyses (Figure 3), that the origin of plicate carpels in various later-emerging angiosperm lineages may have depended on subtle modifications to the NAM/miR164 module that allowed a limited level of early expression of NAM orthologs in the carpel margins, as occurs in present-day M. truncatula. [score:5]
Expression of NAM Orthologs is Absent or Reduced During Carpel Margin Fusion in Arabidopsis thaliana and Medicago truncatulaThe observation that the NAM/miR164 module regulates developmental closure events in the gynoecium in both syncarpous and monocarpous genotypes of A. thaliana led us to speculate that this molecular mechanism might be wi dely conserved within the angiosperms. [score:5]
Comparison of these data strongly suggests that the NAM/miR164 expression balance in A. thaliana lies heavily in favor of miR164 from the earliest stages of gynoecium development. [score:4]
Notably, the NAM/miR164 expression balance at very early stages of carpel development may be important in determining whether carpel margins will fuse congenitally or postgenitally. [score:4]
Thus, the different balances of NAM and miR164 expression observed at very early stages of A. thaliana and M. truncatula carpel development (Figure 3; Galbiati et al., 2013) correlate closely with the different timings of carpel closure observed in these species (Smyth et al., 1990; Benlloch et al., 2003). [score:4]
Expression of a miR164-Resistant form of MtNAM Leads to a Breakdown in Carpel Margin Fusion and Other Developmental Fusion Events in Medicago truncatula Flowers. [score:4]
A detailed comparison of gene expression patterns suggests that fine-tuning of the NAM/miR164 module may regulate species–specific differences in the timing of carpel margin fusion. [score:4]
Thus, it appears reasonable to postulate that the NAM/miR164 module operates in favor of the expression of miR164, and against that of NAM orthologs, from the earliest stages of gynoecium development in A. trichopoda, as it does in A. thaliana. [score:4]
Carpel fusion in A. thaliana is regulated by a genetic module, generically termed here the NAM/miR164 module, which consists of a subset of NAC -family (NAC for NAM, ATAF and CUC; Aida et al., 1997) transcription factors and their post-transcriptional regulator miR164 (Mallory et al., 2004). [score:3]
Plants expressing a miR164-resistant CUC2 gene reveal the importance of post-meristematic maintenance of phyllotaxy in Arabidopsis. [score:3]
Thus, disruption of the NAM/miR164 developmental module in monocarpous mutant gynoecia of A. thaliana causes the failure of developmental closure in these structures in a similar manner to the disruption of carpel fusion in syncarpous, wild-type gynoecia. [score:3]
Despite the differences observed, we concluded that the presence of MtNAM expression in M. truncatula carpel margins suggested that the NAM/miR164 module may be involved in the fusion of these structures, leading us to test this hypothesis experimentally. [score:3]
The observation that the NAM/miR164 module regulates developmental closure events in the gynoecium in both syncarpous and monocarpous genotypes of A. thaliana led us to speculate that this molecular mechanism might be wi dely conserved within the angiosperms. [score:3]
Prior to initiating functional experiments in M. truncatula, we used in situ hybridization to examine the conservation of expression of NAM orthologs in flower tissues between A. thaliana and M. truncatula and thereby ascertain the likelihood that the NAM/miR164 module might function in carpel closure in the latter species. [score:3]
Thus, the establishment of negative regulation by SPT of a miR164-regulated NAM gene in a common ancestor of the angiosperms may have been a crucial step in the evolution of the closed carpel. [score:3]
Redundancy and specialization among plant microRNAs: role of the MIR164 family in developmental robustness. [score:2]
Accordingly, in miR164 triple mutants or CUC2g-m4 transformants, the two carpels of the A. thaliana gynoecium emerge separately and remain unfused and open throughout development. [score:2]
An important test of this hypothesis will depend on the development of plant transformation strategies in basally diverging angiosperms, which would allow, for example, the transformation of A. trichopoda with a miR164-resistant form of AtrNAM. [score:2]
Like the NAM/miR164 module, it seems that SPT may have conserved its function in carpel development from the earliest stages of angiosperm evolution (Reymond et al., 2012). [score:2]
