sort by

37 publications mentioning ath-MIR166c

Open access articles that are associated with the species Arabidopsis thaliana and mention the gene name MIR166c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 488
Expression of miR166/165 was induced and expression of target HD-ZIP IIIs was downregulated after treatment with BAP, ABA and JA, which suggests their transcriptional regulation in root through phytohormone signaling (Figs  1 and 5). [score:11]
Although auxin did not induce miR166/165 expression at 6 hrs of the treatment, the expression of KANs was induced by 2.5 to 5 folds, which could downregulate HD-ZIP IIIs transcription (Fig.   5A). [score:8]
Phytohormones differentially regulate the expression of HD-ZIP IIIs during root developmentSince miR166/165 cleaves and negatively regulates HD-ZIP III transcripts, differential root growth observed in miR166-Oe plants upon phytohormone treatment might be due to the altered expression levels of HD-ZIP IIIs [19]. [score:8]
KANs show differential expression pattern in response to phytohormonesWe showed that phytohormones regulate the expression of miR166/165 and its target HD-ZIP IIIs. [score:8]
Expression of mature miR166/165 was upregulated upon ABA treatment and miR166-Oe roots were more sensitive to ABA treatment, suggesting possible involvement of miR166/165 in ABA mediated stress responses through negative regulation of HD-ZIP IIIs transcript level. [score:7]
To understand whether phytohormones regulate the expression of miR166/165 and contribute to miR166/165 mediated root development, we analyzed the expression of miR166/165 upon treatment with aforesaid phytohormones at different time intervals (1, 6, 12, and 24 hrs). [score:7]
Our results have shown that the expression of miR166/165 is upregulated upon JA and SA treatment, suggesting that miR166/165 may play role in biotic and abiotic stress responses through the regulation of HD-ZIP IIIs transcript level. [score:7]
Roots of npr1-2 show reduced expression level of miR166/165 in comparison to wild type, which further confirmed SA mediated upregulation of miR166/165 in Arabidopsis roots. [score:6]
Differential expression of MIR166 precursors contributes to the altered level of miR166/165 level in response to hormonesWe observed that phytohormones affect the expression of mature miR166/165 and root development. [score:6]
Based on these results, we proposed a mo del showing complex hormonal regulation of miR166, HD-ZIP IIIs and KANs, which advocates that these genes act simultaneously during root development, involve some feedback regulation, and thus regulate root growth in Arabidopsis in a complex regulatory network (Fig.   7). [score:6]
However, the expression of miR166/165 was downregulated after 24 hrs of the treatment (Fig.   1F). [score:6]
miR166/165 regulates diverse developmental processes including shoot apical meristem (SAM) maintenance, leaf polarity, floral development, and root development in plants by negatively regulating HD-ZIP III gene family members - PHABULOSA (PHB), PHAVOLUTA (PHV), REVOLUTA (REV), ARABIDOPSIS THALIANA HOMEOBOX 8 (ATHB8) and ARABIDOPSIS THALIANA HOMEOBOX 15 (ATHB15) 14– 17. [score:6]
Although the expression of miR166/165increased up to 2.3 fold at 6 hrs of the treatment, the upregulation of HD-ZIP IIIs genes could largely be due to their transcriptional induction upon GA treatment. [score:6]
Stem-loop qRT-PCR results showed that the exogenous IAA treatment led to the downregulation of miR166/165 expression level. [score:6]
We showed that phytohormones regulate the expression of miR166/165 and its target HD-ZIP IIIs. [score:6]
After 6, 12, and 24 hrs of ABA treatment, the expression level of mature miR166/165 was upregulated by 2.2, 1.5 and 37–40 folds, respectively (Fig.   1C). [score:6]
To study the hormone dependent regulation of miR166/165 expression, we analyzed the expression level of miR166/165 in response to different phytohormones. [score:6]
In the present study, we have analyzed the effects of various phytohormones on the expression pattern of miR166/165 s (precursors and mature), their target HD-ZIP IIIs and KAN genes during root development. [score:6]
In case of GA, CK, ABA, JA, and SA treatment, expression and accumulation of mature miR166/165 was found to be upregulated at 12 hrs of the treatment (Fig.   1B–F). [score:6]
GA treatment induced the expression level of miR166/165 at all time points, showing highest upregulation up to 2.5 fold at 6 hrs of treatment (Fig.   1B). [score:6]
Decrease in the expression level of total HD-ZIP IIIs and induced expression of miR166/165 upon BAP treatment indicate a complex transcriptional and post-transcriptional regulation of HD-ZIP IIIs by CK. [score:6]
miR166/165 post transcriptionally regulates HD-ZIP IIIs expression, whereas KANs and HD-ZIP IIIs regulate each other transcriptionally through auxin biogenesis, signaling, transport components 36, 37. [score:5]
Thus, the precise spatio-temporal expression of seven MIR166 genes is possibly controlled by their transcriptional regulation in specific cell-types at specific stages of development. [score:5]
Jung JH Park CM MIR166/165 genes exhibit dynamic expression patterns in regulating shoot apical meristem and floral development in ArabidopsisPlanta. [score:5]
These results suggest that phytohormones dynamically regulate the expression of miR166/165 during stages of root development. [score:5]
We showed that CK treatment induced the expression level of both miR166/165 and KANs, whereas reduced the expression of total HD-ZIP IIIs. [score:5]
Thus, SA treatment induced the expression of both miR166/165 and its target HD-ZIP IIIs genes. [score:5]
Our results uncover a complex hormonal crosstalk regulating HD-ZIP IIIs transcript level (at transcriptional/post-transcriptional level) by modulating the expression of miR166/165, KANs and hormone signaling during root development. [score:5]
HD-ZIP IIIs transcript level depend on post-transcriptional regulation by miR166/165 and transcriptional regulation by KANs and phytohormonesmiR166/165 cleaves HD-ZIP III transcripts and differential root growth observed in miR166-Oe plants upon phytohormone treatment might be the result of altered expression levels of HD-ZIP IIIs [19]. [score:5]
These differential expression patterns of seven MIR166 precursors at different time intervals of treatment indicated their temporal transcriptional regulation by developmentally important phytohormones. [score:5]
When we checked the expression of miR166/165 in DELLA pentuple mutant, we found increased expression level of miR166/165, similar to the exogenous GA treatment (Fig.   3B). [score:5]
Over expression of miR166 (miR166-Oe) alters the sensitivity of roots to hormonesWe have recently reported that miR166-Oe affects primary root growth through down regulation of HD-ZIP IIIs transcripts [19]. [score:4]
Mature miR166/165 s are derived from the precursors of their respective MIR166/165 genes, which showed differential expression pattern in response to phytohormone treatment indicating their transcriptional regulation through phytohormones. [score:4]
In comparison to wild type, the expression of miR166/165 was reduced in arr1 arr12 mutant, which further confirmed the CK mediated regulation of miR166/165 (Fig.   3D). [score:4]
Phytohormones dynamically regulate the expression pattern of miR166/165 in roots. [score:4]
Since miR166/165 cleaves and negatively regulates HD-ZIP III transcripts, differential root growth observed in miR166-Oe plants upon phytohormone treatment might be due to the altered expression levels of HD-ZIP IIIs [19]. [score:4]
In addition to miR166/165, KAN genes also regulate the expression of HD-ZIP III genes in an antagonistic manner [22]. [score:4]
