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![]() 18 publications mentioning ath-MIR157aOpen access articles that are associated with the species Arabidopsis thaliana and mention the gene name MIR157a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR172a, ath-MIR172b, ath-MIR159b, ath-MIR172c, ath-MIR172d, ath-MIR156g, ath-MIR156h, ath-MIR159c, ath-MIR172e, ath-MIR156i, ath-MIR156j
The abundance of SPL3 is regulated directly by miR156/miR157 via miRNA -induced transcript cleavage, and indirectly by the effect of miR156/miR157-regulated SPL proteins on the expression of miR172, which in turn represses a group of AP2-like genes that repress the transcription of SPL3, SPL4, and SPL5 [3, 9, 23, 35].
[score:7]
spl9 completely suppressed the precocious abaxial trichome phenotype and partially suppressed the leaf shape phenotype of mir156a/c, whereas spl13 partially suppressed the effect of mir156a/c mir157a/c on both of these traits (Fig 9).
[score:7]
However, the expression pattern of these miRNAs in successive fully expanded leaves (S2C and S2D Fig) and 1 mm LP (Fig 2) is quite similar, indicating that the factors responsible for variation in the expression of miR156/miR157 during shoot development operate at all stages of leaf development.
[score:7]
SPL9 and SPL13 are essential for the expression of adult vegetative traitsThe degree to which the abundance of different SPL transcripts changes in response to changes in the level of miR156/miR157 does not necessarily reflect the developmental importance of these SPL genes because miR156/miR157 can mediate both transcript cleavage [3, 38– 40] and translational repression [23– 26].
[score:6]
In summary, these results provide further evidence that miR156/miR157 regulate the expression of SPL13 primarily by promoting its translational repression, and also demonstrate that SPL13 activity responds non-linearly to changes in the abundance of these miRNAs.
[score:6]
Our results demonstrate that miR156 and miR157 have different expression patterns, different activity, and mediate transcript cleavage and translational repression to different extents at different SPL genes.
[score:5]
Developmental variation in SPL9 and SPL13 protein levels is mediated primarily by miR156/miR157-directed translational repression.
[score:5]
miR156/miR157 regulate SPL9 and SPL13 by different mechanismsWe studied the mechanism by which miR156/miR157 regulate the expression of SPL9 and SPL13 by comparing the abundance of the SPL9 and SPL13 mRNAs with the abundance of their protein products.
[score:5]
We also quantified the effect of varying miR156/miR157 levels on the expression of their SPL targets.
[score:5]
The expression patterns of miR156/miR157-resistant reporter genes suggest that this increase is largely mediated by miR156/miR157 [21], but whether miR156/miR157 are entirely responsible for the temporal expression pattern of SPL genes is still unknown.
[score:5]
In contrast, the only way in which miR156/miR157 have been found to regulate the expression of other SPL genes is through a direct interaction with their transcripts.
[score:5]
miR157 has the same targets as miR156 and produces an over -expression phenotype similar to that of miR156 [20].
[score:5]
miR156/miR157 are responsible for the temporal expression pattern of most SPL genesBoth the transcripts and the protein products of miR156/miR157-regulated SPL genes increase during shoot development [3, 18, 21, 36, 37].
[score:5]
Some SPL genes are expressed at relatively high levels and respond nearly linearly to changes in the level of miR156/miR157, whereas others are expressed at relatively low levels and only respond significantly to a change in the level of miR156/miR157 when these miRNAs are present at very low levels.
[score:5]
miR157 is more abundant than miR156 and is expressed in a similar temporal pattern, but miR156 plays a more important role in vegetative phase change and is a more potent repressor of SPL gene expression.
[score:5]
This combination of direct post-transcriptional regulation by miR156/miR157 and indirect transcriptional regulation via the miR172-AP2 pathway may be responsible for the hypersensitivity of SPL3 transcripts to variation in the abundance of miR156/miR157.
[score:5]
miRNAs with a 5’ terminal uridine, such as miR156 and miR157, repress the expression of their targets via their association with AGO1 [33].
[score:5]
For example, SPL3 is highly expressed in vegetative shoots and is more sensitive to miR156/miR157 than any other SPL gene, but the phenotype of spl3 mutations demonstrate that it plays little or no role in vegetative development [21].
[score:5]
The expression pattern of miR156 in fully-expanded (FE) leaves matched its expression pattern in LP, but miR157 did not decline as dramatically between FE1&2 and FE3&4 as it did between LP1&2 and LP3&4 (S2C and S2D Fig).
[score:5]
Our observation that variation in the abundance of miR156/miR157 produces non-linear changes in the protein level of their targets suggests a molecular mechanism for the qualitative and quantitative changes in leaf morphology that occur during shoot development.
[score:4]
miR156/miR157 are among the oldest miRNAs in plants, and it is therefore reasonable to conclude that miRNA -induced translational repression is an ancient regulatory mechanism in plants.
[score:4]
We studied the mechanism by which miR156/miR157 regulate the expression of SPL9 and SPL13 by comparing the abundance of the SPL9 and SPL13 mRNAs with the abundance of their protein products.
[score:4]
The expression patterns of miR156 and miR157 during leaf and shoot development.
[score:4]
The degree to which the abundance of different SPL transcripts changes in response to changes in the level of miR156/miR157 does not necessarily reflect the developmental importance of these SPL genes because miR156/miR157 can mediate both transcript cleavage [3, 38– 40] and translational repression [23– 26].
[score:4]
The expression patterns and developmental functions of miR156 and miR157.
[score:4]
Our comparison of the expression patterns of miR156 and miR157, as well the phenotype of plants lacking one or both of these miRNAs, demonstrates that these miRNAs work together to regulate vegetative phase change, but are not functionally identical.
