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10 publications mentioning dre-mir-182

Open access articles that are associated with the species Danio rerio and mention the gene name mir-182. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 185
Other miRNAs from this paper: dre-mir-183, dre-mir-31
This study identifies Junb as a novel lymphangiogenic transcription factor and its newly discovered target miR-182 as a novel lymphangiomiR as being required to attenuate foxo1 expression and to allow the development of the lymphatic vasculature in zebrafish. [score:6]
Ectopic miR-182 restores the PL failure evoked upon junb expression silencingNext, we examined whether the phenotypes caused by junb silencing can be rescued by overexpression of miR-182. [score:5]
Since loss of miR-182 is impairing proper PL and TD formation (Figs. 4 and 6), we hypothesized that overexpression of a potential miR-182 target is causing the observed lymphatic vascular malformations. [score:5]
In line with our previous rescue approach, ectopic expression of the 182-Mimic in junba/junbb-MO1 double morphants completely restored TD formation by 5 dpf in 73% of larvae (Fig. 6a,b), which could be re-capitulated with a second set of junb MOs (Fig. 6c), supporting the concept that miR-182 is a Junb target required for lymphatic vascular morphogenesis in zebra-fish. [score:5]
In tumour cells, β-catenin was previously shown to induce miR-182, which in turn leads to an increased invasion by targeting the matrix metalloproteinase inhibitor RECK 40. [score:5]
Knockdown of either foxo1a or foxo1b in miR-182 morphants resulted in a significant amelioration of PL development from 8% to 32% and 40% embryos, respectively, with completely intact PL strongly indicating that Foxo1 is a physiological downstream target of the Junb/miR-182 axis. [score:5]
Therefore, we focused rather on the identification of downstream target(s), preferably a transcript of venous endothelial origin that should be overexpressed upon silencing of either junb or miR-182 in zebrafish and thereby cause the PL phenotype. [score:5]
Comparative miRNA expression profiling of Junb MEFs revealed that miR-182 expression depends on Junb presence. [score:5]
Currently, we cannot rule out that Junb and its target miR-182 are implicated in LEC specification as junb expression has been observed in the gastrointestinal tract of zebrafish 27 (see also Supplementary Fig. S1). [score:5]
Expression of mature miRNAs was normalized to U6 snRNA and plotted relative to miR-182 expression in Junb -deficient cells. [score:5]
Yet, while miR-31 acts as a strong negative regulator by repressing Prox1 in blood endothelial cells 60, we identified miR-182 as a fine-tuner regulating lymphangiogenesis by attenuating foxo1 expression. [score:5]
Taken together, our data identify Junb as transcription factor regulating lymphangiogenesis in zebrafish and the Junb/miR-182/Foxo1 axis as first example for the negative action of Junb through a miRNA -mediated suppression of a downstream transcription factor. [score:4]
Expression levels were normalized to Hprt and B2m and plotted relative to pri-miR-182 in Junb -knockout cells. [score:4]
Due to the low expression of junba and junbb (see Supplementary Fig. S1) and miR-182 57 (see Supplementary Fig. S5) in the trunk region during development, we were not able to decipher the exact site of miR-182 action. [score:4]
Silencing of either foxo1a or foxo1b did neither influence miR-182 expression, nor ISV and DLAV-formation (Supplementary Fig. 4B) but in agreement with previous findings in Xenopus laevis 35 caused a mild developmental retardation with an initial lack of PL formation at 48 hpf (Fig. 7C, Supplementary Fig. 4). [score:4]
In order to identify JUNB -dependently regulated microRNAs, we subjected wild type (wt) and Junb -deficient (Junb [−/−]) mouse embryonic fibroblasts (MEFs) 22 to a global miRNA expression profiling and identified miR-182. [score:4]
miR-182 expression silencing recapitulates the Junb knockdown PL phenotype. [score:4]