Accordingly, we discuss the possibility that the activity of the NAM/miR164 module may be conserved in carpel development throughout the angiosperms, while subtle modulations to this mechanism may determine the distinction between congenital and post-genital carpel margin fusion events in specific angiosperm groups. [score:2]
Such experiments, in quite closely related species showing marked differences in gynoecium anatomy, could provide strong correlative evidence of a role for the subtle modulation of gynoecium development by changes to the balance of the NAM/miR164 module. [score:2]
These data indicate that the NAM/miR164 module has conserved a role in developmental fusion events between carpel margins at least since the MRCA of the eurosids. [score:2]
The NAM/miR164 in Arabidopsis thaliana Plays a Role in Both Syncarpy and the Closure of Single CarpelsAs the NAM/miR164 developmental module is necessary for carpel fusion in wild-type, syncarpous A. thaliana (Nikovics et al., 2006; Sieber et al., 2007), we aimed to discover whether this mechanism could also contribute to the closure of single carpels in this species. [score:2]
Loss of miR164 function through mutations to all three MIR164 paralogs in A. thaliana (Sieber et al., 2007), or genetic transformation of A. thaliana with a miR164-resistant version of CUC2 (CUC2g-m4; Nikovics et al., 2006), results in a breakdown of carpel fusion. [score:2]
In the present work, we show that the role of the NAM/miR164 module in carpel margin fusion was conserved during this developmental transition. [score:2]
As the NAM/miR164 developmental module is necessary for carpel fusion in wild-type, syncarpous A. thaliana (Nikovics et al., 2006; Sieber et al., 2007), we aimed to discover whether this mechanism could also contribute to the closure of single carpels in this species. [score:2]
These data indicate a range of roles of the NAM/miR164 developmental module in fusion events in the corolla, androecium, and gynoecium of M. truncatula flowers. [score:2]
As its genetic components are present in both gymnosperms and angiosperms (Axtell and Bartel, 2005; Larsson et al., 2012), the NAM/miR164 genetic module is clearly of ancient origin in seed plants. [score:1]
From the above observations, we hypothesize that the NAM/miR164 module may have played a role in the fusion of carpel margins in the MRCA of the living angiosperms, as it does in present-day mo del angiosperms. [score:1]
The NAM/miR164 Module Maintained its Role in Carpel Margin Fusion During a Transition from Syncarpy to Monocarpy in an Ancestor of Fabales. [score:1]
A 1.2-kb fragment containing the miR164 -binding site of MtNAM was released from a sub-cloned BAC DNA fragment by cleavage with SstI and re-ligated into the pGEM T-Easy vector. [score:1]
We show that disruption of the NAM/miR164 module in both A. thaliana aux1-22 mutants (Figure 2) and a wild-type background of M. truncatula (Figure 4) produces single carpels that are no longer completely fused at their margins. [score:1]
From the results of these experiments, we conclude that the NAM/miR164 module has conserved a role in carpel margin fusion, at least since the most recent common ancestor (MRCA) of living eurosids. [score:1]
In this study, we show that a previously characterized developmental module involving the post-transcriptional regulation of NAM orthologs by miR164 is involved not only in carpel fusion in syncarpous A. thaliana (Nikovics et al., 2006; Sieber et al., 2007), but also in the closure of the single carpels present in two species whose lineages diverged at the base of the eurosid clade, some 114–113 MYA. [score:1]
A Possible Role for the NAM/miR164 Module in the Timing of Carpel FusionIn A. thaliana, the gynoecium forms as a radially symmetrical cylinder that later differentiates to show the positions of the carpel margins. [score:1]
A Role of the NAM/miR164 Module in the Fusion of Carpel Margins has Been Conserved at Least Since the MRCA of the Eurosids. [score:1]
A Role of the NAM/miR164 Module in the Fusion of Carpel Margins has Been Conserved at Least Since the MRCA of the EurosidsIn this study, we show that a previously characterized developmental module involving the post-transcriptional regulation of NAM orthologs by miR164 is involved not only in carpel fusion in syncarpous A. thaliana (Nikovics et al., 2006; Sieber et al., 2007), but also in the closure of the single carpels present in two species whose lineages diverged at the base of the eurosid clade, some 114–113 MYA. [score:1]