[score:4]
A comparison of the molecular mechanism by which miR156/miR157 regulate the expression of SPL9 and SPL13 will be informative because these genes respond very differently to changes in the level of these miRNAs.
[score:4]
Although it is clear that miR156, and possibly miR157, regulate many of the changes that occur during shoot development, the function of these miRNAs at specific times in development and in specific leaves is poorly understood.
[score:4]
Leaves produced early in shoot development, which have a relatively high level of miR156/miR157, were less sensitive to these mutations than leaves produced later in shoot development, which have a relatively low level of miR156/miR157 (Figs 3 and 4).
[score:4]
The increase in SPL9 activity that occurs during shoot development [21] is probably attributable primarily to a reduction in miR156/miR157 -mediated translational repression because the SPL9-GUS protein increases more significantly in response to a decrease in miR156/miR157 than the SPL9-GUS transcript.
[score:4]
MIR156D and MIR157A are expressed at a much lower level than these loci, but the ability of mir156d and mir157a to enhance the phenotype of plants mutant for mir156a, mir156c, and mir157c demonstrates that they are functionally significant.
[score:3]
To determine which genes produce these transcripts, we identified T-DNA insertions in MIR156A, MIR156C, MIR156D, MIR157A, and MIR157C, and used site-directed mutagenesis to produce mutations in MIR156B.
[score:3]
Our results suggest that the amount of miR156 and miR157 present in both juvenile and adult leaves is sufficient to almost completely saturate the cleavage machinery at most of their targets.
[score:3]
1007337.g006 Fig 6(A) The sequence of miR156 and miR157 transcripts and their target site in SPL transcripts.
[score:3]
However, the response of different SPL transcripts to miR156/miR157 varies between transcripts, suggesting that the susceptibility of these transcripts to miR156/miR157 -induced cleavage depends on sequences outside the miR156/miR157 target site.
[score:3]
The phenotype of plants over -expressing miR156 or miR157 reveals that these miRNAs promote the juvenile vegetative phase, but how they specify heteroblastic patterns of leaf morphology, as well as the individual functions MIR156 and MIR157 genes, are unknown.
[score:3]
miR156/miR157 are responsible for the temporal expression pattern of most SPL genes.
[score:3]
The relative importance of transcript cleavage and translational repression for the activity of miR156/miR157.
[score:3]
Both the transcripts and the protein products of miR156/miR157-regulated SPL genes increase during shoot development [3, 18, 21, 36, 37].
[score:3]
We also show that variation in the level of miR156/miR157 only has a significant effect on SPL gene expression when these miRNAs are present at relatively low levels.
[score:3]
miR156 and miR157 bind to most of their targets with a single mismatch, but this mismatch is located one nucleotide from the cleavage site in the case of miR157 and 3 nucleotides from the cleavage site in the case of miR156.
[score:3]
In these later-formed leaves, a small decrease in the abundance of miR156/miR157 produces a disproportionately large increase in SPL activity, primarily as a result of the increased translation of SPL transcripts.
[score:3]
Previous studies have shown that this phenomenon is regulated by variation in the abundance of the miRNAs, miR156 and miR157, but how miR156/miR157 produce the changes in leaf morphology that occur during shoot development is not understood.
[score:3]
These results demonstrate that miR156/miR157 repress SPL9 both by destabilizing the SPL9 transcript and by repressing its translation.
[score:3]
We found that miR156 and miR157 have similar—but not identical—expression patterns, and that miR157 is more abundant, but less effective, than miR156.
[score:3]
mir156a/c mir157a/c had an even more dramatic effect on the expression of SPL9-GUS, producing a 4-fold increase in the SPL9-GUS transcript and an ~36 fold increase in the SPL9-GUS protein (Fig 10D).
[score:3]
Previous studies have shown that the juvenile forms of these traits require the activity of miR156/miR157 [9], but the relationship between the abundance of these miRNAs and the changes in leaf morphology that occur during shoot development is still unknown.
[score:2]
Our results provide a new view of vegetative phase change in Arabidopsis and the mechanism by which miR156 and miR157 regulate this process.
[score:2]
The effect of mir156 and miR157 mutations on the levels of miR156 and miR157 in 11-day-old seedlings and in 1mm primordia of leaves 1 & 2 is shown in Fig 1. In Col, the miR156 probe hybridized to 20 nt and 21 nt transcripts, with the 20 nt transcripts being more abundant than the 21 nt transcripts (Fig 1A).
[score:2]
miR156/miR157 regulate SPL9 and SPL13 by different mechanisms.
[score:2]
However, plants with multiple mir156 and/or mir157 mutations displayed a significant increase in the level of some SPL transcripts.
[score:2]
The effect of miR156 and miR157 mutations on leaf morphology.
[score:2]
The developmental and molecular functions of miR156 and miR157.
[score:2]
miR157 is more abundant than miR156 and declines more slowly during shoot development.
[score:2]
In general, the morphological phenotype of mir156/mir157 mutations was correlated with their effect on the abundance of miR156 or miR157.
[score:2]
S1 FigRT-qPCR analysis of the effect of mir156 and mir157 mutations on the abundance of the primary transcripts of the corresponding genes.
[score:2]
SPL10, SPL11, SPL13 and SPL15 transcripts, whereas the temporal increase in SPL3 transcripts may be partly regulated by factors that operate independently of miR156/miR157.
[score:2]
A comparison of the effect of different mutations on the intensity of these bands indicates that the 20 nt transcript is miR156 and the 21 band is primarily miR157, with a small contribution from miR156d.
[score:2]
Although the miR156 and miR157 probes cross-hybridize to some extent, the source of the hybridization signal could by determined by comparing the effect of mir156 and mir157 mutations on these signals.
