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15 publications mentioning dre-mir-214

Open access articles that are associated with the species Danio rerio and mention the gene name mir-214. 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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[+] score: 423
This complex process, involving chondrocyte commitment, proliferation, differentiation and hypertrophy, is governed by tightly orchestrated genetic and epigenetic programs and its disruption leads to pathological consequences 1– 3. MicroRNAs (miRNAs) are small non-coding RNAs, usually transcribed by RNA Polymerase II (Pol II), which regulate gene expression by translational repression or by messenger RNA (mRNA) degradation 4, 5. miRNAs have emerged as important regulators of skeleton formation where they exert multiple levels of control from cell fate decision, to proliferation, differentiation and cellular activities 6– 8. In that sense, it is not surprising that skeletal key players, such as Runx2 and Sox9, are regulated by several miRNAs 7– 9. Particularly, miR-214 was shown to inhibit bone formation by regulating Atf4 [10], and to promote osteoclastogenesis by targeting Pten [11]. [score:13]
The following pattern of expression was observed: i) low levels of expression from 18-somite stage to 36 hpf; ii) progressive increase in expression from 2–6 days post fertilization (dpf), with a peak at 6 dpf (over 30-fold change comparing to 24 hours post fertilization, hpf), iii) decrease in miR-214 expression at 15 dpf; iv) progressive increase from 15 to 60 dpf (reaching 110-fold increase compared to 24 hpf); and v) a general decrease in miR-214 expression in young adults (at 81 dpf; similar levels observed in male and female) (Fig.   1A). [score:10]
Since bioinformatic analysis did not indicate Mgp or Oc as direct targets of miR-214 (data not shown), down-regulation of these genes was most likely indirect. [score:8]
Interestingly, miR-214 overexpression lead to an overall down-regulation of Atf4 putative transcriptional targets such as Sox9, Col2a1 and Mgp, where we have identified several conserved putative -binding sites for Atf4, and also for Runx2, one of its skeletal cooperative partners (Supplementary Fig.   S8). [score:8]
miR-214 overexpression impairs zebrafish cartilage formation in vivoIn order to confirm the chondrogenic role of miR-214 in vivo, and since our previous data revealed that miR-214 was poorly expressed or absent in early stages of zebrafish development (Fig.   1A), we decided to overexpress this miRNA in zebrafish embryos by injecting 1-cell stage zebrafish eggs with miR-214 mimic or negative control (NC). [score:8]
For instance, miR-214 regulates the Hedgehog pathway in zebrafish by targeting sufu 19, 43 and was shown to regulate the WNT pathway through direct regulation of β-Catenin in humans [44]. [score:7]
We propose that at least part of miR-214 effects in chondrogenesis are Atf4 -dependent since this gene was consistently decreased upon miR-214 overexpression and unaltered upon miR-214 down-regulation, thus suggesting a direct repressive effect by miR-214 (Fig.   7), as previously validated by other authors [10]. [score:7]
The pattern of expression found for miR-214 during zebrafish development indicate that it might regulate distinct processes of skeleton formation, and further suggests that a tight regulation of miR-214 is required for a proper skeletal development. [score:7]
For chondrocyte differentiation to progress, miR-214 levels decrease thus alleviating the expression of their targets as well as the expression of chondrocyte markers. [score:7]
Upon miR-214 overexpression, Atf4 expression concomitantly decreased, suggesting that this gene could also be a target of miR-214 in chondrogenesis. [score:7]
We found that miR-214 is expressed in the cartilage of zebrafish, and is downregulated during differentiation of murine ATDC5 chondrogenic cells. [score:6]
A miRNA mimic (MmiR-214) and an antagomiR (AmiR-214) with the respective controls (NC) were used to overexpress or down-regulate miR-214. [score:6]
Therefore, in our experimental conditions, down-regulation of both Oc and Mgp upon miR-214 overexpression should represent a drawback in the differentiation process, probably with consequences at mineralization. [score:6]
During differentiation, transcriptional repressors such as AP2α should overcome ETS1 action leading to the repression of miR-214 transcription and downregulate its expression. [score:6]
In order to confirm the chondrogenic role of miR-214 in vivo, and since our previous data revealed that miR-214 was poorly expressed or absent in early stages of zebrafish development (Fig.   1A), we decided to overexpress this miRNA in zebrafish embryos by injecting 1-cell stage zebrafish eggs with miR-214 mimic or negative control (NC). [score:6]
miR-214 was highly expressed in confluent cells but strongly downregulated (over 10-fold change) during early (T9) differentiation (Fig.   3B). [score:6]
In fact, in vitro and in vivo gain-of-function experiments revealed that miR-214 was able to inhibit chondrogenesis, as evidenced by down-regulation of chondrogenic marker genes, and by the observation of phenotypic changes in cartilage formation in zebrafish miR-214 -injected embryos. [score:6]
