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8 publications mentioning gga-mir-183

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-183. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 248
It is interesting to consider that the levels of the miR-183 family are physiologically relevant to retinal function, since they are down-regulated during dark adaptation and up-regulated in light-adapted retina [55]. [score:7]
Functional testing of pGFP-183F expression vector in vitro To examine the role of the miR-183 family in HC development, we employed an overexpression strategy modified from a design reported previously [30]. [score:6]
These developmental expression profiles led Weston and colleagues [24] to propose that the miR-183 family might enforce reciprocal longitudinal gradients on HC target genes that could underlie, at least in part, the acquisition of phenotypic traits responsible for frequency selectivity. [score:6]
AAVs encoding short hairpin RNAs that resemble pre-miR-183 and pre-miR-182 were injected into the retinas of DGCR8-conditional knockout mice in which miRNA biogenesis was blocked, leading to re -expression of miR-183 and miR-182 in Cre -expressing cone photoreceptors and prevention of the loss of outer segments and cone opsins [59]. [score:6]
Gene knockdowns or knockouts in the retina have revealed that down-regulation or loss of the miR-183 family leads to progressive degeneration of photoreceptors and increased susceptibility to light damage [21, 58]. [score:6]
Also, a miRNA target prediction algorithm (TargetScan, version 6.2) applied to the 3’UTR of chicken Sox2 failed to find predicted binding sites for any of the miR-183 family members. [score:5]
Thus, while ectopic HCs are occasionally observed in embryos subjected to electroporation, overexpression of the miR-183 family does not appear to increase the likelihood of their appearance, assuming that GFP is a reliable reporter of miRNA overexpression (Fig 4A–4C). [score:5]
The same study showed that expression of the miR-183 family also varies across the radial axis of the mouse organ of Corti, and that this expression pattern changes with maturation, even as overall levels decrease. [score:5]
We were specifically interested in whether inner ear sensory organs showed evidence of the miR-183 family expression at the prosensory stages, or whether expression was only limited to HCs. [score:5]
We reasoned that genes responsible for imparting neural versus abneural identity to the prosensory cells might be post-transcriptionally regulated by this miR-183 family expression gradient. [score:4]
We hypothesize that expression gradients of the miR-183 family reported along and across the mammalian cochlear axis are meaningful for HC development, and thus would be evolutionarily conserved in the bird BP. [score:4]
During BP development, the miR-183 family is expressed in a gradient along the longitudinal (tonotopic) axis, with highest levels found at the apex. [score:4]
Morpholino -mediated knockdown of the miR-183 family members decreased the number of HCs and otic neurons at 48 hours post fertilization (hpf), while overexpression of miR-96 or miR-182 resulted in ectopic and expanded sensory patches at 26 hpf [26]. [score:4]
To examine the role of the miR-183 family in HC development, we employed an overexpression strategy modified from a design reported previously [30]. [score:4]
Perhaps HCs cannot persistently overexpress the miR-183 family due to the presence of an unknown regulatory pathway that can negatively feedback on the transcription, processing or stability of these miRNAs when their levels are artificially raised. [score:4]
The reductions obtained were 89% knockdown for the miR-96 reporter, 82% knockdown for the miR-182 reporter and 88% knockdown for the miR-183 reporter. [score:4]
Nonetheless, this finding provides indirect evidence that some of the targets for the miR-183 family may be present at the prosensory stage, and may be modulated by changes in the level of the miR-183 family. [score:4]
However, using our experimental approach, ectopic expression of the miR-183 family was insufficient to redirect the differentiation of HCs towards specific radial or longitudinal phenotypes. [score:4]
0132796.g003 Fig 3The bifunctional pT2K-CAG-EGFP-183F plasmid expresses functional members of the miR-183 family in vitro. [score:3]