[score:2]
However, the intensity of the 21 nt band was slightly reduced in mir156d-1 and in genotypes containing this mutation; for example, the 21 nt miR156-hybridizing band was slightly less intense in the mir156a/c/d mir157a/c pentuple mutant than in the mir156a/c mir157a/c quadruple mutant (Fig 1A).
[score:2]
Assuming that the mutations present in this pentuple mutant are null alleles, the amount of miR156/miR157 in this line represents the combined output of MIR156E, F, G, H and MIR157B, D. These six genes therefore contribute relatively little to the production of miR156 and miR157 in seedlings.
[score:2]
The effect of mutations in different MIR156 and MIR157 genes on the abundance of miR156 and miR157 demonstrates that MIR156A and MIR156C produce most of the miR156 in the shoot whereas MIR157C produces most of the miR157.
[score:2]
1007337.g004 Fig 4The effect of miR156 and miR157 mutations on leaf morphology.
[score:2]
RT-qPCR analysis of the effect of mir156 and mir157 mutations on the abundance of the primary transcripts of the corresponding genes.
[score:2]
The effect of mir156 and mir157 mutations on abaxial trichome production and leaf shape was correlated with abundance of miR156/miR157 in different leaves.
[score:2]
We do not know if the miR156 and miR157 transcripts that remain in the mir156a/c/d mir156a/c mutant are derived from one or more these loci or from other MIR156/MIR157 genes because we cannot be certain that the mutations present in this mutant stock are completely null.
[score:2]
Additionally, the amount of miR156/miR157 in leaves 1&2 far exceeds the amount that is actually required to determine their identity; mutations that nearly completely eliminate miR156 have a similar effect on leaves 3 and 5, but a much weaker effect on leaf 1. The only genotypes that caused leaf 1 to resemble leaves 3 and 5 were those that reduce miR156/miR157 by 90%.
[score:2]
SPL9 transcripts are more sensitive to changes in miR156/miR157 than SPL13 transcripts (Fig 7), suggesting that transcript cleavage may play a larger role in the regulation of SPL9 than SPL13.
[score:2]
Thus, SPL9 is more sensitive than SPL13 to miR156/miR157-directed transcript cleavage.
[score:2]
Northern analysis using a mixed miR156/miR157 probe revealed that the amount of miR156 and miR157 in the mir156a/c/d mir157a/c pentuple mutant is about 10% of the wild-type level (Fig 1A and 1B).
[score:1]
SPL13 transcripts were unaffected in mir157a/c, were elevated about 2-fold in both mir156a/c and mi156a/c mir157a/c, and were only slightly more abundant than this in mir156a/c/d mir157a/c.
[score:1]
miR157 is absent in Physcomitrella, but is present in Selaginella and most, but not all, higher plants [61].
[score:1]
For example, mir156a, mir157a, mir157c, and mir157a/c caused abaxial trichomes to be produced on leaves 7 and/or 8, but did not affect abaxial trichome production or the shape of leaf 1, 3, and 5. mir156c produced abaxial trichomes on leaves 7 and 8 and significantly reduced the angle of the leaf base in leaves 3 and 5, but had no effect on leaf 1. miR156a/c and mir156a/b/c/d reduced the angle of the leaf blade in leaves 1, 3 and 5, but had a more significant effect on leaves 3 and 5 than on leaf 1; these genotypes only produced abaxial trichomes on leaves 6 and above.
[score:1]
We also found that heteroblastic variation in leaf morphology is correlated with the relative abundance of miR156/miR157, and that different features of leaf morphology are differentially sensitive to the level of these miRNAs.
[score:1]
SPL transcripts are differentially responsive to miR156/miR157To determine the molecular basis for the effect of mir156 and mir157 mutations on leaf morphology, we compared SPL transcript levels in LP1&2 and LP3&4 in wild-type and mir156/mir157 mutant plants (Fig 7).
[score:1]
MIR156A, MIR156C, MIR157A and MIR157C are the major sources of miR156 and miR157.
[score:1]
mir157a/c did not have a significant effect on SPL9-GUS mRNA or protein levels, but mir156a/c produced a 2-fold increase in the SPL9-GUS transcript and a 5-fold increase in the SPL9-GUS protein (Fig 10D).
[score:1]
The 20 nt band was absent in mir156a/c, and thus represents cross hybridization of the miR157 probe with miR156.
[score:1]
However, the normal function of miR157 is still unknown.
[score:1]
However, we cannot rule out the possibility that the difference in the activity of miR156 and miR157 is a consequence of the difference in their length, rather than the specific features of the miRNA:SPL duplex.
[score:1]
The source of miR156 and miR157.
[score:1]
In addition to two internal nucleotides, miR157 differs from miR156 in possessing an additional U at its 5' end.
[score:1]
Most species also possess another miRNA, miR157, that differs from miR156 at 3 nucleotides [19].
[score:1]
To determine the molecular basis for the effect of mir156 and mir157 mutations on leaf morphology, we compared SPL transcript levels in LP1&2 and LP3&4 in wild-type and mir156/mir157 mutant plants (Fig 7).
[score:1]
1007337.g001 Fig 1(A) Northern blot analysis of miR156 and miR157 levels in the shoot apices of 11-day-old wild-type Col and mir156/mir157 mutants grown in LD.
[score:1]
However, mir157a/c had a significantly weaker effect on abaxial trichome production and leaf shape than mir156a/c (Figs 3 and 4), even though these double mutants have approximately the same amount of miR157 and miR156, respectively (Fig 1).
[score:1]
The miR156 and miR157 transcripts used as references were synthesized by IDT, and the SPL transcripts used as references were synthesized by in vitro transcription.
[score:1]
miR156 is more efficiently loaded into AGO1 than miR157.