Wang X miR-214 targets ATF4 to inhibit bone formationNat. [score:5]
ETS1 promotes miR-214 expression in undifferentiated cells, although other factors might impact on miR-214 expression. [score:5]
Notably, all markers were down-regulated in miR-214 -injected embryos (Fig.   6A) demonstrating that in fact cartilage development was hampered. [score:5]
In order to get further insight into the effect of miR-214 overexpression in these larvae, we performed gene expression analysis for key markers of cartilage formation: sox9, sox10, col2a1, col10a1, runx2 and mgp. [score:5]
Gene expression analysis of ATDC5 cells indicated that miR-214 is differentially expressed during chondrocytic differentiation. [score:5]
Thus, based on the important role of Atf4 on chondrogenesis, and the inverse patterns of expression of Atf4 and miR-214 during ATDC5 differentiation (Supplementary Fig.   S4 and Fig.   3B), we propose that Atf4 could be a target of miR-214 in ATDC5 cells, probably contributing to a mitigation of cell differentiation. [score:5]
More recently, the potential use of miR-214 as a therapeutic target in skeletal disorders was evidenced when miR-214 was shown to transit from osteoclast-derived exosomes to osteoblasts, and inhibit bone formation through Atf4 blockage [12]. [score:5]
Nevertheless, these genes play crucial roles on cartilage development and maintenance 51, 52 and their down-regulation in miR-214 -injected embryos further supports a cartilage hindered phenotype. [score:5]
Since miR-214 expression strongly decreased upon ATDC5 cell differentiation, we speculated if miR-214 could be a natural inhibitor of chondrogenesis. [score:5]
However, the levels expression found for ETS1 during ATDC5 differentiation (Supplementary Fig.   S4) are not in line with miR-214 expression pattern (Fig.   3B). [score:5]
Surprisingly, at this stage the expression levels of Col2a1, Col10a1, Tnap, Sox9 and Sp7 were not affected by miR-214 overexpression (data not shown). [score:5]
On the contrary, the repression of Atf4 by miR-214 overexpression in ATDC5 cells is likely a direct effect, since this regulatory mechanism was previously demonstrated in osteoblasts [10] and upon antagomiR transfection Atf4 levels were restored to those found in the control (Supplementary Fig.   S5). [score:5]
Embryos injected with MmiR-214 had a 5-fold miR-214 up-regulation over NC at 3 dpf (Fig.   5A). [score:4]
miR-214 is downregulated during ATDC5 chondrogenic differentiation. [score:4]
The pattern of expression of miR-214 during zebrafish development and ATDC5 chondrogenic differentiation suggested that this miRNA was most likely associated to chondrogenesis. [score:4]
Altogether, these results indicate that ETS1 could be important to control vertebrate skeletogenesis through a putative regulation of Dnm3os/miR-214 expression. [score:4]
Due to the pattern of expression of miR-214 found in ATDC5 cells, and in order to confirm our results on Dnm3os transcriptional regulation, we performed a ChIP analysis of Dnm3os promoter in undifferentiated ATDC5 cells using antibodies against ETS1, SP1, TWIST1 and RNA polymerase II (positive control). [score:4]
In early development in zebrafish, miR-214 was previously shown to be expressed in somites and in the mesenchyme surrounding developing skeletal elements 15, 19. [score:4]
Supporting this notion, miR-214 gain-of-function in zebrafish was shown to impair cranial cartilage formation, and this was accompanied by a downregulation of atf4 and of crucial cartilage markers, thus unveiling a negative impact of miR-214 on chondrogenesis. [score:4]
Regarding non-skeletal components, miR-214 was detected in zebrafish brain, muscle and kidney (Fig.   1B), consistent with Dnm3os pattern of expression found during mouse development [18]. [score:4]
Not only this pattern of expression suggested that miR-214 could play a negative role on chondrogenesis, similar to what was previously shown during osteogenesis in MC3T3 cells [10], but also that its levels should be tightly regulated during chondrocyte differentiation. [score:4]
To clarify this issue, we first analysed miR-214 expression throughout zebrafish development, from blastula to adulthood, focusing on crucial stages of skeletal formation (Fig.   1A). [score:4]
Nevertheless, Mgp and Oc were still down-regulated upon loss-of-function of miR-214 (Supplementary Fig.   S5), indicating that miR-214 mode of action in chondrogenesis might be more complex. [score:4]
Such TFs could be important for miR-214 down-regulation during ATDC5 differentiation. [score:4]
To further understand a putative involvement of miR-214 in zebrafish skeletogenesis, the spatial component of miR-214 expression was analysed by in situ hybridization (Fig.   1B) at: i) 10 dpf, corresponding to the onset of vertebra calcification; ii) 20 dpf, when vertebra calcification is completed; and iii) 90 dpf, corresponding to young adult fish with active bone remo delling [23]. [score:3]
To further explore this possibility, and to get further insight into the role of miR-214 in chondrogenesis, we altered the expression of miR-214 in ATDC5 cells through gain and loss of function experiments. [score:3]
The lower levels of expression during intermediate and later stages of differentiation suggest that miR-214 might be important to maintain chondrocytes in an undifferentiated condition. [score:3]