The NAM/miR164 in Arabidopsis thaliana Plays a Role in Both Syncarpy and the Closure of Single Carpels. [score:1]
The NAM/miR164 Module Maintained its Role in Carpel Margin Fusion During a Transition from Syncarpy to Monocarpy in an Ancestor of FabalesCharacter-state mapping (Figure 1) further indicates that the monocarpy present in Fabales (including M. truncatula) is a derived condition that occurred by reversion from syncarpy, present in earlier eurosids. [score:1]
These oligonucleotides generate the same four-base mismatch (shown above in lower case) present in the miR164 -binding site of CUC2g-m4 (Nikovics et al., 2006). [score:1]
Analysis of the pathway linking SPT, and its cofactors such as the HECATE transcription factors (Schuster et al., 2015), with the NAM/miR164 module in mo del angiosperms could provide insights into this possibility, and thus potentially indicate a molecular mechanism for the enclosure of the ovule with the carpel in the first angiosperms. [score:1]
The Role of the NAM/miR164 Module in Carpel Evolution. [score:1]
A Possible Role for the NAM/miR164 Module in the Timing of Carpel Fusion. [score:1]
In this work, we hypothesized that the role of the NAM/miR164 module in syncarpous fusion in A. thaliana might reflect a more general role in the fusion of carpel margins in angiosperms. [score:1]
The Role of the NAM/miR164 Module in Carpel EvolutionAs its genetic components are present in both gymnosperms and angiosperms (Axtell and Bartel, 2005; Larsson et al., 2012), the NAM/miR164 genetic module is clearly of ancient origin in seed plants. [score:1]
We further speculate on mechanisms acting upstream of the NAM/miR164 module that may have contributed to the origin of the carpel in the first flowering plants. [score:1]
Thus, our study strongly suggests that the NAM/miR164 module provides an underlying mechanism that is necessary for fusion events at the carpel margins of both syncarpous and monocarpous eurosids. [score:1]
FIGURE 2Gynoecium morphology of A. thaliana aux1-22 mutants transformed with miR164-resistant (CUC2g-m4) or un-mutated control (CUC2g-wt) constructs. [score:1]
The action of the NAM/miR164 module in the A. thaliana leaf margin has been mo deled and found to generate, via effects on the auxin efflux carrier PINFORMED1 (PIN1), an alternating series of auxin maxima and minima that, respectively, generate regions of higher and lower marginal growth (Bilsborough et al., 2011). [score:1]
[1 to 20 of 54 sentences]
4
[+] score: 30
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c
Disruption of miR164 encoding genes or that of its target sequences in CUC1 and CUC2 causes misregulation of their expression, resulting in various developmental defects including abnormal carpel development (Mallory et al., 2004; Baker et al., 2005; Nikovics et al., 2006; Sieber et al., 2007; Larue et al., 2009). [score:8]
For construction of CUC1g-m7, the miR164 target sequence (AG CAC GTG TCC TGT TTC TCC A) of CUC1 was replaced by a mutant sequence (AG CAC GTG AGT TGT TT T AGT A), which contains seven silent mutations (underlined). [score:4]
To this end, we used transgenic plants carrying genomic fragments of CUC1 or CUC2 that carry silent mutations in the target sequences of miR164 (CUC1g-m7 and CUC2g-m4, respectively). [score:4]
Furthermore, the important roles for auxin and miR164 in regulating expression of CUC genes are also conserved among the processes of shoot meristem, leaf margin and carpel margin formation (Aida et al., 2002; Furutani et al., 2004; Nikovics et al., 2006; Larue et al., 2009; Koyama et al., 2010; Bilsborough et al., 2011; Galbiati et al., 2013). [score:4]
Together, the results show that disruption of miR164 -mediated regulation of CUC1 and CUC2 strongly affected the size, positioning, and number of the CMMs. [score:2]
In addition, both CUC1 and CUC2 are negatively regulated by the microRNA miR164, which is encoded by three loci in Arabidopsis. [score:2]
TCP transcription factors regulate the activities of ASYMMETRIC LEAVES1 and miR164, as well as the auxin response, during differentiation of leaves in Arabidopsis. [score:2]
Redundancy and specialization among plant microRNAs: role of the MIR164 family in developmental robustness. [score:2]