[score:1]
Synthetic miR156 and miR157 transcripts were serially diluted in 600ng/μl E. coli RNA, and a standard curve was produced by plotting the concentrations of these miR156 and miR157 standards against 2 [-ct] of the corresponding RT-qPCR reaction.
[score:1]
Sequencing of small RNAs from 11-day-old shoot apices (2 replicates of each genotype) revealed an abundant 20 nt transcript that maps to MIR156A, B, C, D, E, and F, an abundant 21 nt transcript that maps to MIR157A, B, and C, a moderately abundant 21 nt transcript that maps to MIR156D, and 3 rare transcripts that map uniquely to MIR156G, MIR157D and MIR156H (Table 1).
[score:1]
1007337.g002 Fig 2 (A) of miR156 and miR157 levels in successive leaf primordia of plants grown in SD.
[score:1]
of SPL transcript levels in 1 mm leaf primordia of Col and mir156/mir157 mutants grown in SD.
[score:1]
Genes contributing to the production of miR156 and miR157 in vegetative shoots.
[score:1]
Is miR157 less active than miR156?.
[score:1]
Although miR157 is nearly as old and as highly conserved as miR156, this is not wi dely appreciated because miR157 is frequently annotated as miR156 in small studies and in miRBase (http://www.
[score:1]
Most transcripts increase less than 2-fold between LP1&2 and LP3&4 in Col, and increase 2-fold or less in miR156 and miR157 mutants.
[score:1]
The juvenile-to-adult transition occurred during the period when miR156 and miR157 were declining very gradually, and was accompanied by a relatively small change in the abundance of these transcripts.
[score:1]
Hybridization with a mixed miR156/miR157 probe revealed that miR157 (21 nt band) was more abundant than miR156 (20 nt band) in the input fraction, but that miR156 was as abundant as miR157 in the IP fraction (Fig 5).
[score:1]
1007337.g009 Fig 9 SPL9 and SPL13 contribute to the precocious phenotype of mir156 and mir157 mutants.
[score:1]
Thus, the transition between leaves 1&2 and leaves 3&4 is accompanied by a major decline in the level of miR156 and miR157 whereas subsequent changes in leaf morphology are associated with much smaller changes in the abundance these miRNAs.
[score:1]
SPL9 and SPL15 transcripts increased very slightly in mir156a/c and mir157a/c but increased up to 6-fold in mir156a/c mir157a/c and mir156a/c/d mir157a/c.
[score:1]
miR156 was present in LP1&2 at a concentration of 1.96 ± 0.1 x 10 [5] copies per ng total RNA, whereas miR157 was present at a concentration of 2.45 ± 0.2 x 10 [5] copies per ng total RNA (Fig 2B).
[score:1]
To address this question, we introduced spl9 into a mir156a/c mutant background and introduced spl13 into a mir156a/c mir157a/c mutant background.
[score:1]
miR157 also has an additional 5' nucleotide (relative to miR156), which is unpaired in the miR157:SPL13 duplex.
[score:1]
miR157 is more abundant than miR156 and was therefore expected to play a larger role in vegetative phase change than miR156.
[score:1]
Alternatively, the temporal increase in SPL3 may be attributable to the small amount of miR156/miR157 remaining in this quadruple mutant.
[score:1]
miR157 (21 nt) was more abundant than miR156 (20 nt) in the input fraction, whereas miR156 and miR157 were about equally abundant in the IP fraction from AGO1-FLAG/ ago1-36 plants.
[score:1]
However, this is not the only reason for the difference in their activity because the amount of miR157 associated with AGO1 is not dramatically lower than the amount of miR156 associated with AGO1.
[score:1]
miR157 declined to a lesser extent: LP 3&4 had approximately 50%, LP9 had 25%, and LP13 had 17% of the amount of miR157 present in LP1&2 (Fig 2).
[score:1]
SPL2, SPL10 and SPL11 increased 2-fold or less in mir156a/c and mir157a/c, and only about 3-fold in mir156a/c mir157a/c and mir156a/c/d mir157a/c.
[score:1]
Unexpectedly, miR157-related transcripts were more abundant than miR56-related transcripts.
[score:1]
This cannot be the only reason for the difference in the phenotypes of mir156a/c and mir157a/c because the amount of miR156 and miR157 associated with AGO1 is quite similar.
[score:1]
The only unexpected result was the phenotype of mir157a/c.
[score:1]
These findings therefore suggest that the SPL2, SPL9, SPL10, SPL11, SPL13 and SPL15 transcripts are differentially sensitive to destabilization by miR156 and miR157.
[score:1]
1007337.g003 Fig 3(A) Rosettes of three-week-old Col, and miR156 and miR157 single and multiple mutant plants grown in SD.
[score:1]
Consistent with our previous analyses of shoot apices [21], miR156 and miR157 decrease significantly from LP1&2 to LP3&4, and then decline more gradually before reaching a relatively constant level around leaf 13 (Fig 2).
[score:1]
These results demonstrate that abaxial trichome production is more sensitive to miR156/miR157 than leaf morphology, and is strongly repressed by even low levels of these miRNAs.
[score:1]
The intensity of the 20 nt and 21 nt bands on the blot probed with a 1:1 mixture of the miR156 and miR157 probes was quantified by normalizing the intensity of each band to t-Met, and then to Col; these data are shown in the table below the figure.
[score:1]
To compare the sensitivity of the SPL9 and SPL13 transcripts to miR156/miR157 -mediated cleavage, we used a modified form of 5’ RNA Ligase Mediated Rapid Amplification of cDNA Ends (5’ RLM-RACE) [3, 41] to quantify the ratio of un-cleaved/cleaved SPL9 and SPL13 transcripts in wild-type Col and mutants deficient for miR156 and miR157.