Li D Osteoclast-derived exosomal miR-214-3p inhibits osteoblastic bone formationNat. [score:3]
miR-214 overexpression impairs zebrafish cartilage formation in vivo. [score:3]
Higher levels of miR-214 contribute to maintain an undifferentiated cell state, possibly by blocking ATF4 and/or by controling Hh and WNT pathways through targeting of Sufu and β-Catenin, respectively. [score:3]
High levels of miR-214 during early chondrocytic cell differentiation seem to delay this process by affecting the expression of important players of chondrogenesis, as Sox9. [score:3]
Importantly, we found that both aft4 paralogs in zebrafish, atf4a and atf4b, were decreased upon miR-214 overexpression (Fig.   5B). [score:3]
On the contrary, forced expression of miR-214 significantly reduced Mgp, Oc and Atf4 levels by approximately 20%, 60% and 40% respectively (Fig.   4B), suggesting that normal cell differentiation was most likely compromised. [score:3]
Accordingly, precisely in the later stage of differentiation, the expression of miR-214 was slightly increased in WT cells (Fig.   3B), when Mgp and Oc levels are higher. [score:3]
Since in previous studies, Atf4 seemed to be pivotal for miR-214 mechanism of action in the mammalian skeleton, we sought to investigate atf4 expression upon miR-214 ectopic expression. [score:3]
Thus, we analysed the expression of miR-214 in several calcified tissues from zebrafish (branchial arches, vertebra and skull) and mouse (cartilage from the ear, vertebra, calvaria and femur); given the known role of miR-214 in myogenesis, we decided to use muscle as a positive control 19, 27. [score:3]
Li N Flynt AS Kim HR Solnica-Krezel L Patton JG Dispatched Homolog 2 is targeted by miR-214 through a combination of three weak microRNA recognition sitesNucleic Acids Res. [score:3]
Liu J MicroRNA-214 promotes myogenic differentiation by facilitating exit from mitosis via down-regulation of proto-oncogene N-rasJ. [score:3]
miR-214 mitigates the expression of chondrogenic markers during ATDC5 differentiation. [score:3]
This was consistent with the detection of putative binding sites for miR-214 in both transcripts (Fig.   5C), and further supported the hypothesis that both genes are miR-214 targets in zebrafish. [score:3]
Regarding cartilage, miR-214 expression was evident in the chondrocranium, in the pharyngeal cartilage and basal region of branchial filaments, in the ceratohyal, and in the basis of pectoral fins (Fig.   1B). [score:3]
This is also in agreement with previous studies showing similar patterns of expression for miR-199 and miR-214 in different systems 15, 20, 21. [score:3]
Importantly, both targets have conserved binding sites for miR-214 (data not shown). [score:3]
Surprisingly, ETS1 but not TWIST1 was enriched in Dnm3os promoter (Fig.   3C), along with RNA polymerase II, thus confirming that Dnm3os, and miR-214, are expressed in undifferentiated ATDC5 cells. [score:3]
In general, our histological analysis confirmed that chondrogenesis is impaired when miR-214 is overexpressed, and suggested that chondrocytes lost their ability to differentiate and produce the main components of cartilage ECM. [score:3]
Scale bars: 0.2 mm for a, e, f and k; 0.1 mm for b, c, d, h, i and j; and 0.05 mm for g. (C) Relative expression of miR-214 in zebrafish (left panel) and mouse (right panel) adult tissues, determined by miRNA qPCR. [score:3]
Microinjection of zebrafish and in vivo effect of miR-214 overexpressionOne-cell stage embryos were microinjected with 4,6 nl of MmiR-214 or NC at 18 μM in 1 × Danieau solution (58 mM NaCl, 0.7 mM KCl, 0.4 mM MgSO4, 0.6 mM Ca(NO3)2, 5.0 mM HEPES pH 7.6), under a MZ6.0 stereomicroscope (Leica) using a Nanoliter 2010 microinjector (World Precision Instruments LLC). [score:3]
In zebrafish, we also detected miR-214 expression in eye lens and retina (Fig.   1B), consistent with previous data obtained in X. laevies, suggesting that miR-214 could also be associated with cell fate in zebrafish retina [25]. [score:3]
Figure 4Effect of miR-214 on the expression of marker genes for chondrocyte differentiation in ATDC5 cells. [score:3]
To further explore this possibility, we tested the effect of miR-214 overexpression on Hh pathway by assessing the levels of a universal marker for activation of this pathway, Patched 1 (Ptch1). [score:3]
This discrepancy suggests that although ETS1 might contribute for miR-214 expression in undifferentiated ATDC5 cells, other TFs should also be determinant. [score:3]
Even though, one must consider that miR-214 is also known to control signalling pathways crucial for chondrogenesis, such as the Hh and WNT pathways by targeting Sufu and β-Catenin respectively 19, 44. [score:3]
However, miR-214 is known to regulate genes and pathways with important functions in chondrogenesis and alternative targets should be considered. [score:3]
Zhao C miR-214 promotes osteoclastogenesis by targeting Pten/PI3k/Akt pathwayRNA Biol. [score:3]
In the previous section we confirmed that miR-214 and miR-199a have similar temporal expression patterns, consistent with the fact that both miRNAs derive from the same transcript. [score:3]
Microinjection of zebrafish and in vivo effect of miR-214 overexpression. [score:3]
In subsequent stages (T21 and T36), miR-214 expression was somewhat increased, but its levels remained low comparing to T0 (6-fold lower in T36) (Fig.   3B). [score:3]