This finding suggests that the effect of IAA on root growth in miR166-Oe plants is the result of altered expression of HD-ZIP IIIs genes through both transcriptional and post-transcriptional regulation. [score:4]
Overexpression of miR166/165 mediated reduction of HD-ZIP IIIs alters the sensitivity of roots towards phytohormonesWe have previously described that primary root elongation in miR166- Oe is promoted by down regulation of HD-ZIP IIIs [19]. [score:4]
miR166/165 and HD-ZIP IIIs mediated root growth and development is regulated by various hormones such as IAA (red lines), GA (green lines), CK (grey lines), ABA (purple lines), JA (blue lines) and SA (orange lines) through transcriptional regulation of miR166/165, HD-ZIP IIIs and KAN genes. [score:4]
Various hormone insensitive mutants showed differential expression pattern of miR166/165, which further confirmed their hormonal regulation (Fig.   3). [score:4]
To further confirm our result, we checked the expression of miR166/165 in seedlings of IAA insensitive auxin resistant2-1 (axr2-1) mutant, which is defective in auxin perception and root development [25]. [score:4]
On the other hand, BAP treatment induced the expression level of both KANs and miR166/165 at each time point, suggesting their linear temporal regulation by CK signaling in root at transcriptional and post-transcriptional level (Figs  5F and 6D). [score:4]
For the analysis of transcript level of uncleaved or non -targeted HD-ZIP IIIs, primers were designed in coding regions flanking miR166/165 target sites. [score:4]
Stem-loop qRT-PCR results showed that the exogenous GA treatment led to the upregulation of miR166/165 level. [score:4]
Opposite expression of miR166/165 in hormone insensitive mutants, as shown by our qRT-PCR and whole mount in-situ hybridization experiments, further suggests their transcriptional regulation through phytohormones (Fig.   1 and Supplemental Fig.   S3). [score:4]
Phytohormone signaling regulates expression of miR166/165. [score:4]
In contrast to other phytohormones, IAA negatively regulates expression of miR166/165. [score:4]
We observed that phytohormones affect the expression of mature miR166/165 and root development. [score:4]
To confirm the transcriptional regulation of miR166/165 through phytohormones, we analyzed the expression of miR166/165 in hormone insensitive mutants. [score:4]
BAP treatment induced the expression level of both KANs and miR166/165 at all the time points, suggesting their linear temporal regulation by CK signaling in root (Figs  5F and 6D). [score:4]
Collectively these results suggest that the sensitivity of miR166-Oe plant roots vary in response to different phytohormone treatments, which could be the effect of downregulation of HD-ZIP IIIs by increased miR166/165 level in miR166-Oe plants. [score:4]
This strengthens our hypothesis that miR166/165 mediated post-transcriptional regulation of the transcript level of HD-ZIP IIIs, altered expression of KANs and a crosstalk between hormones cumulatively lead to altered root growth in response to phytohormones. [score:4]
To confirm cytokinin mediated regulation of miR166/165, we checked the expression of miR166/165 in arr1-3 arr12-1 double mutant, which shows CK insensitivity towards root elongation, LR formation and callus induction [28]. [score:4]
Therefore, it would be interesting to study the conservation and diversification of phytohormone mediated regulation of miR166/165, its target HD-ZIP IIIs across the plant species. [score:4]
A further increase of the total transcript levels of HD-ZIP IIIs by up to 2.5 folds at 24 hrs may be largely due to the reduced expression and activity of miR166/165 and KAN genes (Fig.   5A). [score:3]
The expression level of miR166/165 was quantified using stem-loop qRT-PCR in (A) axr2-1 mutant. [score:3]
Treatment with IAA and CK resulted in reduced root length in miR166-Oe plants, suggesting the possible involvement of miR166/165 target HD-ZIP IIIs in IAA and CK dependent root growth. [score:3]
Hormone insensitive mutants used in the present study are deficient in respective phytohormone endogenously, hence the expression patterns of miR166/165 was opposite to that of exogenous hormone treatment. [score:3]
We found significant decrease in the expression and accumulation of mature miR166/165 as well as their precursors upon IAA treatment (Figs  1A and 2A). [score:3]
miR165 and miR166 are the two miRNAs that differ by only one nucleotide in their mature sequence and both target transcripts of same HD-ZIP III gene family members [13]. [score:3]
Taken together, our results, in line with previous reports, suggest that miR166/165 post-transcriptionally regulate HD-ZIP IIIs, which are also regulated by various phytohormones and KANs at transcriptional level. [score:3]
Figure 2Phytohormones affect the expression level of precursor genes of MIR166. [score:3]
Over expression of miR166 (miR166-Oe) alters the sensitivity of roots to hormones. [score:3]
Both miR166/165 and KAN genes are involved in maintaining abaxial fate of lateral organs by restricting the expression of HD-ZIP IIIs in the adaxial domain [21]. [score:3]
Singh A Singh S Panigrahi KC Reski R Sarkar AK Balanced activity of microRNA166/165 and its target transcripts from the class III homeodomain-leucine zipper family regulates root growth in Arabidopsis thalianaPlant Cell Rep. [score:3]
HD-ZIP IIIs transcript level depend on post-transcriptional regulation by miR166/165 and transcriptional regulation by KANs and phytohormones. [score:3]
Our results also suggest that root growth is affected by transcriptional regulation of MIR166s and HD-ZIP IIIs genes modulated by hormones, besides post-transcriptional regulation of HD-ZIP IIIs by miR166/165. [score:3]
Localization of miR166/165 in SA treated 7 dag roots at 12 hrs showed slight difference in expression pattern to that of qRT-PCR (Supplemental Fig.   S3A,D). [score:3]
We observed significant induction of miR166/165 expression by ABA treatment in comparison to wild type. [score:3]
Upon SA treatment, the expression of mature miR166/165 was induced at 1, 6 and 12 hrs. [score:3]
Triple mutant roots showed reduced expression of miR166/165 in comparison to wild type (Fig.   3E). [score:3]
The expression of all MIR166 precursors except MIR166A and MIR166C was further induced by up to 1.5 folds and above at 24 hrs of GA treatment (Fig.   2B). [score:3]
The expression level of miR166/165 was quantified using stem-loop qRT-PCR in roots at 1, 6, 12, and 24 hrs after treatment with (A) 10 µM IAA, (B) 10 µM GA, (C) 10 µM ABA, (D) 10 µM BAP, (E) 20 µM JA, and (F) 100 µM SA. [score:3]
JA treated roots showed increased expression of mature miR166/165 at 1, 6, 12, and 24 hrs of the treatment (Fig.   1E). [score:3]
The expression level of seven MIR166(A– G) genes was quantified using qRT-PCR in roots at 1, 6, 12, and 24 hrs with hormone concentrations of (A) 10 µM IAA, (B) 10 µM GA, (C) 10 µM BAP, (D) 10 µM ABA, (E) 20 µM JA and (F) 100 µM SA. [score:3]
To investigate if the accumulation of miR166/165 and reduction in the expression of targets affected the response of roots to hormone treatment, we performed phenotypic analysis of wild type and miR166-Oe plants treated with different phytohormones (Fig.   4). [score:3]
IAA treatment produced similar effect on the expression pattern of both mature miR166 and its precursors. [score:3]
miR166/165 cleaves HD-ZIP III transcripts and differential root growth observed in miR166-Oe plants upon phytohormone treatment might be the result of altered expression levels of HD-ZIP IIIs [19]. [score:3]
Overexpression of miR166/165 (miR166-Oe) has been described earlier [19]. [score:3]
Mutants defective in hormone signaling show altered expression of miR166/165. [score:3]