These results indicate that CUC1 and CUC2 promote CMM formation and, possively through the interaction with miR164, they are required for correct positioning of the CMMs. [score:1]
A transgenic line displaying extra petal number and reduced sepal growth, a typical phenotype described for miR164 resistant 5mCUC1 (Mallory et al., 2004), was selected and subjected to analysis. [score:1]
[1 to 20 of 10 sentences]
5
[+] score: 17
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-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-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
It is likely that carbon starvation induces leaf senescence by suppressing the expression of miR164 and miR319. [score:5]
Leaf senescence allows for the degradation of the nutrients produced during the growth phase of the leaf and their reallocation to developing tissues or organs to maximize the fitness of the plant 43. miR164, whose expression gradually decreased with leaf aging, targets NAC2/ORE1, which functions positively in leaf senescence 44. [score:5]
For example, miR164a and miR164b were downregulated 14-fold by –C, whereas miR164c was not responsive to –C. [score:4]
This suggested that leaf senescence regulation mediated by miR164 and miR319 is specific to –C, whereas –N and –S induce leaf senescence by other regulatory pathways. [score:3]
[1 to 20 of 4 sentences]
6
[+] score: 16
miRNAs were directly implicated in regulating Arabidopsis senescence when it was shown that miR164 is a key player in the senescence regulatory pathway. [score:4]
miR164, which targets the positive regulator of senescence -induced cell death ORE1 (AT5G39610), has been previously reported to decline in leaves as senescence progresses (Kim et al. 2009). [score:4]
In addition to reproducing regulation of miR164, differential expression of seven other Arabidopsis miRNAs during the course of senescence was observed (Fig.   2). [score:4]
Natural reduction of miR164 level during senescence results in increased cell death because of its control on its target, the senescence transcriptional activator gene ORE1 (Kim et al. 2009). [score:3]
Interestingly, miR164 was reduced from young to mature siliques but did not continue to decline as senescence progressed in this tissue (Fig.   2) indicating that levels of senescence-responsive miRNAs may change in a tissue -dependent manner. [score:1]
[1 to 20 of 5 sentences]
7
[+] score: 12
Our third line of evidence comes from our Northern blot analyses where differential accumulation of mature miR163 and miR164 in floral tissues in the hws-1 mutant and the Pro [35]: HWS line were observed, suggesting that during development a differential regulation of mature miRNAs is required, and this is achieved by a pathway implicating HWS. [score:3]
Recently we demonstrated that HWS controls floral organ number by regulating transcript accumulation levels of the MIR164. [score:2]
While miR164 negatively regulates mRNA levels of CUC1 and CUC2 genes to modulate boundary formation in flowers [14, 17– 18]. [score:2]
0189788.g003 Fig 3Northern analyses in a mix of young buds and flowers (up to stage12, [56]) in Col-0 wild type (WT), hws-1 and Pro [35]: HWS using probes for miR163, miR164, and snRNA U6 as internal control. [score:1]
Our Northern blot results provide further evidence for a role of HWS in miRNA pathway and suggest that the sepal fusion phenotype observed in hws-1 maybe due to the over accumulation of miR164 which in turn modulates mRNA levels of CUC1, and CUC2. [score:1]
This phenotype is similar to that of the double mutant cuc1/ cuc2 [CUP-SHAPED COTYLEDON 1 (CUC1) and 2 (CUC2)] [16] and to that of the Pro [35]: 164B ectopic lines for the microRNA gene MIR164B [17, 18]. [score:1]
In agreement with these findings, the levels of miR163 and miR164 mature miRNAs in floral tissues are modified in lines that exhibit a loss or gain of function for HWS. [score:1]
Northern analyses in a mix of young buds and flowers (up to stage12, [56]) in Col-0 wild type (WT), hws-1 and Pro [35]: HWS using probes for miR163, miR164, and snRNA U6 as internal control. [score:1]
[1 to 20 of 8 sentences]
8
[+] score: 11
miR164 plays a significant role in formation of proper organ boundaries [35], floral patterning [36], leaf morphogenesis [37] and lateral root development [38] by negative regulation of its target NAC1, CUC1 and CUC2. [score:5]
We validated expression of three different targets of miR164, such as NAC1 (NO APICAL MERISTEM1) (Fig.   5f), CUC1 (CUP SHAPED COTYLEDON1) (Fig.   5g) and CUC2 (Fig.   5h). [score:5]