We found high levels of miR-214 expression in all skeletal tissues, although the highest level was observed in the muscle of both zebrafish and mouse (Fig.   1C). [score:3]
miR-214 overexpression during ATDC5 cell differentiation. [score:3]
miR-214 temporal expression correlates with skeletogenesis time-points. [score:3]
Levels of miR-214 were determined by miRNA qPCR, normalized using U6 small RNA expression and using day 0 (T0) as reference. [score:3]
This was evidenced by the high levels of miR-214 expression found during early stages of cartilage formation in zebrafish and in undifferentiated ATDC5 cells. [score:3]
Once miR-214 expression decreases, Atf4 levels also increase, and chondrocytic differentiation proceeds (Fig.   7). [score:3]
miR-214 spatial expression correlates with skeletal structures. [score:3]
Not only this result contributed to uncover the transcriptional regulation of Dnm3os (and miR-214) in ATDC5 cells, but also it highlighted a possible role for ETS1 in chondrogenesis, a topic that remains controversial. [score:2]
QPCR analysis confirmed the altered expression of miR-214 in both experiments compared to NC at T14 (Fig.   4A, Supplementary Fig.   S5). [score:2]
Mir-214 expression is associated with skeleton formation of zebrafish. [score:2]
To better understand miR-214 regulation in skeletal cells, in particularly in chondrogenesis, we used the ATDC5 chondrocytic cell line. [score:2]
These putative regulations might also contribute for miR-214 mode of action. [score:2]
In addition, miR-214 was detected in zebrafish vertebral column, reinforcing the idea that miR-214 is important for the onset of calcification during development 10, 26. [score:2]
M. J. N. and E. R. participated in ChIP-assay experiments and P. G. in miR-214 overexpression in vivo experiments. [score:2]
The next set of experiments aimed at exploring a possible conservation of miR-214 transcriptional regulatory mechanisms. [score:2]
In mammalian mo dels, this transcript was shown to be essential for normal growth and development of the skeleton [16], and particularly, miR-214 was found to control both osteogenesis and osteoclastogenesis 10, 11. [score:2]
miR-214 was detected in both skeletal and non-skeletal components of zebrafish body throughout development, confirming previous studies discussed next 16, 18. [score:2]
Altogether, these data suggest that a tight regulation of miR-214 levels is required for a proper control of molecules impacting on chondrogenesis, such as Mgp and Oc, and consequent normal chondrocyte differentiation. [score:2]
Indeed, Ptch1 levels were significantly increased in ATDC5 cells overexpressing miR-214 compared to control cells (Supplementary Fig.   S6), suggesting that this pathway could also be involved in miR-214 effects in chondrogenesis. [score:2]
MiR-214 was also expressed in the notochordal sheath and in scales (Fig.   1B). [score:2]
Although the putative role of miR-214 in chondrogenesis remains generally unknown, it is now accepted that the Dnm3 opposite strand (Dnm3os) transcript, which encodes miR-214 and miR-199a cluster [15], is crucial for normal mouse skeletal development, including cartilage formation [16]. [score:2]
miR-214 mode of action could be in part explained by direct repression of Atf4. [score:2]
Transcriptional regulation of miR-214 in skeletal-related cell lines. [score:2]
Taken together, our results evidence for the first time that miR-214 could have an important role on chondrogenesis and cartilage formation, similarly to what was previously observed in osteogenesis. [score:1]
While almost half of the embryos had severe deformities in the whole body (head and trunk), two thirds presented a clear flattening of the mandible (Fig.   5D,E), a predominant observation in the miR-214 -injected embryos. [score:1]
After 2 h in pre-hybridization solution (50% formamide, 5 × saline sodium citrate buffer (SSC), 500 μg tRNA, 50 μg Heparin, 0.1%Tween and 9.2 mM of citric acid), sections were incubated with 40 nM of LNA ISH probe (Exiqon) specific for detection of dre-miR-214 (Supplementary Table  S1). [score:1]
Although these studies pointed towards a possible role of miR-214 in skeletogenesis, they failed to demonstrate a clear association with tissue calcification. [score:1]
Arrowheads indicate head deformations resulting from flattening of the mandible; arrows indicate differences on staining intensities of main cartilaginous structures (either absent or weak in miR-214 -injected embryos). [score:1]
These reports suggest that a role for miR-214 in chondrogenesis is still to uncover. [score:1]
Analysis of putative miR-214 binding sites analysis was performed using RNAhybrid (https://bibiserv2. [score:1]
The cluster miR-199a-2/miR-214 is transcribed from the opposite strand of Dynamin 3 (Dnm3), in a common primary transcript called Dnm3os 15, 16, 18. [score:1]
Although recent studies have demonstrated that miR-214 plays a role in skeleton formation 10, 11, the involvement of miR-214 in chondrogenesis remains unknown. [score:1]
This analysis revealed different levels of phenotype severity, which could be due to distinct levels of miR-214 mimic incorporation in each embryo. [score:1]
In this study, we explored a putative role for miR-214 on cartilage formation. [score:1]