The bifunctional pT2K-CAG-EGFP-183F plasmid expresses functional members of the miR-183 family in vitro. [score:3]
Until now, deliberate experimental manipulation of the miR-183 family members has mainly relied on knockdown or knockout approaches [21, 58]. [score:3]
We interpret weak hybridization signal for the miR-183 family in developing sensory domains as consistent with the presence of thin cytoplasmic tails of HCs within the SC layer, although we cannot definitely exclude expression in prosensory cells or SCs of the vestibular organs at these immature stages. [score:3]
Ectopic expression of miR-183 family can bias progenitor cells towards HC fate. [score:3]
Thus, the miR-183 family belongs to a small group of genes reported as being differentially expressed across the radial axis of the BP as early as E7, when the proximal organ, while postmitotic, is still at the prosensory stage. [score:3]
Expression of the miR-183 family in the BP at mid to late gestation. [score:3]
Ectopic expression of miR-183 family is confirmed in vivo at S31 and S40. [score:3]
At S28, miR-183 is weakly expressed in the anterior and posterior cristae (A), the saccular macula and the vestibular ganglion (B), but is not detected in the cochlear duct (C). [score:3]
Overexpression of the miR-183 family in vivo. [score:3]
Unlike previous results in zebrafish [26], overexpression of the miR-183 family did not reproducibly induce ectopic HCs beyond the sensory domains. [score:3]
Ectopic expression of miR-183 family does not alter HC fate along and across the BP. [score:3]
To explore the function of the miR-183 family, expression levels were systematically altered in the developing zebrafish [26]. [score:3]
We conclude that in the BP, delivery of the miR-183 family expression plasmid does not impact the differentiation of THC versus SHC phenotypes. [score:3]
Nonetheless, we asked whether ectopic expression of the miR-183 family decreased the level of Sox2 protein in avian SCs, providing a possible mechanism by which they might be pushed toward a HC fate. [score:3]
Our conclusion for the chicken BP stands in contrast to data from the mouse, where qualitative differences in the expression of the miR-183 family were observed for IHCs versus OHCs in both whole mounts and sections [24, 25]. [score:3]
Prior to the appearance of a longitudinal gradient, we observed an early radial gradient in the expression of the miR-183 family (highest on the neural side) in the prosensory BP. [score:3]
Specifically, we speculated that HCs located on the abneural half of the BP, which normally become SHCs, might acquire the morphological phenotypes of THCs if they are forced to overexpress the miR-183 family beginning at the prosensory stage. [score:3]
However, the expression of the miR-183 family in zebrafish inner ear was not detected in prosensory cells, but was only found in HCs [39]. [score:3]
Overexpression of the miR-183 family in vivo Once the functionality of the miRNAs processed from the pGFP-183F construct was confirmed in vitro, pGFP-183F and pT2TP were injected and then electroporated into the right otic cup (S11–12) or otocyst (S15–S16) of chicken embryos. [score:3]
In situ hybridization was used to detect the expression of mature miR-183, miR-96 and miR-182 on sections through the embryonic chicken inner ear at stages when nascent HCs are present in vestibular and auditory sensory organs (E5/S28 and E7/S31, respectively). [score:3]
Both miR-182 and miR-183 were reported to be broadly expressed in the E9.5 mouse otocyst, and present in both prosensory tissues and non-sensory domains in the E12.5 mouse cochlea [25]. [score:3]
Since the miR-183 family was ectopically expressed as early as S26, before cells in the BP begin to pull out of division, we asked whether this experimental manipulation would push bipotential progenitor cells toward a HC fate rather than a SC fate. [score:3]
At S31, miR-183 is strongly expressed in HCs of all the vestibular organs (D-E) and the apical part of the BP (D-F). [score:3]
The ectopic expression of the miR-183 family was observed at S26 (S6 Fig), before the majority of HCs in the inner ear have exited the cell cycle [40]. [score:3]