The total transcripts of HD-ZIP IIIs genes increased by up to 2 folds at 12 hrs of IAA treatment (Fig.   5A), which correlates with the reduced expression of miR166/165 s (Fig.   1A). [score:3]
Treatment with 6-Benzylaminopurine (BAP or CK) induced the expression level of miR166/165 at each time points, except at 1 hr, where miR166/165 level was reduced in comparison to the wild type. [score:3]
Validation of the mature miR166/165 expression profile via stem-loop qRT-PCR. [score:3]
However, ABA reduced the expression of HD-ZIP IIIs nearly equivalent to the control at 12 and 24 hrs of treatment, which could be caused by significant increase in the transcript level of miR166/165 at the same time points (Fig.   1C). [score:3]
The reduced expression of miR166/165 in axr2-1 could be the result of increased endogenous auxin in axr2-1, as observed in case of shy2-2 [26]. [score:3]
Figure 1Phytohormones affect the expression level of mature miR166/165. [score:3]
Roots of aba1-1 mutant showed reduced expression level of miR166/165 in comparison to wild type (Fig.   3C). [score:3]
After 12 and 24 hrs of GA treatment, the expression level of miR166/165 remained higher than the untreated control but lower than that of 6 hrs of the treatment (Fig.   1B). [score:3]
It is also likely that HD-ZIP IIIs and KANs themselves are transcriptionally regulated by multiple hormones and result in a feedback regulatory circuit with miR166/165. [score:3]
Interestingly, we observed that axr2-1 mutant root had significantly reduced level of miR166/165 expression (Fig.   3A). [score:3]
After 1 hr, the expression of miR166/165 was induced in BAP treatment, whereas highest increase upto 5 fold was observed at 6 hrs of treatment (Fig.   1D). [score:3]
ABA treatment led to no significant change in the expression of miR166/165 after 1 hr. [score:3]
We observed that JA treatment induced the expression of miR166/165 significantly. [score:3]
We showed that both SA and IAA induced the expression of miR166/165 (Fig.   1F). [score:3]
To confirm genetically, we further checked the expression of miR166/165 in aba1-1 mutant, an ABA biosynthetic mutant, which is ABA deficient [27]. [score:3]
This indicates that the reduction in the expression level of miR166 in response to auxin, as evidenced by qRT-PCR and in situ localization results, is possibly affected by a complex crosstalk with other hormones (Fig. S3). [score:3]
To further confirm our result, we checked the expression of miR166/165 in roots of GA insensitive pentuple mutant of all five DELLA proteins, gai-t6 rga-t2 rgl1-1rgl2-1rgl3-1 using stem-loop qRT-PCR analysis. [score:3]
Overexpression of miR166/165 mediated reduction of HD-ZIP IIIs alters the sensitivity of roots towards phytohormones. [score:3]
Differential expression of MIR166 precursors contributes to the altered level of miR166/165 level in response to hormones. [score:3]
To genetically confirm this, we checked the expression of miR166/165 in seedlings of coi1-16 ein2-1 pen2-4 triple mutant, which is JA insensitive [30]. [score:3]
Exogenous application of 10 µM BAP induced the expression of all MIR166 members, except MIR166D after 6 hrs of treatment. [score:3]
Our results suggest that phytohormones regulate HD-ZIP IIIs at transcriptional level, besides post-transcriptional regulation through miR166/165 (Fig. 5N). [score:3]
In our experiment, exogenous BAP treatment induced the expression of miR166/165. [score:3]
Figure 3The expression of miR166/165 was affected in hormone insensitive mutants. [score:3]
Two dotted double lines (blue) with arrow/stop bars indicate hormonal regulation of root growth independent of miR166/165 and HD-ZIP IIIs. [score:2]
At cellular level, the transcript level of total HD-ZIP IIIs is ultimately the result of both transcriptional regulation and post-transcriptional cleavage by miR166/165. [score:2]
We have recently reported that miR166-Oe affects primary root growth through down regulation of HD-ZIP IIIs transcripts [19]. [score:2]
The response of miR166-Oe roots to various phytohormones indicates a correlation between levels of miR166/165 and HD-ZIP IIIs transcripts and their transcriptional regulation through phytohormones. [score:2]
Genetic evidences using hormone signaling mutants confirm hormonal regulation of miR166/165. [score:2]
We have previously described that primary root elongation in miR166- Oe is promoted by down regulation of HD-ZIP IIIs [19]. [score:2]
A hormonal crosstalk along with feedback regulation by KANs and HD-ZIP IIIs, and miR166/165 maintain the balance of functional transcript level of HD-ZIP IIIs and phytohormone signaling module, which are critical for maintaining proper root growth. [score:2]
Recently, miR166/165 has been shown to be involved in root development in Arabidopsis 18, 19. [score:2]
Figure 7A hypothetical mo del showing complex crosstalk among phytohormones, miR166/165, HD-ZIP IIIs and KAN genes regulating root growth. [score:2]
We have previously shown that promoter sequences of seven MIR166 genes are significantly dissimilar to each other indicating the variations in the cis-regulatory elements in their promoters [23]. [score:2]
Although mature miR166 derived from all the seven MIR166 genes are same, each individual MIR166 gene exhibits specific spatio-temporal regulation [14]. [score:2]
Before analyzing hormonal regulation of miR166/165, we performed the growth analysis of wild type (Col-0) Arabidopsis roots in response to six phytohormones - IAA, GA, BAP, ABA, JA, and SA to test the reproducibility of phenotype in our growth conditions (Supplemental Fig.   S1). [score:2]
Whole mount in situ localization of miR166/165 was performed in 7 dag roots following 12 hrs of phytohormone treatment (G–J). [score:1]
Thus, the effect of CK on root growth of miR166-Oe plants could be due to the reduced activity of PHB and PHV. [score:1]
RNA isolation and qRT-PCR for the transcript level of MIR166 gene family, HD-ZIP IIIs and KAN gene family were done as described previously 19, 46. [score:1]
The whole mount in situ localization experiment showed the increased accumulation of miR166/165 after the treatment with BAP at 12 hrs (Supplemental Fig.   S3A,B). [score:1]
The treatment with 0.1 μM IAA showed reduction in primary root length of both wild type and miR166-Oe plants in comparison to their respective untreated control, which suggest that miR166-Oe roots were less sensitive to IAA than wild type treated plants (Fig.   4A). [score:1]
Therefore, we analyzed the root growth of miR166- Oe in response to various phytohormones (Fig.   4). [score:1]
At 24 hrs of treatment, insignificant changes in total HD-ZIP IIIs transcript correlate to increased level of miR166/165 and KANs (Figs  5D and 6F). [score:1]
Upon treatment with 100 μM SA, less reduction in primary root length suggested that miR166-Oe plants are less sensitive to SA (Fig.   4E). [score:1]
Figure 4Phytohormones affect the root growth of miR166-Oe and wild type plants. [score:1]
Exogenous application of SA induced the transcript level of miR166/165 in roots. [score:1]
The nearly similar level of total HD-ZIP IIIs transcripts in comparison to the control at 6 hrs of JA treatment correlates with the increased level of both miR166/165 and KANs (Figs  5D and 6F). [score:1]
Primary root growth of miR166-Oe in the presence of (A) 0.1 µM IAA, (B) 0.1 µM BAP, (C) 1 µM ABA, (D) 20 µM JA, and (E) 100 µM SA. [score:1]
We cannot rule out that this difference might be due to fluctuation and stability of mature miR166/165 among treatment points and/or the sensitivity of two techniques. [score:1]
However, the whole mount in situ localization experiment illustrated the increased accumulation of miR166/165 after the treatment with GA at 12 hrs (Supplemental Fig.   S3A,C). [score:1]
In situ localization of miR166/165 in BAP, GA and SA treatment has been provided in Supplemental Fig.   S3. [score:1]