Detection of dre-miR-214 was performed using an ISH protocol adapted from the method described by Kloosterman et al. [56] using LNA (Locked Nucleic Acid) -modified oligonucleotide 5′-Digoxigenin (DIG) labelled probe. [score:1]
However, the putative role of miR-214 in chondrogenesis remains to be explored. [score:1]
Notably, all miR-214 -injected embryos (n = 29) presented a reduced intensity of alcian blue staining indicating that the composition of the matrix in cartilaginous structures was altered and suggesting a defective chondrocyte function (Fig.   5D,E). [score:1]
The levels of miR-214 during chondrogenesis are distinct in undifferentiated cells and in differentiating cells. [score:1]
Concerning skeletal elements of zebrafish, miR-214 was found at sites where new bone is being formed, and also in several cartilaginous structures. [score:1]
Negative effects of mir-214 on chondrogenesis. [score:1]
Altogether, data collected in this report pointed towards a putative negative role of miR-214 on vertebrate cartilage formation. [score:1]
From head to tail, miR-214 was detected in eye lens (arrowhead, a, b), retina (white arrowheads, a, b), brain (arrow, a), chondrocranium (asterisk, a, b), pharyngeal cartilage (white arrows, a, c), kidney (arrows, d), scales (arrow, e), muscle myotomes (arrowheads, e), cartilage in the base of pectoral fins (arrows, f), notochordal sheath (arrow, g), osteoid of haemal arches (arrows, h) and growth zones of vertebral body (arrowheads, i). [score:1]
Figure 7 A mo del for miR-214 mode of action in chondrogenesis. [score:1]
For all groups (MmiR-214, NC and WT), the highest mortality was observed at 24 hpf, although miR-214 -injected embryos presented twice as much mortality (approximately 30%) comparing to NC (approximately 17%) and WT (approximately 12%). [score:1]
Thus, our results provide the first evidence indicating a possible role of miR-214 in chondrogenesis. [score:1]
Based on our results, we propose that low levels of miR-214 are most likely required in order for chondrogenesis to initiate/proceed. [score:1]
Overall, this miR-214 spatial distribution suggests a functional conservation in vertebrates. [score:1]
Nevertheless, one cannot disregard the putative involvement of miR-214 in other processes occurring simultaneously with skeletogenesis, not addressed in the scope of this study. [score:1]
Figure 3Analysis of miR-214 transcriptional activity in skeletal-derived cell lines. [score:1]
Nevertheless, some cartilaginous structures, e. g. pharyngeal arch cartilage (Supplementary Fig.   S7A and B), seemed to be properly placed and resembled a chondrocyte packing, but lacked reactivity to safranin-O in the miR-214 -injected embryos. [score:1]
Cells were seeded in 24-well plates (2.5 × 10 [4] cells/well), incubated for 16 h and transfected with miRIDIAN microRNA mimic for mmu-miR-214 (from now on designated MmiR-214) or negative control scrambled miR 1 (NC) (Dharmacon) at a final concentration of 50 nM, using EzWay (Koma Biotech) transfection reagent. [score:1]
This result suggested a functional conservation of miR-214 in skeletogenesis between zebrafish and mammals. [score:1]
In fact, we could not detect the presence of mature chondrocytes in miR-214 -injected embryos as evidenced in NC (Fig.   6B and Supplementary Fig.   S7). [score:1]
Flynt AS Li N Thatcher EJ Solnica-Krezel L Patton JG Zebrafish miR-214 modulates Hedgehog signaling to specify muscle cell fateNat. [score:1]
Cartilage associated proteoglycans (evidenced by safranin-O) are either absent or present in low amounts in the Ethmoid plate (Ep) or hyosympletic (Hs), respectively, of miR-214 -injected embryos comparing to NC. [score:1]
However, to the best of our knowledge, miR-214 was never detected in cartilage. [score:1]
We further investigated the distribution of miR-214 in adult zebrafish calcified tissues, and argued if its expression could be comparable to other vertebrates. [score:1]
As for newly forming bone, miR-214 was detected in arches and in the growth zones of the vertebral centra (Fig.   1B). [score:1]
Herein, we show that miR-214 has a role in chondrogenesis and an underlying mechanism for miR-214 action is proposed. [score:1]
Loss-of-function experiments further supported that miR-214 levels should be important for proper chondrocyte differentiation, although it also revealed that the role of miR-214 might be more complex than originally expected. [score:1]
However, data collected in our study suggests that miR-214 might have a role in chondrogenesis. [score:1]
Gross morphology analysis revealed four phenotypes in miR-214 -injected embryos comparing to NC: i) the embryos were generally smaller; ii) pericardium was enlarged; iii) the eyes were smaller and less developed; and iv) larvae presented alterations in the size and number of otoliths. [score:1]
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[+] score: 36
For instance zebrafish, common carp, Atlantic cod, coelacanth, spotted gar, cave fish and elephant shark follow the single copy pattern of non-fish species whilst platyfish, stickleback, medaka, fugu, tetraodon and Nile tilapia possess two copies of miR-214 and Dnm3. [score:1]
Additionally the highly conserved sequence and organizational pattern within all gnathostome species indicates that miR-214 would have experienced similar evolutionary pressures that kept it under strong selective constraint. [score:1]