Expression of miR-182 is JUNB -dependently regulated. [score:4]
An in silico search for validated miR-182 targets revealed foxo1 as a putative valuable candidate. [score:3]
Based on published data and our own findings we can tell that junb, miR-182 and foxo1 share common or neighbouring sites of expression, such as eye (foxo1 54; junb 27 and miR-182 36, see also Supplementary Fig. S1 and Fig. S5, respectively), lateral line (junbb 55 and miR-182 36) and gut (junb 27 and foxo1 56) or notochord (miR-182, see Supplementary Fig. S5) versus hypochord (foxo1 56), respectively. [score:3]
Next, we examined whether the phenotypes caused by junb silencing can be rescued by overexpression of miR-182. [score:3]
Strict miR-182–mediated control of foxo1 expression is required for PL formation in zebra-fish. [score:3]
By contrast, only 17% of junba/junbb double morphants and 11% of zebrafish larvae with silenced miR-182 expression developed a continuous TD by 5 dpf, respectively (Fig. 6a,b). [score:3]
Silencing of either junb or miR-182 inhibits thoracic duct formation in zebrafish. [score:3]
In support of the assumption that foxo1 is one important downstream target of Junb and miR-182, we identified significantly increased foxo1 mRNA levels in junb -deficient MEFs (Fig. 7a). [score:3]
Importantly, co-silencing of either foxo1 paralog in miR-182 morphants reduced the penetrance of the PL failure at 72 hpf from formerly 77% to 29% or to 37% when either foxo1a or foxo1b, respectively, was suppressed (Fig. 7c). [score:3]
The penetrance of the PL phenotype provoked upon miR-182 silencing was nearly identical to that of combined junb silencing, providing strong evidence that miR-182 is an important functional Junb target. [score:3]
Ectopic miR-182 restores the PL failure evoked upon junb expression silencing. [score:3]
Supplementary Video 1. Supplementary Video 2. Supplementary Video 3. Supplementary Video 4. Supplementary Video 5. Supplementary Video 6. Supplementary Video 7. Supplementary Video 8. miR-182 is JUNB -dependently expressed. [score:3]
These findings indicate that foxo1 is one major downstream target of miR-182 and that strictly balanced Foxo1 levels are required for proper lymphatic vascular morphogenesis in zebrafish (Fig. 7d). [score:3]
Yet, with regard to increasing observations, that microRNAs can be released from their producer cell, circulate, re-enter another recipient cell and thereby act as mediators of cell-cell communication 58 59, knowing the site of miR-182 expression may be of secondary importance. [score:3]
MiR-182 is abundantly expressed in neurosensory cells in the eye, ear and nose 36 and implicated in retinal development 37 38. [score:3]
Interestingly, the transcription factor Foxo1 was recently validated as a miR-182 target in zebrafish implicated in osteoblast proliferation and differentiation 33. [score:3]
These data indicate that development of the lymphatic vascular system was not delayed but completely aborted upon knockdown of junb or miR-182. [score:3]
MiR-182 expression was validated in three distinct Junb [−/−] and wt MEF clone pairs by a Taqman miRNA assay, proving that miR-182 is consistently lost or strongly reduced upon Junb ablation (Fig. 1a,b). [score:2]
Consequently, miR-182 is required to ensure precise Foxo1 levels that are a prerequisite for proper lymphatic vascular development in zebrafish. [score:2]
Taken together, knockdown of miR-182 yields a similar lymphatic vascular phenotype as the loss of junb in zebrafish with a specific and striking effect on the formation of the PL. [score:2]
Remarkably, silencing of miR-182 mimicked the double knockdown of junb with regard to the PL phenotype in both temporal occurrence and strength of the defects (Fig. 4d,e). [score:2]
Foxo1 knockdown rescues the PL formation failure of miR-182 morphants. [score:2]
Yet so far, miR-182 has neither been associated with Junb or AP-1 nor with a function in vascular development. [score:2]
To address this question, we chose the morpholino -mediated knockdown of either junb or miR-182 in zebrafish embryos. [score:2]