Sequence of the miR166 LNA probe is provided in Supplemental Table  S1. [score:1]
Whole mount in situ hybridization experiment illustrated the reduced accumulation of miR166/165 in IAA treated roots than control roots (Fig.   1G,H). [score:1]
We observed significant induction in the transcript levels of all MIR166 genes, except MIR166G, after 12 hrs of treatment (Fig.   2B). [score:1]
Treatment with 10 µM IAA significantly reduced the level of mature miR166/165 at each time point, except at 1 hr of the study, as observed in stem loop qRT-PCR analysis (Fig.   1A). [score:1]
In brief, 7 days old seedlings were transferred to control and hormone plates and after 12 hrs, the treated seedlings were used for in situ hybridization using locked nucleic acid (LNA) probe complementary to miR166/165 (Eurogentec, Belgium). [score:1]
Treatment with SA showed induction of both HD-ZIP IIIs genes and miR166/165 after 1 and 6 hrs of the treatment followed by a further increase at 12 hrs (Fig.   5E). [score:1]
Treatment of miR166-Oe plants with other phytohormones like ABA, JA and SA also leads to change in root growth (Fig.   4). [score:1]
At 24 hrs of the treatment, nearly unchanged level of the total HD-ZIP IIIs transcripts correlates with the level of miR166/165, which might be below the control and insufficient to reduce HD-ZIP III transcripts post-transcriptionally (Fig.   5E). [score:1]
Additionally, primary root growth of miR166-Oe plants was more sensitive to 20 μM JA treatment (Fig.   4D). [score:1]
The whole mount in situ localization showed increased accumulation of miR166/165 in 7 dag roots treated with JA for 12 hrs in comparison to control (Fig.   1G,J). [score:1]
Arabidopsis genome encodes seven MIR166 (MIR166A– G) and two MIR165 (MIR165A-B), which finally produce same mature miR166 and miR165, respectively. [score:1]
Whole mount in situ localization experiment also confirmed the stem-loop qRT-PCR results exhibiting increased accumulation of miR166/165 upon ABA treatment (Fig.   1G,I). [score:1]
We observed that primary root growth of miR166-Oe was more sensitive towards 1 μM ABA treatment than that of wild type plants (Fig.   4C). [score:1]
[1 to 20 of 145 sentences]
2
[+] score: 101
Given the well-established expression patterns and roles of miR166 and its targets in leaf polarity determination (reviewed in [50], [51]), an obvious outstanding question is why the normal expression of the PHB and PHV genes in the adaxial domain of leaf primordia in wild type plants is not sufficient to cause the ectopic expression of seed maturation genes. [score:9]
In wild type seedlings, AGO1 and miR166 repress the expression of PHB/ PHV, which promotes the seed maturation program by directly activating LEC2 expression and indirectly that of other positive regulators of the seed maturation program. [score:8]
1003091.g008 Figure 8In wild type seedlings, AGO1 and miR166 repress the expression of PHB/ PHV, which promotes the seed maturation program by directly activating LEC2 expression and indirectly that of other positive regulators of the seed maturation program. [score:8]
To demonstrate that the specific loss of miR166 can cause the ectopic expression of seed maturation genes, we obtained the recently developed transgenic lines that exhibit a dramatic reduction in miR165/166 accumulation achieved by the expression of a short tandem target mimic (STTM165/166) [41]. [score:7]
These gain-of-function alleles have mutations in the miR166 target regions to cause a mismatch between the miRNA and the target mRNA and thus render the transcripts resistant to miRNA -mediated degradation and consequently the ectopic accumulation of HD-ZIPIII transcripts. [score:6]
Further, we show that the targets of miR166, type III HD-ZIP transcription factors PHB and PHV, are sufficient for derepressing seed maturation genes in seedlings, likely by binding directly to the promoter of a master regulator gene of maturation. [score:5]
Overexpression of miRNA166 Rescues the essp5/ ago1-100 Mutant Phenotype and Loss of miR166 Causes Ectopic Expression of Seed Maturation GenesPost-germination repression of seed genes is critical in order for the seedling to develop normally. [score:5]
1003091.g005 Figure 5Over-Expression of miRNA166 Rescues the essp5 GUS Phenotype, and Loss of miR166 Causes Ectopic Expression of Seed Maturation Genes. [score:5]
Figure S4qRT-PCR analysis of PHB expression in wild type and miR166 overexpressors. [score:5]
Over-Expression of miRNA166 Rescues the essp5 GUS Phenotype, and Loss of miR166 Causes Ectopic Expression of Seed Maturation Genes. [score:5]
Overexpression of miRNA166 Rescues the essp5/ ago1-100 Mutant Phenotype and Loss of miR166 Causes Ectopic Expression of Seed Maturation Genes. [score:5]
We demonstrated that targets of miR166, the class III homeodomain leucine zipper (HD-ZIPIII) family of transcription factor genes, PHB and PHV, are positive regulators of seed genes. [score:4]
These observations suggest that the reduction of miRNA166 and the concomitant accumulation of its target gene transcripts are likely the cause underlying the ectopic GUS phenotype of essp5/ ago1-100 seedlings. [score:3]
We first demonstrated that miR166 reduction is a major cause of the mutant phenotype and further showed that the targets of miR166, PHB and PHV, are sufficient for derepressing seed maturation genes in seedlings. [score:3]
In this context, it is worth noting that the transcript level of PHB was found to be decreased in miR166 overexpressors (Figure S4). [score:3]
The miR166 overexpressors analyzed here were the wild type siblings of miR166ox-1 and miR166ox-2 shown in Figure 5 (the miR166 construct was initially introduced into an essp5 heterozygous background). [score:3]
We only observed loss of leaf GUS activity in miR166 and miR156 overexpressing lines. [score:3]
Similar aberrant structures were observed by Zhou et al in miRNA166 overexpressors [40]. [score:3]
This work thus uncovered an important role of miR166 in the repression of seed genes during seedling development. [score:2]
As shown in Figure 5E, there were clearly higher levels of miR166 in lines miR166ox-1-2 than lines miR166ox-3-4. In addition, we observed the formation of aberrant structures on leaves of miRNA166ox-1-2 (Figure 5F). [score:1]
To confirm that the loss of leaf GUS activity in the transgenic lines was indeed due to the elevated accumulation of miR166, a northern blot analysis was performed. [score:1]
5′-end-labeled [32]P antisense DNAs or an LNA oligonucleotide (for miRNA166) were used to detect miRNAs from total RNAs (10 µg each sample). [score:1]
This observation indicates that miR166 plays an important role in repressing seed genes in seedlings. [score:1]
The extremely low rate of positive transgenic plants for miR166 is likely due to the fact that some transgenic seedlings failed to develop the shoot apical meristem and could not survive in soil, as observed by others [40]. [score:1]
The miR166 transgene driven by the CaMV 35S promoter was introduced into essp5/+ background. [score:1]
Taking advantage of the weak ago1 allele identified in this work, we were able to identify the miRNA species (miR166) responsible for the repression of seed genes. [score:1]
T2 seeds were germinated on selective MS agar plates such that only seedlings transgenic for miR166 were selected. [score:1]
We first demonstrate that the decrease in miR166 in ago1 is a major cause of the mutant phenotype. [score:1]
[1 to 20 of 28 sentences]
3
[+] score: 36
This is likely due to the fact that MIR166c/d locus has the highest enrichment among all targeted loci, resulted from an additive effect of two target sites (Fig. S2, 4 [th] panel). [score:5]