We then looked at the miR-214-par precursor sequences and verified that they were distinct to precursors of the canonical miR-214 by twelve to fifteen nucleotide substitutions in 90 bp nucleotide sequences. [score:1]
However neither the wi dely distributed nor the paralog copy have shown a conserved intronic localization among vertebrates, indicating singularities of miR-214 organization in the genomes analyzed. [score:1]
In the phylogenetic tree, all miR-214-par branched out together, founding an isolated clade from the canonical miR-214 (Figure  4). [score:1]
miR-214 duplication. [score:1]
Thereby, it indicates two possibly scenarios where (1) the duplication event occurred in a bony fish ancestor, and miR-214-par was lost in diverse lineages but kept in superorder Acanthopterygii; or (2) the duplication event was specific to superorder Acanthopterygii. [score:1]
Therefore, we suggest that the intronic miR-214-par emerged by the duplication of its host gene Dnm3, followed by the transposition of both genes to another chromosome or scaffold. [score:1]
Then, we can infer that miR-214-par derived from miR-214 by duplication and divergence, being secondarily lost in a few fish lineages. [score:1]
For instance, the tetraodon genome experienced a rearrangement in the miR-214 neighbor genes Pigc, Tmed5, Suco, Mysm1 and Oma1 moved from downstream to an upstream segment, likely by a translocation episode (Figure  1E). [score:1]
This extra miRNA copy turns out to be a novel paralog of miR-214, henceforth called miR-214-par. [score:1]
Conversely, the miR-214-par and miR-214 have shown poor synteny for their respective surrounding protein coding genes. [score:1]
Figure 4 of miR-214 in vertebrates. [score:1]
In general, miR-214 orthologs have been organized as syntenic blocks in fishes although particular features were also uncovered. [score:1]
Overall, our analysis supports a scenario where the origin of miR-214 in vertebrate genomes took place during Paleozoic and extant paralogs came out after a gene duplication event restricted to an Acanthopterygii ancestor during Mesozoic. [score:1]
Furthermore, miR-214 is clusterized (with miR-199) and intronic of Dnm3 gene as reported in mammals [35]. [score:1]
All the results presented here confirm the miR-214-par as a new paralog of miR-214 and highlight a duplication event restricted to superorder Acanthopterygii, thus fostering the need for a new nomenclature to these miRNA genes (i. e. miR-214-1 and miR-214-2). [score:1]
Phylogenetic relationships were constructed based on the 80 bp alignment of precursor sequences of miR-214 from diverse vertebrate species (retrieved from miRBase and Ensembl) as well as miR-214 paralog sequences from fish species, recovered by BLAST, as previously mentioned. [score:1]
Figure 5 Schematic representation of the genomic organization and synteny analysis of miR-214 and its paralog detected on fish genomes. [score:1]
For the miR-214, we propose a gene-birth in a gnathostome common ancestor, because our deep genome search did not recover this miRNA neither in lamprey (agnatha) nor in any other basal chordate. [score:1]
Our analysis suggests that the duplication event of miR-214 was restricted to medaka, stickleback, tetraodon, fugu, Nile tilapia and platyfish. [score:1]
Figure 3 Secondary structures of miR-214 and miR-214-par. [score:1]
In the case of miR-214-par, it was embedded within a conserved syntenic block on all studied species (Figure  1F). [score:1]
Amid these genes, only Suco and Myoc were duplicated along with miR-214-par, while Mettl13, Vamp4, Prrc2c and Pigc were maintained neighboring the canonical miR-214 wi dely distributed in vertebrates. [score:1]
Furthermore, in fish species we observed that genes nearby miR-214-par were highly syntenic, excepting the Jun gene that was solely retained in Nile tilapia, medaka and stickleback genomes (Figure  5). [score:1]
In the comparative screening of the genomic context of muscle miRNAs in vertebrates, we found that all non-fish species carry a single copy of miR-214 and its host gene Dnm3. [score:1]
Highlighted square represents the divergent clade of miR-214-par. [score:1]
Interestingly, the Prdx6 gene that is located near to miR-214-par was exclusively held by those fish species carrying this miRNA paralog copy. [score:1]
The interrogation dot on 3’ region of stickleback indicates no detection of any gene once miR-214 and its host gene were detected on the region of the scaffold that are not anchored with other scaffold yet. [score:1]
As major outcomes we show that (1) miR-208 was unexpectedly absent in cartilaginous and ray-finned fish genomes whereas it still exist in other vertebrate groups; (2) miR-499 was intergenic in medaka and stickleback conversely to other vertebrates where this miRNA is intronic; (3) the zebrafish genome is the unique harboring two extra paralogous copies of miR-499 and their host gene (Myh7b); (4) a rare deletion event of the intergenic and bicistronic cluster miR-1-1/133a-2 took place only into Tetraodontiformes genomes (pufferfish and spotted green puffer); (5) the zebrafish genome experienced a duplication event of miR-206/-133b; and (6) miR-214 was specifically duplicated in species belonging to superorder Acanthopterygii. [score:1]