[score:1]
This result indicates that miR156 is more efficiently loaded onto AGO1 than miR157.
[score:1]
miR156- and miR157-related transcripts in 11-day-old FRI FLC and FRI flc-3 seedlings.
[score:1]
a = significantly different from Col; b = significantly different from mir56a and miR156c; c = significantly different from miR15a and miR157c; d = significantly different from miR156a/c and miR157a/c; e = significantly different from miR156a/c mir157a/c; f = significantly different from mir156a/c/d mir157a/c (Student's t test; p < 0.01; n = 18 to 23).
[score:1]
MIR156A, MIR156C, MIR157A and MIR157C are the major sources of miR156 and miR157In Arabidopsis, miR156 is encoded by 8 genes and miR157 is encoded by 4 genes.
[score:1]
miR156 and miR157 bind to the SPL2, SPL9, SPL10, SPL11, and SPL15 transcripts with only one mismatched nucleotide, although the position of this nucleotide is different for the two miRNAs (Fig 6A).
[score:1]
a = significantly different from Col; b = significantly different from mir156a/c, c = significantly different from miR156a/c mir157a/c.
[score:1]
The phenotype of plants mutant for genes encoding miR156 and miR157.
[score:1]
RT-qPCR (S2A Fig) and Northern analysis (S2B Fig) demonstrate that miR156 and miR157 increase as leaves expand.
[score:1]
The intensity of the 21 nt miR157-hybridizing band was reduced to 81 ± 13% (± SD, n = 4) of wild-type in mir157a-1, to 26 ± 5% (± SD, n = 7) of wild-type in mir157c-1 (mir157c), and to 13 ± 2% (± SD, n = 3) of wild-type in the mir157a/c double mutant.
[score:1]
The difference in the activity of these miRNAs may be due, in part, to the lower efficiency with which miR157 is loaded onto AGO1.
[score:1]
In Arabidopsis, miR156 is encoded by 8 genes and miR157 is encoded by 4 genes.
[score:1]
miR156/miR157 are present at very high levels in the first two rosette leaves, where they act as buffers to stabilize leaf identity.
[score:1]
This 5’ U is unpaired in the miR157-SPL13 duplex (Table 1).
[score:1]
We suspect that this phenomenon is attributable to functional differentiation between SPL genes, coupled with variation in their sensitivity to miR156 and miR157.
[score:1]
A 1:1 ratio of miR156 and miR157 probes was used for mixed probe hybridizations.
[score:1]
We then determined the absolute amount of these miRNAs in LP by comparing the RT-qPCR results obtained with leaf samples to the results obtained using known quantities of miR156 and miR157.
[score:1]
miR156 subsequently declined to approximately 2.6 x 10 [4] copies per ng total RNA in LP9, whereas miR157 declined to 6.1 x 10 [4] copies per ng total RNA.
[score:1]
Consequently, instead of using this ratio to compare the relative abundance of cleaved SPL9 and SPL13 transcripts, we asked whether the cleavage of these transcripts is differentially sensitive to variation in the level of miR156/miR157.
[score:1]
The ratio of un-cleaved:cleaved SPL13 transcripts was about 2-fold greater in mir156a/c and mir156a/c mir157a/c than in Col, whereas the ratio of un-cleaved:cleaved SPL9 transcripts was 5-fold greater in mir156a/c and 15-fold greater in mir156a/c mir157a/c than in Col (Fig 10E).
[score:1]
Hybridization with a 1:1 mixture of miR156/miR157 probes revealed that 21 nt transcripts are significantly more abundant than 20 nt transcripts in 11 day-old seedlings and in the primordia of leaves 1&2 (Fig 1A and 1B).
[score:1]
In contrast, SPL3 transcripts were relatively insensitive to a decrease in miR157, except in genotypes that were also deficient for miR156.
[score:1]
The 21 nt band was reduced significantly in mir157a/c, and therefore corresponds primarily to miR157, whereas the 20 nt band was nearly absent in mir156a/c, and therefore corresponds to miR156.
[score:1]
This result suggests that miR156/miR157 are entirely responsible for the temporal increase in the SPL2, SPL9.
[score:1]
1007337.g008 Fig 8RT-qPCR analysis of SPL transcript levels in successive 1 mm leaf primordia of the mir156a/c mir157a/c mutant.
[score:1]
of SPL transcript levels in successive 1 mm leaf primordia of the mir156a/c mir157a/c mutant.
[score:1]
Only genotypes with very low levels of miR156/miR157 (e. g., miR156a/c mir157a/c, mir156a/c/d mir157a/c, 35S:: MIM156) cause these leaves to resemble adult leaves (Figs 3B and 4B).
[score:1]
Given that SPL genes are not functionally identical [9, 21, 50], conditions that produce small changes in miR156/miR157, or which elevate the transcription of particular SPL genes above the threshold established by miR156/miR157, could lead to unusual combinations of phase-specific traits.
[score:1]
We found that leaves 1&2 have a significantly more miR156/miR157 than other juvenile leaves, and that the largest absolute as well as relative decrease in these miRNAs occurs between leaves 1&2 and leaves 3&4.
[score:1]
These results are consistent with the results of (Table 1), and demonstrate that miR157 is more abundant than miR156 in young seedlings.
[score:1]
In Col, the miR156 and miR157 probes hybridize to 21 and 20 nt bands.
[score:1]
SPL transcripts are differentially responsive to miR156/miR157.
[score:1]
This observation demonstrates that miR157 is less important for vegetative phase change than miR156, and suggests that it may be less active than miR156.
[score:1]
This combination of quantitative and qualitative changes, as well as the morphological plasticity of late juvenile leaves, can be explained by the relatively low and gradually decreasing level of miR156/miR157 in successive leaves, and by the non-linear response of some SPL genes to changes in the abundance these miRNAs.