There are several technical caveats that might explain why the delivery of a miR-183 family overexpression vector ectopically to the inner ear on E2/E3 did not alter HC phenotypes 10–14 days later. [score:3]
To ensure that mature members of the miR-183 family were produced from the miRNA expression plasmid, HEK293T cells were transfected with pGFP-183F, and their lysates were analyzed using. [score:3]
HC morphologies and HC subtypes are unaltered by transfection with a miR-183 family expression vector. [score:3]
The overexpression of the miR-183 family persisted for two weeks, as HCs were differentiating. [score:3]
The expression of miR-183 in the inner ear at S28 and S31. [score:3]
At S28 when HCs in the basal (proximal) BP start to exit the cell cycle [40], there was no detectable expression of the miRNA-183 family anywhere along its length (n = 3 embryos; S2 and S3 Figs). [score:3]
Progenitor cells are biased toward an HC fate by transfection with a miR-183 family expression vector. [score:3]
The 3 members of the miR-183 family (miR-183, miR-96, miR-182) are processed from a single primary transcript [20, 21] and are expressed in sensory cells in mice and zebrafish [20, 22, 23]. [score:3]
Ectopic HCs in non-sensory epithelia did not correlate with delivery of a miR-183 family expression vector. [score:3]
Thus, robust expression of the miR-183 family in BP HCs is tightly linked to the initiation of HC differentiation. [score:3]
With the exception of a mild bias toward the HC fate within the middle regions of the sensory BP, there were no obvious changes in HC or hair bundle morphologies induced by the delivery of the overexpression vector for the miR-183 family. [score:3]
Expression of the miR-183 family was specific to HCs throughout these ages (Fig 2B–2E), and began to decline after S40. [score:3]
We predicted that increasing the expression of the miR-183 family might cause basal HCs to acquire the characteristics of apical HCs, because the apex is where their expression levels are normally highest. [score:3]
Inner ear expression of the miR-183 family at E5 and E7. [score:3]
0132796.g004 Fig 4Ectopic expression of miR-183 family is confirmed in vivo at S31 and S40. [score:3]
Therefore, we posited that overexpression of miR-183 family might also induce non-sensory epithelia to take on a sensory fate in the chicken inner ear. [score:3]
This suggests that delivery of miR-183 family expression plasmids does not generate a persistent mixed HC-SC phenotype, when assayed with the markers used. [score:2]
Samples (600ng of small RNA) were subsequently probed for miR-183 family expression using DNA probes against the mature miRNA human sequences (Signosis) in conjunction with a chemiluminescence system, the High Sensitive miRNA Northern Blot Assay Kit (Signosis), according to the manufacturer’s instructions. [score:2]
While confirmed that the miRNA-183 family members were expressed from an artificial intron housed within a Tol2 construct, we sought evidence that each mature miRNA was processed and functional in chicken cells by using an in vitro dual luciferase assay. [score:2]
Compared to the controls (cells transfected with pGFP), HEK 293T cells transfected with pGFP-183F display expression of mature miR-183, -96, and -182. [score:2]
All 3 members of the miR-183 family exhibit dynamic longitudinal gradients postnatally in the mouse organ of Corti [24]. [score:1]
In the apical (distal) BP at the same stage, all three members of the miR-183 family were detected in nascent HCs (Fig 1C for miR-182; S2 and S3 Figs). [score:1]
Genomic sequences from the murine miR-183/96 and miR-182 loci were fused and placed within an artificial intron, which is located downstream of the EGFP reporter gene. [score:1]
We found that manipulating the levels of the miR-183 family can mildly influence the HC-SC fate decision. [score:1]
At both stages, the miR-183 family members were detected in the statoacoustic ganglion neurons and in vestibular HCs of the anterior crista, posterior crista, lateral crista, utricular macula and saccular macula (Fig 1A–1C, S2 and S3 Figs). [score:1]
To evaluate a possible role in establishing or maintaining HC phenotypic gradients in the chicken BP, the miR-183 family was overexpressed in the inner ear prior to and during HC differentiation. [score:1]