However, the predicted secondary structure of miR-214-par precursors mounts into a hairpin conformation consistent with the miRNA biogenesis mo del (reviewed in [5]), therefore denoting functionality to the paralog copy detected (Figure  3). [score:1]
By contrast, only Prdx6 gene was retained near of miR-214-par. [score:1]
The homologs of ancient miRNAs that emerged more recently by duplication and are still not under functional constraint, may either evolve fast, potentially originating other miRNAs, or be conserved, as verified for the miR-214 paralog identified in the present study (below discussed). [score:1]
For instance Myoc, Suco, Ppapdc2 genes are maintained in synteny into both miR-214 variants, contrasting to the majority of remaining protein coding genes which have evolved distinctively after duplication. [score:1]
Furthermore, we performed an analysis of secondary structure of precursor sequences of miR-214 and miR-214 paralog copy obtained from each fish species in order to verify the paralog compliance to the hairpin structure required by the miRNA biogenesis mo del. [score:1]
It is probably caused by the proximity of miR-214 and its host gene to the 3’end of the scaffold sequence they are located. [score:1]
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3
[+] score: 25
The results of qRT-PCR showed that all three miRNAs exhibited significant inhibitory effects on mRNA expression of the N gene, while for the P gene, only miR-130c-5p and miR-214 exhibited inhibitory effects (Figure 5A). [score:7]
Similar to the effects on mRNA expression of SHVV, miR-130c-5p and miR-214 also exhibited a significant inhibitory effect on protein expression of SHVV. [score:7]
SSN-1 cells in 12-well plates were transfected with 100 nM mimics or 50 nM inhibitors of miR-130c-5p, miR-214, miR-216b, as well as mimic control or inhibitor control using Lipofectamine 2000 (Invitrogen, USA). [score:5]
Among the three miRNAs, miR-214 exhibited the most significant inhibitory effect (Figure 5A). [score:3]
Three differentially-expressed miRNAs, including miR-130-5p, miR-214 and miR-216b, were chosen to evaluate their effects on SHVV multiplication. [score:1]
Together, these data demonstrated the three miRNAs, at least miR-130c-5p and miR-214, could efficiently repress SHVV multiplication. [score:1]
miR-130-5p and miR-216b were predicted to bind to N, G and L genes, while miR-214 was predicted to bind to N and P genes (Table 2). [score:1]
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[+] score: 9
Other miRNAs from this paper: dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-205, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-7a-3, dre-mir-30c, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-206-1, dre-mir-206-2, dre-mir-375-1, dre-mir-375-2, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j
Morpholinos are wi dely applied to knock down genes in zebrafish development [19] and have recently been used to target mature miR-214 in zebrafish [20]. [score:5]
In a recent study, mature miR-214 was targeted by a morpholino in zebrafish, and this resulted in a change in somite shape, reminiscent of attenuated hedgehog signaling [20]. [score:3]
In addition, data were lacking that showed an effect of the morpholino on endogenous miR-214 levels. [score:1]
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5
[+] score: 8
The Hh pathway regulator, Suppressor of Fused (SuFu), is directly targeted by miR-214 and this interaction affects muscle fibre specification in the developing zebrafish embryo by regulating the transcription factor Gli1 and maintaining the required levels of Hh activity in the muscle progenitor cells [20]. [score:8]
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[+] score: 6
Tian X. Zeng G. Li X. Wu Z. Wang L. Cantharidin inhibits cell proliferation and promotes apoptosis in tongue squamous cell carcinoma through suppression of miR-214 and regulation of p53 and Bcl-2/Bax Oncol. [score:6]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-23a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-205, hsa-mir-214, hsa-mir-221, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-184, hsa-mir-193a, hsa-mir-1-1, hsa-mir-29c, hsa-mir-133b, dre-mir-205, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-1-2, dre-mir-1-1, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-107a, dre-mir-122, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-184-1, dre-mir-193a-1, dre-mir-193a-2, dre-mir-202, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, hsa-mir-202, hsa-mir-499a, dre-mir-184-2, dre-mir-499, dre-mir-724, dre-mir-725, dre-mir-107b, dre-mir-2189, hsa-mir-499b, dre-mir-29b3
Interestingly, several VTGs are targets of miRNAs for silencing [119]: VTG-3 is targeted by miR-122, the most abundant miRNA in the liver, as well as miR-107, VTG-7 by miR-107, VTG-2 by miR-214 and VTG-6 by miR-23a, highlighting the importance that miRNAs have on vitellogenesis, oocyte maturation and reproduction. [score:5]
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[+] score: 4