Normalized coverages of bins that were within nine kb from any one of the target sites were different from one with statistical significance (p<0.05), indicating that the size of the enriched regions was about 19 kb on average (totaling 135 kb for the eight targeted loci, MIR166c and MIR166d considered as a single locus as they are just two bins apart). [score:4]
Successful enrichment at all MIR166 and MIR165 lociAn Arabidopsis genomic DNA sample prepared with the optimized targeted enrichment protocol was fragmented to an approximate mean size of 400 bp and sequenced on one lane of an Illumina GAIIx sequencer. [score:3]
In this study, we tested the strategy with a 21 nt probe against the miR166 mature sequence in Arabidopsis thaliana, and found that this methodology was highly specific and sensitive to enrich regions flanking the targeted loci. [score:3]
Shaded panels are regions surrounding the eight MIR165/166 loci (MIR166c and MIR166d are two bins apart, therefore are shown in the same panel). [score:1]
Table S1 Summary of mapped reads from long-range miR166 enrichment in Arabidopsis thaliana. [score:1]
At 20 reads per nt, all but MIR166c/d (highest enrichment, Fig. S2, 4 [th] panel) were recovered (Table S4). [score:1]
All contigs harboring a miR166 matching sequence, together with all contigs long than 1000 bp, were BLASTed against the reference genome to identify the origin. [score:1]
Seven out of the eight MIR165/166 loci were recovered in the assembled contigs, missing only MIR166c/MIR166d. [score:1]
Next, the enrichment pattern was assessed across the genome, focusing on all “enriched” regions regardless of whether or not they were MIR166 or MIR165 loci. [score:1]
Indeed, an analysis of the 20 kb flanking regions of 12 maize MIR166 loci showed an average 20mer frequency of 317 (Fig. S3A), while the average 20mer frequency of the 20 kb flanking regions was 6.6 for the nine Arabidopsis MIR165/166 loci (Fig. S3B). [score:1]
Figure S3 (A) Average 20mer frequency of the 20 kb flanking regions of 12 maize MIR166 loci. [score:1]
All the loci with zero or one mismatches are MIR165 or MIR166 loci, and Student's t test revealed that the mean normalized coverage of loci with perfect complementarity and with one mismatch were both significantly different from the null hypothesis of one with p-values <0.01 and <0.05, respectively (Fig. 5A). [score:1]
Successful enrichment at all MIR166 and MIR165 loci. [score:1]
20mer frequency of the 20 kb flanking regions of 12 maize MIR166 loci [38] was averaged and shown in Fig. S3A. [score:1]
There are seven MIR166 loci with perfect matches to the probe, and two MIR165 loci with a single mismatch to the probe (miR165 and miR166 are highly similar miRNA families; Fig. 2A). [score:1]
Assembled contigs were searched for complementary sequences to miR166 with BLASTn. [score:1]
de novo assembly of enriched MIR166 and MIR165 loci. [score:1]
A peak enrichment of 100-fold or more was evident for the seven MIR166 loci in the genome with full complementarity to the capture probe, while a slightly lower peak of enrichment was evident for both MIR165 loci in the genome which have one mismatch to the probe (Fig. 2A–B). [score:1]
0083721.g006 Figure 6 de novo assembly of enriched MIR166 and MIR165 loci. [score:1]
** MIR166c and MIR166d were assembled into separate contigs, despite their ∼2 kb distance. [score:1]
An enrichment experiment performed with both Arabidopsis and maize in parallel ruled out technical errors as the reason for the failure in maize, as over ∼1,000 fold of enrichment was observed for an Arabidopsis MIR166 locus, while enrichment was barely seen for two maize MIR166 loci (Table S5). [score:1]
After merging and extending, a total of 64 highly enriched regions were generated (Fig. S2), including all eight MIR165/166 loci (MIR166c and MIR166d are closely linked on chromosome five, and as such were merged into a single locus in this analysis). [score:1]
All contigs greater than one kb in length and having sequence complementary to the capture probe (identified by BLASTn against the miR166 sequence) were indeed MIR165/166 flanking regions (identified by BLASTn against the genome) (Fig. 6). [score:1]
A pilot enrichment experiment was performed with Arabidopsis genomic DNA and a 21 nt, biotinylated LNA capture probe complementary to the mature miR166 DNA sequence. [score:1]
[1 to 20 of 25 sentences]
4
[+] score: 27
[36, 61]SHR → MIR166 SCR → MIR166 SHR and SCR promote the expression of microRNA165a/6b in the endodermis; the expression of microRNA166b in the QC is reduced in the shr mutant background. [score:5]
Finally, we used MIR166 as a generic node to mo del the role of MIR165a/6b, as MIR166b is expressed in a broader domain than MIR165a [30]. [score:3]
[50] CK-|MIR166 Cytokinin treatment strongly represses the expression of MIR165 in the RAM. [score:3]
Moreover, the mo del elucidated a potential new role of MIR166 in the maintenance of the QC cells, proving that the core system-level module that we uncovered is a valuable theoretical framework that can be used to predict and discern on the regulatory role of a component in the context of the rest of the interactions integrated in the mo del. [score:2]
Experimentally, the role of MIR166 in the QC cells had not been conclusive [30], but in the context of our mo del it becomes clear that it is a necessary restriction to repress PHB to indirectly maintain the QC activity configuration. [score:2]
A mutual degradation between MIR166 and PHB has been suggested to form sharp boundaries of activity [50]. [score:1]
Experimentally, the importance of MIR166 in the QC has not been conclusive [30], and our mo del shows that it might be an important constraint to maintain PHB out of these cells as a necessary condition for WOX5 activity. [score:1]
These simulations that do not recover the QC attractor (LOF SCR, SHR, JKD and MIR166), show that additionally to not having WOX5 activity, these mutants might have activity of ARF10 in all the PD cells. [score:1]
[30]PHB– | MIR166 In computational simulations, the mutual degradation between MIR165/6 and PHB create sharp boundaries between the MIR165/6 and PHB activity domains. [score:1]
We recovered 6 additional cyclic attractors when we solved with the synchronous updating regime; these cyclic attractors result from the coexistence of MIR166 and PHB, and of MGP and WOX5 (S2 Appendix). [score:1]
MIR166 moves from its site of synthesis in the adjacent layer to the pro-vascular tissues, where it promotes the degradation of PHB. [score:1]
In this case, the mo del suggests that MIR166 at the QC might have a key and previously unknown role in maintaining this cell type. [score:1]
The simulation of LOF of MIR166 also lost the QC attractor. [score:1]
Similarly, there is no QC attractor in the simulation of the LOF of MIR166 (Fig 6B) that is a repressor of PHB. [score:1]
For example, the GOF of MIR166 and PHB [30, 64], and the LOF of JKD [28, 36], SCR [37], SHR [38], MIR166 [64] and PHB [30, 64] are among these cases that result in the loss of the endodermis, peripheral or central pro-vascular tissues (Fig 6 and S7 Appendix). [score:1]
We followed this assumption such that the non-cell autonomous role of microRNA MIR166 was mo deled considering that is active either in its site of synthesis (where SHR and SCR are active) or if PHB is not present. [score:1]
[30]MIR166 – | PHB microRNA165a/6b post-transcriptionally promotes the degradation of PHB transcript. [score:1]
[1 to 20 of 17 sentences]
5
[+] score: 15