The miRNA reporters, composed of two complementary miRNA binding sites (to either miR-183, miR-96, or miR-182) housed downstream of the Renilla luciferase gene, were co -transfected into DF-1 cells with pGFP-183F or pGFP. [score:1]
An approximately 800 base pair fragment containing genomic sequences from the mouse miR-183 family locus, flanked by splice donor and acceptor sites, was obtained from pME-MCS-sd-miR183F-sa [30]. [score:1]
In this study, we show that the miR-183 family briefly presents with a neural-to-abneural gradient in the chicken BP at E7 and that it also displays an apical-to-basal gradient at E16-18. [score:1]
There are two studies using gain-of-function approaches of the miR-183 family. [score:1]
The detection of the miR-183 family members in both immature HCs and in statoacoustic neurons is similar to that previously described for both mouse [24, 25] and zebrafish [26]. [score:1]
A similar gradient was evident in adjacent sections probed for miR-183 (n = 3/4 ears from 2 embryos) or miR-96 (n = 2/5 ears from 3 embryos, S3 Fig bracket). [score:1]
The miR-183 intron was inserted into pT2K-CAG-EGFP-attR through a Gateway LR recombination reaction, creating pT2K-CAG-EGFP-183F (abbreviated pGFP-183F). [score:1]
miR-96 is conserved among the four species, while miR-182 and miR-183 show differences in the last few nucleotides at their 3’ ends. [score:1]
We suspect that we are too close to the detection threshold to always see radial gradients of miR-96 and miR-183 in the BP, but they are probably present nonetheless. [score:1]
The longitudinal gradient of miR-183 family was observed after S42. [score:1]
The LNA probes used were dre/hsa-miR-183, hsa-miR-96 and dre-miR-182. [score:1]
These data suggest that the precise level of the miR-183 family members can influence HC specification. [score:1]
In the mouse, all 3 miR-183 family members are derived from a common transcript and are located within an intronic region of a potential protein-coding gene [21]. [score:1]
miR-183 family is present in HCs in S38–S45 BPs. [score:1]
To ask whether delivery of miR-183 family expression plasmids could affect these morphological parameters, pGFP-183F -transfected BPs were triple-labeled with antibodies to GFP (to identify transfected cells), HCS-1 (to measure HC cross-sectional areas) and phalloidin (to label HC bundles). [score:1]
S1 Fig shows a comparison of the miR-183 family mature sequences among human (hsa), mouse (mmu), chicken (gga) and zebrafish (dre). [score:1]
Although many HCs were obviously GFP+ when viewed in immunostained whole-mounts, we were unable to confirm that the miR-183 family levels exceeded endogenous levels in HCs by whole mount in situ hybridizations of the BP (Fig 4D). [score:1]
However, miR-183 was significantly weaker on than the other two miRNAs. [score:1]
Arrows point to examples where GFP+ cells superimpose with a higher intensity of signal for miR-183. [score:1]
The sequence of miR-96 is fully conserved between these species, while miR-182 and miR-183 differ by 1–3 nucleotides at their 3’ ends, but are otherwise identical. [score:1]
S1 Fig miR-96 is conserved among the four species, while miR-182 and miR-183 show differences in the last few nucleotides at their 3’ ends. [score:1]
A further correlation between the miR-183 family and the tonotopic organization of the mouse cochlea is seen by in situ hybridization. [score:1]
Sequence comparison of the miR-183 family members among human, mouse, chicken and zebrafish. [score:1]
Gallus gallus mature miR-183 (gga-miR-183) sequence was obtained from miRBase while the miR-182 and miR-96 sequences were obtained from published Gallus gallus short RNA sequencing reads [31]. [score:1]
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[+] score: 60
a ADIPOR2 is targeted by miR-20b and let-7c, b INSIG1 is targeted by miR-182, miR-183, and miR-454, c MAPK4K4 is targeted by miR-29a, d FASN is targeted by miR-107, e FADS2 is targeted by let-7c, f ELOVL2 is targeted by miR-10b, g HMGCS1 is targeted by miR-18a, and h MSMO1 is targeted by miR-20b and miR-454 To further explore miRNA regulatory networks associated with the metabolic switch, we identified potential metabolic mRNA targets for let-7c, miR-20b, and miR-183 using in silico target prediction in combination with IPA pathway analysis. [score:22]