Knockdown of miR-182 mimics the lymphatic vascular phenotype of junb morphants. [score:2]
Silencing of either junb or miR-182 inhibits thoracic duct formation in zebrafishAlthough we analysed PL formation at 72 hpf, a time point at which PL formation should be completed 28, we also investigated the formation of the thoracic duct (TD) at 5 dpf in order to exclude that the PL phenotype is simply caused by a developmental delay. [score:2]
Our functional analyses for Junb and miR-182 in zebrafish revealed a novel essential role for both in lymphatic vascular development. [score:2]
Morpholino -mediated knockdown of miR-182 provoked a failure in the formation of the PL and, subsequently, of the TD. [score:2]
The inability to rescue PL formation completely upon foxo1 co-silencing in miR-182 morphants can be explained by our observations that mani-pulation of either foxo1 paralog in zebrafish already caused a vascular developmental delay. [score:2]
How to cite this article: Kiesow, K. et al. Junb controls lymphatic vascular development in zebrafish via miR-182. [score:2]
The optimal mimic concentration was established and miR-182 overexpression was validated by Taqman miRNA assay (see Supplementary Fig. S3). [score:2]
Marker analyses for muscle pioneers, rostral primary motoneurons and dorsal root ganglia at 30 hpf, hence shortly before PL formation initiates as early as 32 hpf 52 53, did not reveal any major morphological aberrations (see Supplementary Fig. S6) suggesting that the structural scaffold guiding lymphangioblasts per se is still present upon junb or miR-182 knockdown. [score:2]
PL failure frequency of embryos co -injected with the miR-182-5MM-MO and either foxo1a- or foxo1b-MO was 9% and about similar to std-MO injected embryos. [score:1]
Thus, we attempted to rescue the PL failure in miR-182 morphant embryos by co-injection of a submaximal dose of either foxo1a- or foxo1b-MO. [score:1]
MiR-182 plays also a central role in the physiological regulation of IL-2 -driven helper T cell -mediated immune responses 39. [score:1]
For the future, time-lapse studies in a reporter zebrafish line such as Tg(fli1:gal4 [ubc3] ; UAS:Kaede [rk8]) 50 with genetically ablated junb or miR-182 shall be helpful to decipher the involvement of Junb-miR-182 in LEC specification. [score:1]
The impairment of junb or miR-182 morphants in forming the PL may be due to (i) failure in LEC specification, (ii) defective sprouting angiogenesis from the PCV, (iii) impairment in the dorsal extension of the secondary ISV sprouts, or (iv) failure in the turning of the sprouts towards the horizontal myoseptum. [score:1]
These findings indicate that miR-182 acts downstream of Junb and strongly suggest that Junb and miR-182 act in a common signalling pathway crucial for lymphatic vascular morphogenesis in zebrafish. [score:1]
For breast and colorectal cancer entities it has been shown that miR-182 promotes proliferation and invasion 40 41. [score:1]
Equal amounts of control CRISPR gRNA (derived from original pT7-gRNA), 5-mismatch miRNA morpholino (miR-182-5MM-MO) or standard control morpholino (std-MO) were used as negative controls, respectively. [score:1]
Nucleotides of mature miR-182 and substituted nucleotides of miR-182-5MM-MO are marked in bold and red, respectively. [score:1]
n = 82 (12 ng miR-182-MO), n = 248 (12 ng miR-182-MO + 2 ng foxo1a-MO), n = 118 (12 ng miR-182-5MM-MO + 2 ng foxo1a-MO), n = 163 (12 ng miR-182-MO + 2 ng foxo1b-MO), n = 103 (12 ng miR-182-5MM-MO + 2 ng foxo1b-MO). [score:1]
Thus, it will be highly interesting to investigate in future stu-dies whether this Junb/miR-182/Foxo1 regulatory axis is equally important in mammalian development. [score:1]
Recent publications have shown that miR-182 is a member of the miRNA cluster miR-183~96~182 likely co-transcribed as a single precursor 23. [score:1]
In control zebrafish larvae, injected with a std-MO or a miR-182-5MM-MO, the TD was formed in 93% larvae by 5 dpf as a continuous lymphatic vessel (Fig. 6a,b). [score:1]