Other miRNAs from this paper: dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-210, dre-mir-219-1, dre-mir-219-2, dre-mir-221, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-21-1, dre-mir-21-2, dre-mir-25, dre-mir-30e-2, dre-mir-101a, dre-mir-103, dre-mir-107a, dre-mir-122, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-126a, dre-mir-129-2, dre-mir-129-1, dre-mir-130b, dre-mir-130c-1, dre-mir-130c-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-135c-1, dre-mir-135c-2, dre-mir-140, dre-mir-142a, dre-mir-142b, dre-mir-150, dre-mir-152, dre-mir-462, dre-mir-196a-2, dre-mir-196b, dre-mir-202, dre-mir-203b, dre-mir-219-3, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-mir-455-1, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-135b, dre-mir-135a, dre-mir-499, dre-mir-738, dre-mir-429b, dre-mir-1788, dre-mir-196c, dre-mir-107b, dre-mir-455-2, dre-mir-222b, dre-mir-126b, dre-mir-196d, dre-mir-129-3, dre-mir-129-4
In some ZF samples, the number of miRNA* reads was higher than that of mature miRNA sequences, namely dre-miR-129*, dre-miR-140*, dre-miR-142a*, dre-miR-202*, dre-miR-210* and dre-miR-214*. [score:1]
However, six miRNA* were more abundant than their corresponding mature miRNAs, namely dre-miR-129*, dre-miR-140*, dre-miR-142a*, dre-miR-202*, dre-miR-210* and dre-miR-214*. [score:1]
In the case of dre-miR-129, dre-miR-140, dre-miR-142a, dre-miR-202, dre-miR-210 and dre-miR-214, the number of miRNA* reads was considerably higher than that of mature miRNA reads, suggesting that the miRNA* strand was more stable than the miRNA strand. [score:1]
Similar results were observed before for dre-mir-129*, dre-mir-142a*, dre-mir-142b* and dre-mir-214* [20]. [score:1]
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9
[+] score: 4
107.149377 17947801 32. van Mil A. Grundmann S. Goumans M. -J. Lei Z. Oerlemans M. I. Jaksani S. Doevendans P. A. Sluijter J. P. MicroRNA-214 inhibits angiogenesis by targeting Quaking and reducing angiogenic growth factor release Cardiovasc. [score:4]
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[+] score: 3
ReagentsMature miRNA mimics (mmu- miR-218a, mmu-miR-492, mmu-miR-214 and miR-Ct) were synthesized by GenePharma (Shanghai, China), morpholinos (Gene Tools, LLC USA. [score:1]
The total numbers of embryos analyzed were as follows: Ct miRNA (1 ng) n = 293; miR-214 mimic (1 ng) n = 104; miR-492 mimic (1 ng) n = 103; miR-218 mimic (35 pg) n = 107; miR-218 mimic (135 pg) n = 180; miR-218 mimic (260 pg) n = 318; miR-218 mimic (2 ng) n = 180; MO-Ct (8 ng) n = 207; MO [D]-218 (12 ng) n = 323; MO [M]-218 (2 ng) n = 112; MO [M]-218 (4 ng) n = 165; MO [M]-218 (8 ng) n = 182. [score:1]
As specificity controls, 2 ng of either miR-492, a control miRNA, that is not annotated in zebrafish, or miR-214, which is not heart-specific, were injected without generating embryos with cardiac defects in significant percentages (Fig. 2C). [score:1]
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[+] score: 3
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-191, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-let-7d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, mmu-mir-429, mmu-mir-449a, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, mmu-mir-449c, mmu-mir-449b, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-124b
By contrast, we identified 12 miRNAs corresponding to 9 families (miR-199, miR-140, miR-152, miR-214, miR-205, miR-200, miR-183, miR-182, miR-96) that displayed highly enriched expression in the olfactory system (Figure 1A). [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, mmu-mir-376a, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, hsa-mir-429, mmu-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-130b, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The most abundant miRs expressed in the developing mouse OE are: the miR-200-class (- 200a, - 200b, - 200c, - 141 and - 429), miR-199, miR-152, miR-214, miR-205, miR-183, miR-182 and miR-96 (Choi et al., 2008). [score:3]
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[+] score: 2
For example, miR-214 is required for proper muscle formation, miR-375 is needed for pancreatic islet development, and the large miR-430 family is needed for deadenylation and clearance of maternal mRNAs at the midblastula transition [21- 23]. [score:2]
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[+] score: 1
In Zebrafish, miR-430 [20] has been shown to silence maternal RNAs, miR-214 is involved in proper somite specification [21] and miR-375 is necessary for the maintenance of embryonic pancreas integrity [22]. [score:1]
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15
[+] score: 1
Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-204-1, dre-mir-181a-1, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-25, dre-mir-26a-1, dre-mir-26a-2, dre-mir-26a-3, dre-mir-30d, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-100-1, dre-mir-100-2, dre-mir-125a-1, dre-mir-125a-2, dre-mir-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-125c, dre-mir-126a, dre-mir-143, dre-mir-146a, dre-mir-462, dre-mir-202, dre-mir-204-2, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-181a-2, dre-mir-1388, dre-mir-222b, dre-mir-126b, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-204-3
Modifications at 5′ end were detected in 8 miRNAs; miR-100-5p, miR-10a-5p, miR-10b-5p, miR-10c-5p, and miR-126a-5p were truncated, while miR-202-5p, miR-202-3p, and miR-214-3p had templated additions (Supplementary Dataset S6). [score:1]
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