FADS2, SCD and other genes in this network are predicted targets of miRNA, including let-7c and miR-183 Fig. 3Examples of reciprocal expression of metabolic genes and some their targeting miRNAs during the metabolic switch in developing chickens. [score:7]
ELOVL6, a validated miR-183 target (Fig. 4c), encodes for a lipogenic enzyme involved in the de novo synthesis of long-chain fatty acids, along with FASN, a validated let-7c (Fig. 4a) and miR-183 target (Fig. 4c), and SCD, a validated let-7c target (Fig. 4a). [score:7]
Among the regulators of ELOVL6 are INSIG1, also a validated miR-183 target (Fig. 4c) and SCAP, a validated let-7c target (Fig. 4a). [score:6]
FADS2, SCD and other genes in this network are predicted targets of miRNA, including let-7c and miR-183. [score:3]
INSIG1 mRNA is a predicted target of three miRNAs (miR-182, miR-183, and miR-454), all of which decreased 2-fold between D1 and D3 (Figs. 1 and 3b). [score:3]
Other validated miRNA target genes include FADS1 (let-7c, miR-20b, and miR-183), FADS2 (let-7c), and SQLE (let-7c and miR-183) (Fig. 4). [score:3]
This analysis revealed that all three miRNAs, (let-7c, miR-20b, and miR-183), potentially regulate a number of genes associated with lipid metabolism and carbohydrate metabolism (Table 2). [score:2]
Similar mechanisms might involve other miRNAs such as let-7c and miR-183, which we have confirmed can regulate ADIPOR2, ELOVL6, FADS1, FADS2, FASN, HMGCR, LSS, SCD, and SQLE, which also control fatty acid and cholesterol synthesis. [score:2]
Luciferase assays for (a) let-7c, (b) miR-20b, (c) miR-183, and a scrambled sequence (SC) for target gene validation are shown. [score:2]
These included ACAT2 and CYP51A1 for let-7c (Fig. 4a), ABCD3 and ACSBG2 for miR-20b (Fig. 4b), and HACD2 for miR-183 (Fig. 4c). [score:1]
DF1 cells were infected with either RCAS- gga-let-7c, RCAS- gga-miR-20b, RCAS- gga-miR-183 or RCAS- SC (M. O. I. of 1) and maintained in a 96-well plate in RPMI 1640 with 1% heat-inactivated FBS, L-glutamine, penicillin (100 U/ml), streptomycin (100 μg/ml), and fungizone (4 μg/ml), at 37 °C with 5% CO [2]. [score:1]
For miR-20b, 10 genes were selected for validation, and for miR-183, 11 genes were chosen for validation. [score:1]
[1 to 20 of 13 sentences]
[+] score: 8
Notably however, gga-mir-183 which targets EZR mRNA (which did not change), was decreased and EZR (important in metastasis) protein increased; i. e. we suggest that one reason for the increase in EZR protein is decreased gga-mir-183 translation -inhibition. [score:7]
Of these, nine (gga-mir-1b, gga-mir-7, gga-mir-7b, gga-mir-10b, gga-mir-31, gga-mir-130b, gga-mir-204, gga-mir-215, gga-mir-489) are increased, and five (gga-mir-223, gga-mir-124b, gga-mir-140, gga-mir-183, gga-mir-222a) are decreased in CD30 [hi] cells. [score:1]
[1 to 20 of 2 sentences]
[+] score: 5
Other miRNAs from this paper: mmu-mir-183
We showed that HDAC2 cooperates with MYCN to suppress apoptosis mediated by miR-183 [36], and that HDAC3 interacts with MYCN to transcriptionally repress the GRHL1 transcription factor, which exerts tumor suppressive effects in neuroblastoma [19]. [score:5]
[1 to 20 of 1 sentences]
[+] score: 5
Expression patterns of miR-96, miR-182 and miR-183 in the development inner ear. [score:4]
MicroRNA-183 family members regulate sensorineural fates in the inner ear. [score:1]
[1 to 20 of 2 sentences]
[+] score: 2
Several miRNAs, including the miR-183 family, miR-96, miR-15, miR-99, miR-100, miR-125, and miR-133, all might contribute to hair cell development and maintenance [23– 26]. [score:2]
[1 to 20 of 1 sentences]
[+] score: 2
Results of the analysis are shown in Fig.   2. All miRNAs previously detected in both fluids were found to be consistently present and gga-mir-183 was not detected in any sample. [score:1]
These were gga-mir-control, as an endogenous positive control and for calculating relative expression; gga-mir-183, which was not present in either fluid, as an endogenous negative control; gga-mir-2188, gga-mir-30c-5p, gga-mir-215-5p and gga-mir-92-3p all of which were present in both fluids. [score:1]
[1 to 20 of 2 sentences]
[+] score: 1
Fifteen known microRNA altered by ZnO-NP-5μg/ml and/or ZnSO [4]-10μg/ml are related to evolution including miRNA-7441-5p, miRNA-7455, miRNA-183, miRNA-211, and miRNA-204 and others [38, 55]. [score:1]
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