In the previous report, there is the indication of the involvement of miR164 in seed germination in maize [20]. [score:1]
[1 to 20 of 3 sentences]
9
[+] score: 11
ORE1/NAC2 was genetically identified as a positive regulator of leaf senescence, because knockout of ORE1/NAC2 extends plant longevity in Arabidopsis [25], and miR164 mediates the cleavage of a group of NAC family genes, of which ORE1/NAC2 is a positive regulator of aging -induced cell death and leaf senescence [25, 31]. [score:4]
Overexpression of miR164 represses EIN3 -induced early-senescence phenotypes in Arabidopsis thaliana leaves [23, 25]. [score:3]
NAC is reportedly regulated by miR164 [3]. [score:2]
Kim et al. (2009) found that senescence was accelerated in the miR164 mutant [25]. [score:1]
They demonstrated that miR164 repressed ORE1 via cleavage of ORE1 mRNA. [score:1]
[1 to 20 of 5 sentences]
10
[+] score: 10
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c
EIN2 (ethylene insensitive 2) and its downstream component EIN3 of the ethylene signalling pathway negatively block miRNA164 expression in an age -dependent manner, through the direct binding of EIN3 to the promoter of miRNA164, which allows ORE1 mRNA to accumulate (Kim et al., 2009; Li et al., 2013). [score:4]
Plant Growth Regulation 53, 195– 206 Li Z Peng J Wen X Guo H 2013 ETHYLENE-INSENSITIVE3 is a senescence -associated gene that accelerates age -dependent leaf senescence by directly repressing miR164 transcription in Arabidopsis. [score:3]
Physiologia Plantarum 109, 211– 216 Kim JH Woo HR Kim J Lim PO Lee IC Choi SH Hwang D Nam HG 2009 Trifurcate feed-forward regulation of age -dependent cell death involving miR164 in Arabidopsis. [score:2]
The control of the ORE1 transcript involves miR164 (microRNA164), which interacts with ORE1 mRNA to trigger its degradation. [score:1]
[1 to 20 of 4 sentences]
11
[+] score: 10
A different type of leaf serration was caused by MIM164 (Figure 2), similar to what has been reported for plants expressing a non-targetable version of CUC2, one of the miR164 targets, and for plants lacking one of the miR164 isoforms, miR164a [13]. [score:7]
Although carpel fusion defects have been described for plants lacking miR164c [12], the carpel defects in MIM164 plants seemed to be different, with ectopic growths forming at the valve margins (Figure 3D), resembling those seen in the cuc2-1D mutant, in which a point mutation affects the miR164 complementary motif in CUC2 [46]. [score:2]
ARF10, ARF16, ARF17 1, 3, 4 MIM164 miR164 Partially serrated leaves. [score:1]
[1 to 20 of 3 sentences]
12
[+] score: 8
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]
For example, Bazzini et al (2009) demonstrated that miR164 promoter respond to virus and gibberellins displaying a positive correlation of the miRNA/target pair [61]. [score:3]
[1 to 20 of 2 sentences]
13
[+] score: 8
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-MIR162a, ath-MIR162b, ath-MIR164a, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR168a, ath-MIR168b, ath-MIR169a, ath-MIR172a, ath-MIR172b, ath-MIR159b, 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-MIR162a, osa-MIR164a, osa-MIR164b, 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-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, ath-MIR396a, ath-MIR396b, 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-MIR396a, osa-MIR396b, osa-MIR396c, 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-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-MIR160e, osa-MIR160f, osa-MIR162b, osa-MIR164c, osa-MIR164d, osa-MIR164e, osa-MIR166k, osa-MIR166l, osa-MIR167d, osa-MIR167e, osa-MIR167f, osa-MIR167g, osa-MIR167h, osa-MIR167i, osa-MIR168a, osa-MIR168b, 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-MIR171h, osa-MIR408, osa-MIR172d, osa-MIR167j, osa-MIR166m, osa-MIR166j, osa-MIR164f, zma-MIR156d, zma-MIR156f, zma-MIR156g, zma-MIR156b, zma-MIR156c, zma-MIR156e, zma-MIR156a, zma-MIR156h, zma-MIR156i, zma-MIR160a, zma-MIR160c, zma-MIR160d, zma-MIR160b, zma-MIR164a, zma-MIR164d, zma-MIR164b, zma-MIR164c, zma-MIR169a, zma-MIR169b, zma-MIR167a, zma-MIR167b, zma-MIR167d, zma-MIR167c, zma-MIR160e, zma-MIR166a, zma-MIR162, zma-MIR166h, zma-MIR166e, zma-MIR166i, zma-MIR166f, zma-MIR166g, zma-MIR166b, zma-MIR166c, zma-MIR166d, zma-MIR172a, zma-MIR172d, zma-MIR172b, zma-MIR172c, osa-MIR396e, zma-MIR395b, zma-MIR395c, zma-MIR395a, zma-MIR396b, zma-MIR396a, zma-MIR399a, zma-MIR399c, zma-MIR399b, zma-MIR399d, zma-MIR399e, zma-MIR399f, zma-MIR156j, zma-MIR159a, zma-MIR159b, zma-MIR159c, zma-MIR159d, zma-MIR166k, zma-MIR166j, zma-MIR167e, zma-MIR167f, zma-MIR167g, zma-MIR167h, zma-MIR167i, zma-MIR168a, zma-MIR168b, zma-MIR169c, zma-MIR169f, zma-MIR169g, zma-MIR169h, zma-MIR169i, zma-MIR169k, zma-MIR169j, zma-MIR169d, zma-MIR169e, zma-MIR172e, zma-MIR166l, zma-MIR166m, zma-MIR171h, zma-MIR408a, zma-MIR156k, zma-MIR160f, osa-MIR529a, osa-MIR395m, osa-MIR395n, osa-MIR395o, osa-MIR395p, osa-MIR395q, osa-MIR395v, osa-MIR395w, osa-MIR395r, osa-MIR529b, osa-MIR169r, osa-MIR396f, zma-MIR396c, zma-MIR396d, 