Other miRNAs from this paper: ath-MIR159a, ath-MIR162a, ath-MIR162b, ath-MIR166a, ath-MIR166b, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR169a, ath-MIR171a, ath-MIR159b, ath-MIR319a, ath-MIR319b, osa-MIR162a, osa-MIR166a, osa-MIR166b, osa-MIR166c, osa-MIR166d, osa-MIR166e, osa-MIR166f, osa-MIR169a, osa-MIR171a, ath-MIR169b, ath-MIR169c, ath-MIR169d, ath-MIR169e, ath-MIR169f, ath-MIR169g, ath-MIR169h, ath-MIR169i, ath-MIR169j, ath-MIR169k, ath-MIR169l, ath-MIR169m, ath-MIR169n, ath-MIR171b, ath-MIR171c, ath-MIR390a, ath-MIR390b, ath-MIR396a, ath-MIR396b, ath-MIR398a, ath-MIR398b, ath-MIR398c, ath-MIR399a, ath-MIR399b, ath-MIR399c, ath-MIR399d, ath-MIR399e, ath-MIR399f, osa-MIR396a, osa-MIR396b, osa-MIR396c, osa-MIR398a, osa-MIR398b, osa-MIR399a, osa-MIR399b, osa-MIR399c, osa-MIR399d, osa-MIR399e, osa-MIR399f, osa-MIR399g, osa-MIR399h, osa-MIR399i, osa-MIR399j, osa-MIR399k, ath-MIR408, ath-MIR159c, ath-MIR319c, osa-MIR156k, osa-MIR159a, osa-MIR159b, osa-MIR159c, osa-MIR159d, osa-MIR159e, osa-MIR159f, osa-MIR319a, osa-MIR319b, osa-MIR162b, osa-MIR166k, osa-MIR166l, osa-MIR169b, osa-MIR169c, osa-MIR169d, osa-MIR169e, osa-MIR169f, osa-MIR169g, osa-MIR169h, osa-MIR169i, osa-MIR169j, osa-MIR169k, osa-MIR169l, osa-MIR169m, osa-MIR169n, osa-MIR169o, osa-MIR169p, osa-MIR169q, osa-MIR171b, osa-MIR171c, osa-MIR171d, osa-MIR171e, osa-MIR171f, osa-MIR171g, osa-MIR166g, osa-MIR166h, osa-MIR166i, osa-MIR171h, osa-MIR408, osa-MIR171i, osa-MIR166m, osa-MIR166j, ath-MIR414, osa-MIR414, osa-MIR390, osa-MIR396e, ptc-MIR156k, ptc-MIR159a, ptc-MIR159b, ptc-MIR159d, ptc-MIR159e, ptc-MIR159c, ptc-MIR162a, ptc-MIR162b, ptc-MIR166a, ptc-MIR166b, ptc-MIR166c, ptc-MIR166d, ptc-MIR166e, ptc-MIR166f, ptc-MIR166g, ptc-MIR166h, ptc-MIR166i, ptc-MIR166j, ptc-MIR166k, ptc-MIR166l, ptc-MIR166m, ptc-MIR166n, ptc-MIR166o, ptc-MIR166p, ptc-MIR166q, ptc-MIR169a, ptc-MIR169aa, ptc-MIR169ab, ptc-MIR169ac, ptc-MIR169ad, ptc-MIR169ae, ptc-MIR169af, ptc-MIR169b, ptc-MIR169c, ptc-MIR169d, ptc-MIR169e, ptc-MIR169f, ptc-MIR169g, ptc-MIR169h, ptc-MIR169i, ptc-MIR169j, ptc-MIR169k, ptc-MIR169l, ptc-MIR169m, ptc-MIR169n, ptc-MIR169o, ptc-MIR169p, ptc-MIR169q, ptc-MIR169r, ptc-MIR169s, ptc-MIR169t, ptc-MIR169u, ptc-MIR169v, ptc-MIR169w, ptc-MIR169x, ptc-MIR169y, ptc-MIR169z, ptc-MIR171a, ptc-MIR171b, ptc-MIR171c, ptc-MIR171d, ptc-MIR171e, ptc-MIR171f, ptc-MIR171g, ptc-MIR171h, ptc-MIR171i, ptc-MIR319a, ptc-MIR319b, ptc-MIR319c, ptc-MIR319d, ptc-MIR319e, ptc-MIR319f, ptc-MIR319g, ptc-MIR319h, ptc-MIR319i, ptc-MIR390a, ptc-MIR390b, ptc-MIR390c, ptc-MIR390d, ptc-MIR396a, ptc-MIR396b, ptc-MIR396c, ptc-MIR396d, ptc-MIR396e, ptc-MIR396f, ptc-MIR396g, ptc-MIR398a, ptc-MIR398b, ptc-MIR398c, ptc-MIR399a, ptc-MIR399b, ptc-MIR399d, ptc-MIR399f, ptc-MIR399g, ptc-MIR399h, ptc-MIR399i, ptc-MIR399j, ptc-MIR399c, ptc-MIR399e, ptc-MIR408, ptc-MIR482a, ptc-MIR171k, osa-MIR169r, ptc-MIR171l, ptc-MIR171m, ptc-MIR171j, ptc-MIR1448, osa-MIR396f, osa-MIR2118a, osa-MIR2118b, osa-MIR2118c, osa-MIR2118d, osa-MIR2118e, osa-MIR2118f, osa-MIR2118g, osa-MIR2118h, osa-MIR2118i, osa-MIR2118j, osa-MIR2118k, osa-MIR2118l, osa-MIR2118m, osa-MIR2118n, osa-MIR2118o, osa-MIR2118p, osa-MIR2118q, osa-MIR2118r, osa-MIR396g, osa-MIR396h, osa-MIR396d, ptc-MIR482d, ptc-MIR169ag, ptc-MIR482b, ptc-MIR482c, pde-MIR159, pde-MIR162, pde-MIR166a, pde-MIR166b, pde-MIR169, pde-MIR171, pde-MIR390, pde-MIR396, pde-MIR482a, pde-MIR482b, pde-MIR482c, pde-MIR482d, pde-MIR946, pde-MIR947, pde-MIR949a, pde-MIR950, pde-MIR951, pde-MIR952a, pde-MIR952b, pde-MIR952c, pde-MIR1311, pde-MIR1312, pde-MIR1313, pde-MIR1314, pde-MIR3701, pde-MIR3704a, pde-MIR3704b, pde-MIR3712
Pde-MIR171 family had two conserved targets, while pde-MIR162 and pde-MIR166 families each had only one conserved target. [score:5]
For example, HD-ZIP and GRAS family transcription factors, which are important to root and nodule development in Medicago truncatula and nutrient homeostasis in maize, were predicted to be targets of pde-MIR166 and pde-MIR171, respectively [50, 51]. [score:4]
It includes DCL1 targeted by pde-miR162, GRAS family transcription factor cleaved by pde-miR171, Class III HD-Zip protein HDZ33 regulated by pde-miR166 and CC-NBS-LRR resistance-like protein sliced by pde-miR2118. [score:4]
It includes pde-MIR159, pde-MIR162, pde-MIR166, pde-MIR169, pde-MIR171, pde-MIR390, pde-MIR396 and pde-MIR399. [score:1]
The result suggests that pde-miR166 may play key roles in a variety of physiological processes in P. densata needles. [score:1]
[1 to 20 of 5 sentences]
6
[+] score: 15
While the expressions of 14 families (miR156/miR157, miR158, miR160, miR162, miR165/miR166, miR168, miR169, miR171, miR390, miR393, miR394, miR396, miR398, and miR399) were dramatically reduced, 3 families (miR159, miR167, and miR172) were up-regulated in CsCl -treated seedlings. [score:6]
Among the down-regulated miRNAs, it is worthwhile to take note of the miR165/166 family—consisting of seven individual MIR166 and two MIR165 genes—which specifically responded to CsCl-treatment. [score:4]
B. The processing pattern of pri-miR166. [score:1]
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]
Likewise, the intermediate fragments of pri-miR166 and pri-miR172 were clearly detected in CsCl -treated seedlings (Fig 6B and 6C). [score:1]
At first glance, in accordance with the reduced levels of miR160 and miR166 (Fig 3B), the accumulations of pri-miR160a (~ 3.5-fold) and pri-miR166a (~ 3-fold) seemingly reflected the interference with the miRNA processing pathway. [score:1]
Conversely, the accumulated levels of ARF17 and REV should be monitored due to the reduction of miR160 and miR166. [score:1]
[1 to 20 of 7 sentences]
7
[+] score: 12
It is well established that the miR166 family miRNAs target the transcripts of the HD-ZIPIII genes, controlling the level and domain of their expression to allow their proper functions in plant development [62– 64]. [score:6]
Our genome-wide H3K27me3 profiling data also reveal that BRM is involved in the regulation of a number of other important developmental genes including, most noticeably, members of the miR166 and miR156 families (S2 Dataset). [score:3]
More recently, we uncovered a new role for miR166 in repressing the seed maturation program during vegetative development [65]. [score:2]
Our new data presented here thus provide a potential link between the two early studies [33, 65]: it strongly suggests that BRM promotes the accumulation of miR166, which in turn represses seed maturation genes in developing seedlings. [score:1]
[1 to 20 of 4 sentences]
8
[+] score: 11
In total about 86 targets genes were predicted among which most of them encode transcription factors (TFs) targeted by miR156, miR159, miR165, miR166, miR169, miR319, miR408, miR829, miR2934, miR5029 and miR5642. [score:5]
In addition, the sequencing results also revealed that various other stress-regulated miRNAs were expressed in response to LPS which include: miR161, miR165, miR166, miR167, miR168 miR401, miR403, miR405 and miR5635. [score:4]
are regulated by the identified miR156, miR159, miR165, miR166, miR169, miR319, miR408, miR829, miR2934, miR5029 and miR5642 (Tables  3 and 4). [score:2]
[1 to 20 of 3 sentences]
9
[+] score: 11
For instance, Boualem and collegues have shown that miR166 that targets class III HD-ZIP transcription factors (with known developmental roles in Arabidopsis) can control root and nodule development in M. truncatula [103]. [score:5]
Thus, overexpression of miR166 led to a decreased capability to form LR and nodules in hairy roots. [score:3]
Although miR166 has a link with auxin in Arabidopsis and despite a strong miR166 expression in LRP, nodule primordia and vascular tissues in M. truncatula, no link between the action of miR166 and auxin was shown in this study. [score:3]
[1 to 20 of 3 sentences]
10
[+] score: 11
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR164a, ath-MIR164b, ath-MIR166a, ath-MIR166b, ath-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
BLAST2GO helped in localization of predicted targets and KEGG (Kyoto Encyclopedia for Genes and Genomes) pathway analysis concluded that miR9662, miR894, miR172, and miR166 might be involved in regulating saponin biosynthetic pathway. [score:4]