[score:1]
mir156b and mir156d have very minor effects on the abundance of mir156 (Fig 1) and also have minor effects on shoot morphology; mir156b did not significantly enhance the phenotype of mir156a or mir156a/c, and mir156d only produced a significant effect on leaf morphology in combination with mir156a/c and mir157a/c.
[score:1]
We were particularly interested in determining whether SPL9 and SPL13 contribute to the precocious phenotype of mir156/mir157 mutants because SPL9 transcripts increase as miR156/miR157 levels decline, whereas SPL13 transcripts are relatively insensitive to changes in these miRNAs (Fig 7).
[score:1]
These results demonstrate that the major miR157 transcript is 21 nt, and that MIR157C is the major source of this transcript.
[score:1]
In wild-type Col, the miR157 probe hybridized strongly to 21 nt transcripts and more weakly to 20 nt transcripts (Fig 1A).
[score:1]
SPL13 plays a major role in vegetative phase change [21] and if this mismatch reduces the ability of miR157 to repress the activity of SPL13, this would be expected to have a significant phenotypic effect.
[score:1]
Another possibility is that the AGO1-miR157 complex is inherently less active than the AGO1-miR156 complex.
[score:1]
miR156a/c mir157a/c and mir156a/c/d mir157a/c had a significant effect on the shape of leaves 1, 3, and 5, but rarely produced abaxial trichomes on leaf 2, and never produced abaxial trichomes on leaf 1 (Figs 3 and 4).
[score:1]
The blots were hybridized with 1:1 mixed miR156 and miR157 probes, and the results were quantified as described above.
[score:1]
SPL9 and SPL13 contribute to the precocious phenotype of mir156 and mir157 mutants.
[score:1]
We then examined the amount of miR156 and miR157 in these stocks by hybridizing RNA blots with probes for miR156, miR157, and a combination of both probes.
[score:1]
They also reveal that the amount of miR156/miR157 in leaves 1&2 far exceeds the amount required to specify their identity.
[score:1]
The absence of abaxial trichomes on leaves 1 and 2 is attributable to the small amount of miR156/miR157 remaining in these mutants because 35S:: MIM156 consistently produced abaxial trichomes on both of these leaves (Fig 4A).
[score:1]
Nucleotides that are mis-paired in the miR156/miR157:SPL duplex are shown in different colors.
[score:1]
The fact that miR157 has been conserved along with miR156 during plant evolution suggests that it is not completely redundant with miR156, and raises the possibility that the relative activity of these miRNAs may differ in different species.
[score:1]
1007337.g007 Fig 7RT-qPCR analysis of SPL transcript levels in 1 mm leaf primordia of Col and mir156/mir157 mutants grown in SD.
[score:1]
Indeed, we only observed a major increase in SPL transcripts in the mir156a/c mir157a/c quadruple mutant, implying that transcript cleavage does not require high levels of these miRNAs.
[score:1]
For example, SPL3 was elevated nearly 20 fold in LP3&4 of the mir156a/c/d mir157a/c pentuple mutant.
[score:1]
This result demonstrates that MIR156D is less effective than MIR156A, and suggests that the additional 5' U in miR157 is partly responsible for its lower biological activity.
[score:1]
These results provide a foundation for detailed studies of the molecular mechanism of miR156/miR157 activity and their role in shoot morphogenesis.
[score:1]
We suspect that this extra 5' uracil is primarily responsible for the relatively low activity of miR157 because miR156d also has an extra 5' uracil and is significantly less active than miR156, despite being otherwise identical to miR156.
[score:1]
Small RNAs were then extracted from both the IP and non-IP fractions and subjected to Northern analysis using a mixed miR156/miR157 probe.
[score:1]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR156g, ath-MIR156h, ghr-MIR156a, ghr-MIR156b, ghr-MIR156c, ghr-MIR156d, gra-MIR157a, gra-MIR157b, ath-MIR156i, ath-MIR156j
Liu et al. [8] reported the expression level of GhSPLs and two MADS-box genes (orthologs of AtAGL6 and SITDR8) were repressed in the miR157 over -expression cotton lines.
[score:5]
Motif 7 contained the miR156/miR157 recognition element as a target site for the miR156/miR157 in 3′ UTR.
[score:3]
Thus, SPL gene function analysis mainly through significantly represses the SPL transcriptions by over -expression of miR156/miR157.
[score:3]
Interestingly, motif 7 was existed in those SPLs, and it is a potential target site for the miR156/miR157.
[score:3]
Hypothesized that the miR157/SPL may regulate floral organ size and ovule production in cotton.
[score:2]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR161, ath-MIR164a, ath-MIR164b, ath-MIR165a, ath-MIR165b, ath-MIR169a, ath-MIR172a, ath-MIR172b, ath-MIR159b, 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-MIR390a, ath-MIR390b, ath-MIR395a, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, ath-MIR402, ath-MIR156g, ath-MIR156h, ath-MIR159c, ath-MIR164c, ath-MIR172e, ath-MIR417, ath-MIR447a, ath-MIR834, ath-MIR824, ath-MIR854a, ath-MIR854b, ath-MIR854c, ath-MIR854d, ath-MIR2112, ath-MIR854e, ath-MIR156i, ath-MIR156j
Among the ten SPLs in Arabidopsis, we chose SPL3 (Fig. 4h), SPL9 (Fig. 4i) and SPL10 (Fig. 5a), since they are the targets of both miR156 and miR157.
[score:3]
Similar expression patterns were observed in case of both miR156h (Fig. 2e) and miR157a/c or, d (Fig. 2f).
[score:3]
In both of the cases, we observed highest level of expression at 24 h/4 °C (2 fold in miR156 and ~5 fold in miR157).