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-MIR2275a, osa-MIR2275b, zma-MIR2118a, zma-MIR2118b, zma-MIR2118c, zma-MIR2118d, zma-MIR2118e, zma-MIR2118f, zma-MIR2118g, zma-MIR2275a, zma-MIR2275b, zma-MIR2275c, zma-MIR2275d, osa-MIR396g, osa-MIR396h, osa-MIR396d, zma-MIR156l, zma-MIR159e, zma-MIR159f, zma-MIR159g, zma-MIR159h, zma-MIR159i, zma-MIR159j, zma-MIR159k, zma-MIR160g, zma-MIR164e, zma-MIR164f, zma-MIR164g, zma-MIR164h, zma-MIR166n, zma-MIR167j, zma-MIR169l, zma-MIR169m, zma-MIR169n, zma-MIR169o, zma-MIR169p, zma-MIR169q, zma-MIR169r, zma-MIR395d, zma-MIR395e, zma-MIR395f, zma-MIR395g, zma-MIR395h, zma-MIR395i, zma-MIR395j, zma-MIR395k, zma-MIR395l, zma-MIR395m, zma-MIR395n, zma-MIR395o, zma-MIR395p, zma-MIR396e, zma-MIR396f, zma-MIR396g, zma-MIR396h, zma-MIR399g, zma-MIR399h, zma-MIR399i, zma-MIR399j, zma-MIR408b, zma-MIR529, osa-MIR395x, osa-MIR395y, osa-MIR2275c, osa-MIR2275d, ath-MIR156i, ath-MIR156j
Beyond miR156 and miR172, miR164 targets genes encoding NAM proteins, and may be involved in regulating ear development (Table  3), similar to how miR164 is postulated to regulate NAC-domain targets in Arabidopsis [58]. [score:8]
[1 to 20 of 1 sentences]
14
[+] score: 7
Overexpression of miR164, that targets NAC1 reduced LRF but had no significant effect on nodulation in soybean [77] whereas it reduced nodule number without any effect on LRF in M. truncatula [80]. [score:5]
Mao G. Turner M. Yu O. Subramanian S. miR393 and miR164 influence indeterminate but not determinate nodule development Plant Signal. [score:2]
[1 to 20 of 2 sentences]
15
[+] score: 7
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]
The involvement of miRNAs as key regulators of flowering time (miR159, miR172, miR156, and miR171), hormone signaling (miR159, miR160, miR167, miR164, and miR393), or shoot and root development (miR164), was reviewed by (Wang and Li, 2007). [score:3]
[1 to 20 of 2 sentences]
16
[+] score: 6
The transcription factor CUC2 which is expressed at the leaf sinuses and is negatively regulated by miR164 (Nikovics et al., 2006), promotes generation of these PIN1 -dependent auxin maxima, which was supported by computer simulations (Bilsborough et al., 2011). [score:4]
TCP transcription factors regulate the activities of ASYMMETRIC LEAVES1 and miR164, as well as the auxin response, during differentiation of leaves in Arabidopsis. [score:2]
[1 to 20 of 2 sentences]
17
[+] score: 5
For instance, we speculated that the increased levels of miR159, miR164, and miR172 should lead to a decrease in the target mRNAs, MYB33, CUC1, and AP2, respectively. [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]
However, the dramatic accumulations of pri-miR159a (~ 4.5-fold), pri-miR164a (~3-fold), and pri-miR172a (~2.5-fold) were proportional to the levels of mature miR159 (~ 2-fold), miR164 (~ 1.6-fold) and miR172 (~ 2-fold) present. [score:1]
[1 to 20 of 3 sentences]
18
[+] 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]
19
[+] score: 5
The NAC1 transcription factor is targeted by miR164 and acts on lateral root development through regulating auxin responses [45, 53– 56]. [score:5]
[1 to 20 of 1 sentences]
20
[+] score: 5
TCP fine-tunes the expressional patterns of CUC through the regulation of microRNA164 to shape the serrations (Nikovics et al., 2006; Koyama et al., 2007, 2010; Kawamura et al., 2010). [score:3]
TCP transcription factors regulate the activities of ASYMMETRIC LEAVES1 and miR164, as well as the auxin response, during differentiation of leaves in Arabidopsis. [score:2]
[1 to 20 of 2 sentences]
21
[+] score: 5
In rice, osa-miR160, osa-miR164 and osa-miR172 are co-expressed with their targets in root, leaf, seedling, endosperm and embryo [46]. [score:5]
[1 to 20 of 1 sentences]
22
[+] score: 4
On the contrary, miR156, miR158, miR164, miR165, miR400, miR5654, miR775, miR829, miR838 and miR852 were down-regulated by TCV infection. [score:4]