Out of all, on the basis of bioinformatic analysis maximum expression was observed for miR159 family i. e. 315,441 reads followed by miR166 and miR167 family with 56,445 and 25,592 reads respectively and 17 miRNA families were reported to have less than 10 reads. [score:3]
On the basis of data analysis, it can be predicted that miR159 and miR166 have maximum expression in leaf during the period of its active growth. [score:3]
miR166 family with 56 member followed by miR159 (52 members) family were found to have maximum number of members in the library, although 14 miRNA families such as miR393, miR444, miR473, miR531, miR1425, miR1862, miR1873, miR3623, miR3634, miR5072, miR5077, miR7486, miR9662, and miR9674 were found to have only one member. [score:1]
[1 to 20 of 4 sentences]
11
[+] score: 11
MIR166/165 genes exhibit dynamic expression patterns in regulating shoot apical meristem and floral development in Arabidopsis. [score:5]
Arabidopsis Argonaute10 specifically sequesters miR166/165 to regulate shoot apical meristem development. [score:3]
Thus, wus was described as epistatic to miR166 over -expression caused by the jabba1-D allele [43] and to ago10-12 [35], while ago10 clv3 double mutants failed to display any meristem enhancement (Fig 2). [score:3]
[1 to 20 of 3 sentences]
12
[+] score: 10
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-MIR164b, ath-MIR166a, ath-MIR166b, 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
The seed regions of the newly identified maize miRNAs t0002967, t0511822, t0207061, t0448353 and t0053880 were identical to those of ctr-miR171 and ctr-miR166, respectively, indicating that they may share the same targets. [score:3]
Previous studies indicated that MiRNA166 targets HD-ZIP transcription factors that are involved in plant leaf morphogenesis. [score:2]
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]
Not only the miRNA166 and miRNA156 families were abundant during this stage of seed germination, but also they had more family members than other miRNA families, suggesting the importance of these two miRNA families at this very early stage of seed germination. [score:1]
The largest miRNA family size identified was miR166 that consisted of 14 members and miR156, miR169 and miR167 possessed 12, 12 and 10 members, respectively; whereas other miRNA families such as miR162, miR529, miR827 and miR1432 had only one member detected in this period. [score:1]
For example, miR156/157, miR159/319, miR166, miR169, and miR394 have been found in 51, 45, 41, 40 and 40 plant species, respectively [36- 38]. [score:1]
In our datasets, miRNA166 showed the highest abundance followed by miRNA156 and miRNA528, respectively, during the very early stage of seed germination. [score:1]
[1 to 20 of 7 sentences]
13
[+] score: 8
In our study, the sequencing material consisted of total RNA pools collected from each stage of somatic embryogenesis, the detailed expression of a given miRNA at a certain developmental stage could not be identified, but some miRNA families exhibited dominant place in family members and copy reads, they presumably played an important role in this process, such as miR156 and miR166. [score:4]
miR166 -mediated regulation of PHB and PHV is also important during early embryonic patterning [33]. [score:2]
Among these families, the miR156 family had the most family members (13), with 93.7% of all conserved miRNA reads, followed by miR166 (6), miR168 (5), miR167 (4), miR397 (4), miR390 (3), and miR399 (3) etc. [score:1]
The reads of different members within a given family were not evenly distributed: miR156 with 13 family members had 47 to 4,750,907 reads; miR166 with 6 members had 10 to 216,840 reads; miR390 with 3 members had 5 to 2,768 reads. [score:1]
[1 to 20 of 4 sentences]
14
[+] score: 7
Arabidopsis argonaute10 specifically sequesters miR166/165 to regulate shoot apical meristem development. [score:3]
For example, miR159, miR165, miR166, and miR168 are usually incorporated into AGO1 -based RISCs, but associate with other AGOs in AGO1 -deficient Arabidopsis mutants, where this redirection is supposed to be mediated by stabilizing proteins (Vaucheret, 2009; Zhu et al., 2011). [score:2]
By contrast, AGO10 (also referred to as ZWILLE or PINHEAD) specifically associates with members of the miR165 and miR166 families (Mallory et al., 2009; Zhu et al., 2011). [score:1]
For example, the miR165 and miR166 families were surmised to be bound by AGO10 as opposed to AGO1 because of the higher number of unpaired bases than can be tolerated by AGO1 (Zhu et al., 2011). [score:1]
[1 to 20 of 4 sentences]
15
[+] score: 7
For example, analysis of the MIR156, MIR159, and MIR166 families revealed differences in the spatial and temporal expression of genes within these families, which suggests that expression diversification occurred after gene duplication [17]. [score:5]
1003218.g004 Figure 4miRNA abundance in pwr-1 and pwr-2. (A) Abundance of miR159, miR172, miR173, miR166, and miR390 in L er, pwr-1, Col, and pwr-2 detected by small RNA northern blotting. [score:1]
Decreased accumulation was not observed for miR166 or miR390 in either allele. [score:1]
[1 to 20 of 3 sentences]
16
[+] score: 6
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR166a, ath-MIR166b, ath-MIR166d, ath-MIR166e, ath-MIR166f, ath-MIR166g, ath-MIR169a, ath-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-MIR395a, ath-MIR395b, ath-MIR395c, ath-MIR395d, ath-MIR395e, ath-MIR395f, ath-MIR396a, ath-MIR396b, ath-MIR399a, ath-MIR408, ath-MIR156g, ath-MIR156h, gma-MIR156d, gma-MIR156e, gma-MIR156c, gma-MIR166a, gma-MIR166b, gma-MIR156a, gma-MIR396a, gma-MIR396b, gma-MIR156b, gma-MIR169a, ath-MIR848, gma-MIR169b, gma-MIR169c, gma-MIR171a, gma-MIR171b, gma-MIR1527, gma-MIR1533, gma-MIR396c, pvu-MIR166a, pvu-MIR399a, gma-MIR396d, gma-MIR156f, gma-MIR169d, gma-MIR171c, gma-MIR169e, gma-MIR156g, gma-MIR396e, gma-MIR156h, gma-MIR156i, gma-MIR166c, gma-MIR166d, gma-MIR166e, gma-MIR166f, gma-MIR166g, gma-MIR166h, gma-MIR169f, gma-MIR169g, gma-MIR171d, gma-MIR171e, gma-MIR171f, gma-MIR171g, gma-MIR408d, ath-MIR5021, gma-MIR171h, gma-MIR171i, gma-MIR169h, gma-MIR169i, gma-MIR396f, gma-MIR396g, gma-MIR171j, gma-MIR395a, gma-MIR395b, gma-MIR395c, gma-MIR408a, gma-MIR408b, gma-MIR408c, gma-MIR156j, gma-MIR156k, gma-MIR156l, gma-MIR156m, gma-MIR156n, gma-MIR156o, gma-MIR166i, gma-MIR166j, gma-MIR169j, gma-MIR169k, gma-MIR169l, gma-MIR169m, gma-MIR169n, gma-MIR171k, gma-MIR396h, gma-MIR396i, gma-MIR171l, ath-MIR156i, ath-MIR156j, gma-MIR399a, gma-MIR156p, gma-MIR171m, gma-MIR171n, gma-MIR156q, gma-MIR171o, gma-MIR169o, gma-MIR171p, gma-MIR169p, gma-MIR156r, gma-MIR396j, gma-MIR171q, gma-MIR156s, gma-MIR169r, gma-MIR169s, gma-MIR396k, gma-MIR166k, gma-MIR156t, gma-MIR171r, gma-MIR169t, gma-MIR171s, gma-MIR166l, gma-MIR171t, gma-MIR171u, gma-MIR395d, gma-MIR395e, gma-MIR395f, gma-MIR395g, gma-MIR166m, gma-MIR169u, gma-MIR156u, gma-MIR156v, gma-MIR156w, gma-MIR156x, gma-MIR156y, gma-MIR156z, gma-MIR156aa, gma-MIR156ab, gma-MIR166n, gma-MIR166o, gma-MIR166p, gma-MIR166q, gma-MIR166r, gma-MIR166s, gma-MIR166t, gma-MIR166u, gma-MIR169v, gma-MIR395h, gma-MIR395i, gma-MIR395j, gma-MIR395k, gma-MIR395l, gma-MIR395m, gma-MIR169w
In the present study pvu-miR166d was predicted to target kinase mRNA, which is in agreement with the reported target kinase for miR166 family in soybean [67]. [score:5]
Among these miRNAs, the miR166 family had the most number of reads. [score:1]
[1 to 20 of 2 sentences]
17
[+] score: 6
Here it must be noted that Vaucheret et al. (2006) reported modest increases in the accumulation of mature miR159a and miR166 in transgenic plants over -expressing AtAGO1, the opposite result to what we observed. [score:3]