[score:3]
According to the previous report, miR156 and its closely related miR157 [33] are the principal regulators of transition from juvenile to adult phase.
[score:2]
Among these eighteen precursor miRNA, miR157a, miR157c, miR157d consist of same mature sequence; so we took only one mature sequence of miR157 (Fig. 2f) among the three.
[score:1]
The miR157 families a, c and d constitute the same mature miRNA sequences.
[score:1]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR172a, ath-MIR172b, ath-MIR171b, ath-MIR172c, ath-MIR172d, ath-MIR156g, ath-MIR156h, ath-MIR172e, ath-MIR156i, ath-MIR156j
miR156/miR157 are expressed at high levels in organs produced early in shoot development, where they repress the expression of their targets, SQUAMOSA PROMOTER BINDING PROTEIN (SBP) transcription factors [3, 5– 9].
[score:8]
miR156, and the closely related miRNA, miR157, are the master regulators of the transition from the juvenile to the adult phase of vegetative development (vegetative phase change) [3, 4].
[score:3]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR170, ath-MIR171a, ath-MIR171b, ath-MIR171c, ath-MIR156g, ath-MIR156h, ath-MIR156i, ath-MIR156j
Binding of the miR156 and miR157 Families with the mRNAs of SPL Paralogs.
[score:1]
The maximal interaction energy (Δ G [m]) for miR156, miR157, miR170, miR171, and their families was equal to the binding energy of perfectly complementary sequences.
[score:1]
The miR157a–c sequences differ from the miR156a sequence by one nucleotide at the 5′-end.
[score:1]
For example, Oryza sativa and Zea mays have only the miR156 family and not the miR157 family (miRBase).
[score:1]
We found that, among 328 miRNAs in A. thaliana, the miR156 and miR157 families are shown to have strong binding sites within the squamosa promoter binding protein-like (SPL) gene family of transcription factors.
[score:1]
Binding of the miR156 and miR157 Families with the mRNAs of SPL ParalogsWe found that, among 328 miRNAs in A. thaliana, the miR156 and miR157 families are shown to have strong binding sites within the squamosa promoter binding protein-like (SPL) gene family of transcription factors.
[score:1]
miR157a–d bind to the mRNAs of the SPL family at the same site as miR156a–j (Table 2).
[score:1]
It is likely that ath-miR156a–j and ath-miR157a–d are members of the same family.
[score:1]
Therefore, we suggest that the miRNAs of the miR156 and miR157 families belong to the same family.
[score:1]
According to the miRBase database, ath-miR156a–j and ath-miR157a–d belong to different families.
[score:1]
The Δ G/Δ G [m] value of the miR157a–d -binding sites ranged from 89.5% to 92.5% (Table 2).
[score:1]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR158a, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR162a, ath-MIR162b, ath-MIR164a, ath-MIR164b, ath-MIR165a, ath-MIR165b, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR168a, ath-MIR168b, ath-MIR169a, ath-MIR170, ath-MIR171a, 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-MIR171c, ath-MIR172c, ath-MIR172d, ath-MIR390a, ath-MIR390b, ath-MIR393a, ath-MIR393b, ath-MIR394a, ath-MIR394b, ath-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, ath-MIR396a, ath-MIR396b, ath-MIR397a, ath-MIR397b, ath-MIR398a, ath-MIR398b, ath-MIR398c, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, ath-MIR403, ath-MIR156g, ath-MIR156h, ath-MIR158b, ath-MIR159c, ath-MIR319c, ath-MIR164c, ath-MIR167c, ath-MIR172e, ath-MIR156i, ath-MIR156j
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]
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]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR164a, ath-MIR164b, ath-MIR396a, ath-MIR398a, ath-MIR398b, ath-MIR398c, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, ath-MIR408, ath-MIR156g, ath-MIR156h, ath-MIR164c, ath-MIR447a, ath-MIR447b, ath-MIR447c, ath-MIR827, ath-MIR156i, ath-MIR156j
Despite overlapping predicted targets, it has recently been reported that miR156 and miR157 family members do mediate differential cleavage of specific SPL transcripts (Meng et al. 2012).
[score:3]
The senescence repression of miR157 in leaves without any change in miR156 therefore may be a fine-tuning mechanism to control expression of specific SPLs as senescence progresses in leaves.
[score:3]
Both miR156 and miR157 had different expression patterns in siliques compared with leaves, where they both increased strongly in late senescence.
[score:2]
Intriguingly, miR157 showed a slight decrease during senescence in leaves while its close relative, miR156 was unchanged (Fig. 3a).
[score:1]
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Other miRNAs from this paper: ath-MIR168a, ath-MIR168b, ath-MIR171a, ath-MIR171b, ath-MIR171c, ath-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, ath-MIR396a, ath-MIR396b, ath-MIR397a, ath-MIR397b, ath-MIR398a, ath-MIR398b, ath-MIR398c, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, ath-MIR408, ath-MIR167c, ath-MIR826a, ath-MIR857, ath-MIR826b
Moreover, several pri-miRNAs seemed to be Cd-specific in this experimental design, by which is meant that these pri-miRNAs (in roots: pri-miR157a, pri-miR397a and pri-miR857; in leaves: pri-miR167c and pri-miR857) were only expressed after exposure to Cd and not (or very lowly) expressed in control conditions as well as after Cu exposure (Table 1).
[score:5]
Striking is the opposite regulation after Cu and Cd exposure of miR398b/c in the leaves and the specific Cd-responsive miRNAs, namely miR157a, miR167c, miR397a and miR857 that were not (or very low) expressed under control conditions or after Cu exposure (Table 1).