[1 to 20 of 1 sentences]
23
[+] score: 4
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c, tae-MIR164
The target gene of tae-miR164, a novel NAC transcription factor from the NAM subfamily, negatively regulates resistance of wheat to stripe rust. [score:4]
[1 to 20 of 1 sentences]
24
[+] score: 4
Trifurcate feed-forward regulation of age -dependent cell death involving miR164 in Arabidopsis. [score:2]
For instance, four copies of miR164 (miR164a to miR164d) were identified in E. salsugineum while three copies were found in A. thaliana, which have been reported to post-transcriptionally regulate mRNA transcripts of NAC, a transcription factor required for ABA-independent pathway in response to a variety of abiotic stresses (Kim et al., 2009). [score:2]
[1 to 20 of 2 sentences]
25
[+] score: 4
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c
For instance, in the SAM CUC1 and CUC2 but not CUC3 are regulated by miR164, which restricts the expression of CUC1 and CUC2 mRNAs to the boundary domain (Laufs et al., 2004). [score:4]
[1 to 20 of 1 sentences]
26
[+] 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-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, ath-MIR398a, 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
5, miR164c-5p, miR164b. [score:1]
4, miR164b. [score:1]
Total 29 miRNAs (miR172d-3p, miR164b. [score:1]
[1 to 20 of 3 sentences]
27
[+] 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]
28
[+] score: 3
The direct binding of CUC2 to the MiR164c promoter identifies an additional reciprocal regulation between CUC genes and MiR164 miRNAs (Laufs et al, 2004; Mallory et al, 2004). [score:3]
[1 to 20 of 1 sentences]
29
[+] score: 3
miRNA -mediated signaling is also involved in the development of various tissues; several miRNA families such as miR160, miR164, miR167, and miR390 have been demonstrated to be involved in root cap formation and lateral root development [42]. [score:3]
[1 to 20 of 1 sentences]
30
[+] score: 3
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]
[1 to 20 of 1 sentences]
31
[+] score: 2
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c
Journal of Biochemstry 146, 463– 469 Kim JH Woo HR Kim J Lim PO Lee IC Choi SH Hwang D Nam HG 2009 Trifurcate feed-forward regulation of age -dependent cell death involving miR164 in Arabidopsis. [score:2]
[1 to 20 of 1 sentences]
32
[+] score: 2
For example, transcripts of the NAC1 gene (At1g56010), which is a target of microRNA ath-Mir164 [33], have both cis- and trans-NATs. [score:2]
[1 to 20 of 1 sentences]
33
[+] score: 2
Both the miR164 and miR167 families were identified as stem-specific miRNAs from A. thaliana and tobacco [50, 51]. [score:1]
In addition, most of the petiole-specific miRNAs were members of the conserved miRNA families miR164 and miR167, although there was one novel miRNA (bra-miR6104). [score:1]
[1 to 20 of 2 sentences]
34
[+] score: 2
Known miRNAs also failed due to length (miR163), an incorrectly predicted foldback (miR164b and miR167d) or because the MIRNA gene yielded bidirectional small RNAs (miR156d and miR161). [score:2]
[1 to 20 of 1 sentences]
35
[+] score: 2
Other miRNAs from this paper: ath-MIR164a, ath-MIR164c
Crop Science 40, 1049– 1055 Kim JH Woo HR Kim J Lim PO Lee IC Choi SH Hwang D Nam HG 2009 Trifurcate feed-forward regulation of age -dependent cell death involving miR164 in Arabidopsis. [score:2]
[1 to 20 of 1 sentences]
36
[+] score: 1
Regulation ofs by miRNA in A. thaliana can be considered as auxin-independent because auxin treatment does not alter appreciably miR160, miR164, and miR167 accumulation, at least in seedlings [49]. [score:1]
[1 to 20 of 1 sentences]
37
[+] score: 1
Sequence data from this article can be found in the EMBL/GenBank data libraries under the following accession numbers: NF-YA2 (At3g05690), NF-YA3 (At1g72830), NF-YA5 (At1g54160), NF-YA7 (At1g30500), NF-YA10 (At5g06510), SPX1 (At5g20150), HEN1 (At4g20910), MIR169a (At3g13405), MIR169h (At1g19371), MIR169i (At3g26812), MIR169j (At3g26813), MIR169k (At3g26815), MIR169l (At3g26816), MIR169m (At3g26818), MIR169n (At3g26819), MIR156g (At2g19425), MIR164a (At2g47585), MIR164b (At5g01747), MIR164c (At5g27807), ACTIN 2 (At3g18780). [score:1]
[1 to 20 of 1 sentences]
38
[+] score: 1
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]
[1 to 20 of 1 sentences]
39
[+] score: 1
ath-miR159a, ath-miR164b, ath-miR172a, ath-miR319a, and osa-miR528 recently been developed and tested. [score:1]