Arabidopsis Argonaute10 specifically sequesters miR166/165 to regulate shoot apical meristem development. [score:3]
[1 to 20 of 2 sentences]
18
[+] score: 5
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157a, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR165a, ath-MIR165b, ath-MIR166a, ath-MIR166b, 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
Further targets were predicted for certain more conserved miRNAs including miR166, miR167, miR319, miR 396 and miR408, miR856 and miR1310 (Additional file 2 Table S1). [score:3]
In addition, miR167 and miR394 were found to have some thousands to tens of thousands of redundancies while miR319, miR166 and miR156 had more than one hundred redundancies. [score:1]
Further, the largest miRNAs family size identified was miR166 that consisted of 17 members. [score:1]
[1 to 20 of 3 sentences]
19
[+] score: 5
MiR166, which targets HD-Zip transcription factors, is up-regulated by heat in Arabidopsis (Zhong et al., 2013), wheat (Xin et al., 2010), and barley (Hordeum vulgare; Kruszka et al., 2014). [score:5]
[1 to 20 of 1 sentences]
20
[+] score: 5
microRNA Target Gene familymir165 [51] HD-ZIPIII family members including PHV, PHB, REV, ATHB-8, and ATHB-15 mir166 [97] HD-ZIPIII family members including PHV, PHB, REV, ATHB-8, and ATHB-15 mir319 [51], [52] TCP family members. [score:3]
mir165 [97] HD-ZIPIII family members including PHV, PHB, REV, ATHB-8, and ATHB-15 mir166 [97] HD-ZIPIII family members including PHV, PHB, REV, ATHB-8, and ATHB-15 mir167 [93] ARF family members ARF6 and ARF8. [score:1]
Gene ID microRNA At1g30490 mir165a, mir165b, mir166a, mir166b, mir166c, mir166d, mir166e, mir166f, mir166g At1g30210 mir319a, mir319b. [score:1]
[1 to 20 of 3 sentences]
21
[+] score: 5
The mature miRNAs 1, 2, 4, and 5 have high complementarity to transcription factor encoding mRNAs targeted by MIR166 and MIR169 miRNAs [18], [21] (Table 4); however mature miRNAs 2, 4 and 5 have predicted novel target cleavage sites within these transcripts. [score:5]
[1 to 20 of 1 sentences]
22
[+] score: 4
miR166 expression served as control. [score:3]
Antisense miR167 (5′-TAGATCATGCTGGCAGCTTCA-3′) and miR166 (5′-GGGGAATGAAGCCTGGTCCGA-3′) probes were prepared by end-labelling with T4-polynucleotide kinase (New England Biolabs, Ipswich MA, USA) in the presence of γ [32]P-ATP. [score:1]
[1 to 20 of 2 sentences]
23
[+] score: 4
During early seedling development the regulation mediated by the presence of miR165, miR166, miR164, and miR319 is of special importance for germination and developmental phase transitions (Wang and Li, 2007; Rubio-Somoza and Weigel, 2011). [score:4]
[1 to 20 of 1 sentences]
24
[+] score: 4
In contrast, negative seed regulators such as PICKLE (PKL; Ogas et al., 1999), POLYCOMB REPRESSIVE COMPLEX 2 (PRC2; Bouyer et al., 2011), SET DOMAIN GROUP 8 (SDG8; Tang et al., 2012b), BRAHMA (BRM; Tang et al., 2008), VP1/ABSCISIC ACID INSENSITIVE 3-LIKE (VAL) genes (Suzuki et al., 2007) and microRNA166 (miR166; Tang et al., 2012a) are responsible for suppressing the seed program in vegetative tissues. [score:4]
[1 to 20 of 1 sentences]
25
[+] score: 4
In Arabidopsis, AGO10 has been shown to regulate the function of miR166/165 [28, 29]. [score:2]
AGO10 specifically sequesters miR166/165 from AGO1, which is essential for shoot apical meristem development [28, 29]. [score:2]
[1 to 20 of 2 sentences]
26
[+] score: 3
Prigge and Clark [73], and Floyd and Bowman [75] have previously suggested that HD-Zip III sequences across all land plants produce transcripts that could be targeted by miRNA165 and miRNA166. [score:3]
[1 to 20 of 1 sentences]
27
[+] score: 3
5. Zhu H, Hu F, Wang R, Zhou X, Sze S-H, et al. (2011) Arabidopsis Argonaute10 Specifically Sequesters miR166/165 to Regulate Shoot Apical Meristem Development. [score:3]
[1 to 20 of 1 sentences]
28
[+] 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-MIR162a, ath-MIR162b, ath-MIR164a, ath-MIR164b, ath-MIR166a, ath-MIR166b, 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
The six most abundantly expressed miRNA families were miR166, miR168, miR167, miR156, miR159, and miRs6. [score:3]
[1 to 20 of 1 sentences]
29
[+] score: 2
This pattern was specific to the MIR166g precursor and was not observed in any of the other eight MIR165 or MIR166 genes. [score:1]
MIR166 Organizing center Phyllotaxis Stem cells WUSCHEL In plants, all above-ground organs develop post-embryonically from a small group of pluripotent stem cells that reside at the shoot tips in a highly organized structure called the shoot apical meristem (SAM). [score:1]
[1 to 20 of 2 sentences]
30
[+] score: 2
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157a, ath-MIR157b, ath-MIR157c, ath-MIR157d, ath-MIR159a, ath-MIR165a, ath-MIR165b, ath-MIR166a, ath-MIR166b, 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 Oryza and Populus, we find no new miSquare families, but three new members of known miRBase families (oza-MIR399, ptc-MIR166, and ptc-MIR395; see Table 2). [score:1]
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]
[1 to 20 of 2 sentences]
31
[+] score: 2
MiR166 reads were depleted 5 fold, whereas miR166* reads were enriched 16 fold in wild-type HC-Pro immunoprecipitates. [score:1]
For example, miR166 reads were enriched 30 and 45 fold in HA-AGO1 [DAH] immunoprecipitates from inflorescences of mock-inoculated and TuMV-infected plants, respectively. [score:1]
[1 to 20 of 2 sentences]
32
[+] score: 2
The partial results are shown in Table  5, and the complete results are available in Additional file 5. Table 5 Top 5 prediction results for miRNAs responding to high-salt conditions and TMV-Cg stress Stress miRNA Score High-salt ath-miR418 0.932 ath-miR166 0.929 ath-miR160 0.908 ath-miR841 0.892 ath-miR169 0.816 TMV-Cg ath-miR165 1.000 ath-miR156 0.939 ath-miR418 0.932 ath-miR160 0.908 ath-miR8177 0.899 To our knowledge, most of the existing methods mentioned previously have not been implemented as publicly available software packages. [score:1]
We also predicted several new miRNAs that are likely to respond to high-salt conditions, including miR418, miR166 [36, 40], miR160 [36, 38], miR841 [41], miR169 [37, 42, 43]. [score:1]
[1 to 20 of 2 sentences]
33
[+] score: 2
Of these six genes, BrARF3.1, BrARF4.1, BrKAN1, and BrKAN2.1 were identified as homologs of Arabidopsis abaxial polarity genes, and BrHYL1.1 is the homolog of Arabidopsis HYL, which is involved in the biogenesis of the abaxial determinant, miRNA166. [score:1]
The HYL1 gene is responsible for the leaf abaxial determinant-miR166 (Han et al., 2004; Wu et al., 2007), and the rosette leaves of Arabidopsis hyl1 mutants are curved inward (Wu et al., 2004; Liu et al., 2011). [score:1]
[1 to 20 of 2 sentences]
34
[+] score: 1
Among these miRNAs, the miR168 and miR166 families had the most reads in the control and treatment groups, respectively. [score:1]
[1 to 20 of 1 sentences]
35
[+] score: 1
The abundance of some miRNA (miR172 and miR397) induced by cold stresses increased in the OE lines but many other miRNAs (miR166, miR393, miR396 and miR408) induced by cold were unaltered [36]. [score:1]
[1 to 20 of 1 sentences]
36
[+] score: 1
NAC1, CUC1, CUC2, ANAC079, ANAC092, ANAC100, AT3G12977 1 MIM165/166 miR165/miR166 Rounder leaves. [score:1]
[1 to 20 of 1 sentences]
37
[+] score: 1
Other miRNAs from this paper: ath-MIR156a, ath-MIR156b, ath-MIR156c, ath-MIR156d, ath-MIR156e, ath-MIR156f, ath-MIR157d, ath-MIR158a, ath-MIR159a, ath-MIR160a, ath-MIR160b, ath-MIR160c, ath-MIR161, ath-MIR162a, ath-MIR162b, ath-MIR163, ath-MIR164a, ath-MIR164b, ath-MIR165a, ath-MIR165b, ath-MIR166a, ath-MIR166b, ath-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
In all four libraries, the miR156 family was the most abundant, followed by the miR167 and miR166 families. [score:1]
[1 to 20 of 1 sentences]