[score:4]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR164a, ath-MIR164b, ath-MIR156g, ath-MIR156h, ath-MIR164c, ath-MIR156i, ath-MIR156j
To test whether SPL suppression of LAS expression has biological relevance to AM initiation, we analyzed AM initiation in the spl9-4 spl15-1 mutant and in a pSPL9::rSPL9 line containing mutations in the target sites for miR156 and miR157 (Wu & Poethig, 2006; Wang et al, 2008; Li et al, 2012).
[score:8]
[1 to 20 of 1 sentences]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR158a, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR161, ath-MIR162a, ath-MIR162b, ath-MIR165a, ath-MIR165b, ath-MIR167a, ath-MIR167b, ath-MIR168a, ath-MIR168b, ath-MIR171a, ath-MIR172a, ath-MIR172b, ath-MIR173, ath-MIR159b, ath-MIR319a, ath-MIR319b, ath-MIR167d, ath-MIR171b, ath-MIR172c, ath-MIR172d, ath-MIR390a, ath-MIR390b, ath-MIR396a, ath-MIR396b, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, ath-MIR402, ath-MIR403, ath-MIR156g, ath-MIR156h, ath-MIR158b, ath-MIR159c, ath-MIR319c, ath-MIR167c, ath-MIR172e, ath-MIR773a, ath-MIR774a, ath-MIR778, ath-MIR827, ath-MIR829, ath-MIR845a, ath-MIR855, ath-MIR854a, ath-MIR854b, ath-MIR854c, ath-MIR854d, ath-MIR859, ath-MIR845b, ath-MIR2933a, ath-MIR2933b, ath-MIR2934, ath-MIR2936, ath-MIR2937, ath-MIR2938, ath-MIR2939, ath-MIR773b, ath-MIR774b, ath-MIR854e, ath-MIR156i, ath-MIR156j
Given the presence of miRs targeting transcription factor families such as SPL (miR156/miR157), MYB/TCP (miR159, miR319), ARF (miR160, miR167), AP2 (miR172), and GRF (miR396) there can be no doubt that miRs modulate the expression of many transcription factors during later stages of pollen development.
[score:6]
miR157, miR845 and ath-MIR2939 were not amplified from leaf material and may therefore be pollen-specific, or very strongly pollen enriched (Figure 2).
[score:1]
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Other miRNAs from this paper: ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR398a, ath-MIR398b, ath-MIR398c, ath-MIR824, bol-MIR824, bra-MIR824, bra-MIR157a, bol-MIR157a, bol-MIR398a, ath-MIR5021, bra-MIR398
These miRNAs are reported to function in regulation of genes related to growth (miR157/171/824) [59], Brassica-specific stomatal organization (miR824), pollen development (miR824) [60], abiotic stress tolerance, and plant–pathogen interactions (miR398) [61].
[score:3]
[1 to 20 of 1 sentences]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR156g, ath-MIR156h, ath-MIR5021, ath-MIR156i, ath-MIR156j
Genes AT4G12080, AT1G53160 and AT2G03750 had target sites for the miR156/miR157 in their 3′ UTRs.
[score:3]
[1 to 20 of 1 sentences]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, osa-MIR156a, osa-MIR156b, osa-MIR156c, osa-MIR156d, osa-MIR156e, osa-MIR156f, osa-MIR156g, osa-MIR156h, osa-MIR156i, osa-MIR156j, ath-MIR156g, ath-MIR156h, osa-MIR156k, osa-MIR156l, osa-MIR818a, osa-MIR818b, osa-MIR818c, osa-MIR818d, osa-MIR818e, osa-MIR1436, ath-MIR5021, ath-MIR156i, ath-MIR156j, osa-MIR818f
In Arabidopsis, AT1G53160.2-2 (represents the 2 [nd] intron of the transcription form AT1G53160.2 of the gene AT1G53160) was regulated by ath-miR156 and ath-miR157 (Figure 1A).
[score:2]
[1 to 20 of 1 sentences]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, 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-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
miR156, miR159, miR167, miR319, miR396 and miR172 possessed 5, 8, 10, 8, 7 and 6 members respectively whereas other miRNA families such as miR157, miR160, miR169, miR858, miR894, miR2111 etc.
[score:1]
Only one read was detected form miR157, 160, 403, 414, 482, 1511, 2111, 3520, 5084.
[score:1]
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR165a, ath-MIR165b, 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]
As a negative test case, we took 21 Arabidopsis “a” precursors (ath-MIR156a, ath-MIR157a, etc. )
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Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR172a, ath-MIR172b, ath-MIR172c, ath-MIR172d, ath-MIR156g, ath-MIR156h, ath-MIR172e, ath-MIR156i, ath-MIR156j
Therefore, from a molecular perspective juvenility can be defined as the period during which the abundance of antiflorigenic signals such as miR156/miR157 is sufficiently high to repress the transcription of FT and SPL genes (Matsoukas, 2014).
[score:1]
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Other miRNAs from this paper: ath-MIR158a, ath-MIR160b, ath-MIR167a, ath-MIR167b, ath-MIR168a, ath-MIR168b, ath-MIR171a, ath-MIR167d, ath-MIR171b, ath-MIR171c, ath-MIR398a, ath-MIR398b, ath-MIR398c, ath-MIR167c
In contrast, the precursors of miR157A, miR158A, miR160B, and miR167D are clock-controlled (Hazen et al., 2009).
[score:1]
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Other miRNAs from this paper: ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR163, ath-MIR164a, ath-MIR164b, ath-MIR165a, ath-MIR165b, ath-MIR166a, ath-MIR166b, ath-MIR166c, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR167a, ath-MIR167b, ath-MIR169a, ath-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-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-MIR319c, ath-MIR164c, ath-MIR167c, ath-MIR472, ath-MIR859
mir157 [87] [88] SPL family members, including SPL3, SPL4, and SPL5.
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