[1 to 20 of 1 sentences]
40
[+] score: 1
As a control, three MIR164 loci which have no significant complementarity to the probe were analyzed and indeed showed no evidence of enrichment (Fig. 2C–D). [score:1]
[1 to 20 of 1 sentences]
41
[+] score: 1
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-MIR162a, ath-MIR162b, ath-MIR164a, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR169a, ath-MIR171a, ath-MIR172a, ath-MIR172b, ath-MIR159b, 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-MIR162a, osa-MIR164a, osa-MIR164b, osa-MIR166a, osa-MIR166b, osa-MIR166c, osa-MIR166d, osa-MIR166e, osa-MIR166f, osa-MIR167a, osa-MIR167b, osa-MIR167c, osa-MIR169a, osa-MIR171a, 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-MIR171c, ath-MIR172c, ath-MIR172d, ath-MIR393a, ath-MIR393b, ath-MIR394a, ath-MIR394b, ath-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, osa-MIR393a, osa-MIR394, 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, 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-MIR160e, osa-MIR160f, osa-MIR162b, osa-MIR164c, osa-MIR164d, osa-MIR164e, 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-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-MIR393b, osa-MIR172d, osa-MIR171i, osa-MIR167j, osa-MIR166m, osa-MIR166j, osa-MIR164f, zma-MIR156d, zma-MIR156f, zma-MIR156g, zma-MIR156b, zma-MIR156c, zma-MIR156e, zma-MIR156a, zma-MIR156h, zma-MIR156i, zma-MIR160a, zma-MIR160c, zma-MIR160d, zma-MIR160b, zma-MIR164a, zma-MIR164d, zma-MIR164b, zma-MIR164c, zma-MIR169a, zma-MIR169b, zma-MIR167a, zma-MIR167b, zma-MIR167d, zma-MIR167c, zma-MIR160e, zma-MIR166a, zma-MIR162, zma-MIR166h, zma-MIR166e, zma-MIR166i, zma-MIR166f, zma-MIR166g, zma-MIR166b, zma-MIR166c, zma-MIR166d, zma-MIR171a, zma-MIR171b, zma-MIR172a, zma-MIR172d, zma-MIR172b, zma-MIR172c, zma-MIR171d, zma-MIR171f, zma-MIR394a, zma-MIR394b, zma-MIR395b, zma-MIR395c, zma-MIR395a, zma-MIR156j, zma-MIR159a, zma-MIR159b, zma-MIR159c, zma-MIR159d, zma-MIR166k, zma-MIR166j, zma-MIR167e, zma-MIR167f, zma-MIR167g, zma-MIR167h, zma-MIR167i, zma-MIR169c, zma-MIR169f, zma-MIR169g, zma-MIR169h, zma-MIR169i, zma-MIR169k, zma-MIR169j, zma-MIR169d, zma-MIR169e, zma-MIR171c, zma-MIR171j, zma-MIR171e, zma-MIR171i, zma-MIR171g, zma-MIR172e, zma-MIR166l, zma-MIR166m, zma-MIR171k, zma-MIR171h, zma-MIR393a, zma-MIR156k, zma-MIR160f, osa-MIR528, osa-MIR529a, osa-MIR395m, osa-MIR395n, osa-MIR395o, osa-MIR395p, osa-MIR395q, osa-MIR395v, osa-MIR395w, osa-MIR395r, ath-MIR827, osa-MIR529b, osa-MIR1432, osa-MIR169r, osa-MIR827, 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-MIR2275a, osa-MIR2275b, zma-MIR2118a, zma-MIR2118b, zma-MIR2118c, zma-MIR2118d, zma-MIR2118e, zma-MIR2118f, zma-MIR2118g, zma-MIR2275a, zma-MIR2275b, zma-MIR2275c, zma-MIR2275d, zma-MIR156l, zma-MIR159e, zma-MIR159f, zma-MIR159g, zma-MIR159h, zma-MIR159i, zma-MIR159j, zma-MIR159k, zma-MIR160g, zma-MIR164e, zma-MIR164f, zma-MIR164g, zma-MIR164h, zma-MIR166n, zma-MIR167j, zma-MIR169l, zma-MIR169m, zma-MIR169n, zma-MIR169o, zma-MIR169p, zma-MIR169q, zma-MIR169r, zma-MIR171l, zma-MIR171m, zma-MIR171n, zma-MIR393b, zma-MIR393c, zma-MIR395d, zma-MIR395e, zma-MIR395f, zma-MIR395g, zma-MIR395h, zma-MIR395i, zma-MIR395j, zma-MIR395k, zma-MIR395l, zma-MIR395m, zma-MIR395n, zma-MIR395o, zma-MIR395p, zma-MIR482, zma-MIR528a, zma-MIR528b, zma-MIR529, zma-MIR827, zma-MIR1432, osa-MIR395x, osa-MIR395y, osa-MIR2275c, osa-MIR2275d, ath-MIR156i, ath-MIR156j
This was also the case for some other miRNA families, such as zma-miR164 (from 14 read to 25,253 reads) and zma-miR166 (from 931 reads to 300,478 reads). [score:1]
[1 to 20 of 1 sentences]
42
[+] score: 1
mir164 [90] NAC domains including NAC1 and ORE1. [score:1]
[1 to 20 of 1 sentences]
43
[+] score: 1
The newly identified genes were members of diverse gene families such as major facilitator super family (MFS) transporters [AT1G08900, AT1G30560, AT1G33440, AT1G72140, AT1G80530, AT2G26690, AT2G34355, AT3G20460, AT3G45680, AT3G47960, AT4G19450, STP8 (AT5G26250), AT5G27350, and AT5G62680], MATE efflux transporters (AT1G71140, AT5G17700, AT5G19700, and AT5G38030), microRNA genes [MIR156b (AT4G30972), MIR161 (AT1G48267), MIR162b (AT5G23065), MIR164 (AT5G01747), MIR167c (AT3G04765), MIR168b (AT5G45307), MIR396a (AT2G10606), MIR402 (AT1G77235), MIR777a (AT1G70645), and MIR848a (AT5G13887)], various transcription factors (MYB, NAC domain, WRKY, etc. [score:1]
[1 to 20 of 1 sentences]