n = 181 (14 ng std-MO), n = 77 (12 ng miR-182-5MM-MO). [score:1]
As proof of our hypothesis that miR-182 -mediated silencing of foxo1 is required for normal PL formation in zebrafish, we aimed to co-inject foxo1 morpholinos into miR-182 morphants to rescue the phenotype of miR-182 morphants. [score:1]
By contrast, only 46% of miR-182 morphants were able to develop at least a partial PL. [score:1]
Nonetheless, it is possible that signalling events driven by these cell types fail to properly orchestrate the formation of the PL and subsequent TD in junb or miR-182 morphants. [score:1]
Ectopic miR-182 restores PL formation in Junb morphants. [score:1]
At 48 hpf, 88% of embryos exhibited a complete lack of the PL upon injection of miR-182-MO vs. [score:1]
At 72 hpf, ectopic miR-182 administration restored the PL in junba/junbb double morphants such that now 67% (MO1) and 60% (MO2) of embryos displayed an entirely intact PL compared to 11% and 10 % of junba/junbb-MO1 and -MO2 knockdown embryos, respectively (Fig. 5b,c). [score:1]
Failure in TD formation of Junb morphants is restored by ectopic miR-182. [score:1]
For this purpose, we co -injected a double-stranded miR-182 (182-Mimic) or a negative control oligonucleotide (Neg-Mimic) into junba +  junbb double morphants generated by two independent sets of junba- and junbb-specific MOs (MO1 and MO2). [score:1]
Thus, it is feasible that the guidance of the lymphatic sprouts towards the horizontal myoseptum may be hampered upon miR-182 loss. [score:1]
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2
[+] score: 45
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-15a, hsa-mir-17, hsa-mir-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, 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-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376c, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-183, dre-mir-181a-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-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, 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-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-181d, hsa-mir-507, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
Wang et al. (2012) miR-96, miR-182 Chloride intracellular channel 5 (Clic5) Co -expression in mouse auditory HEI-OC1 cells; luciferase assay in A549 cells; down-regulation of target. [score:7]
In the presence of miR-182, the mRNA levels of Tbx1 were restored as compared to infected cells, suggesting target inhibition. [score:4]
Therefore the tightly regulated transcriptional regulation of Tbx1 in the mammalian ear may be influenced in part by miR-182, providing a function in crucial inner ear developmental pathways. [score:4]
Expression patterns of miR-96, miR-182 and miR-183 in the development inner ear. [score:4]
After confirming direct binding between miR-182 and the Tbx1 3′UTR by luciferase assay, degradation of the target on an mRNA level was tested (Wang et al., 2012). [score:3]
To demonstrate that miR-182 is a direct target of Sox2, a luciferase assay was performed both with a luciferase reporter vector with the 3′UTR of Sox2 and a mutated version of the 3′UTR at the seed region of miR-182 (Weston et al., 2011). [score:3]
Clic5, a chloride intracellular channel that is associated with stereocilia in the inner ear, was identified as a target of both miR-96 and miR-182 (Gu et al., 2013). [score:3]
Isolated IHC infected with rA-miR-182 and transfected miR-182 inhibitor were collected and harvested to explore Tbx1 transcription. [score:3]
Moreover, the transcription factor Tbx1 was found to be a target of miR-182. [score:3]
MicroRNA-182 regulates otocyst-derived cell differentiation and targets T-box1 gene. [score:3]
Targeted deletion of miR-182, an abundant retinal microRNA. [score:3]
In a study on cells derived from mouse otocysts, miR-182 promoted differentiation of these cells to a hair cell-like fate (Wang et al., 2012). [score:1]
” For specific miRNAs, the approach taken to examine loss of miR-182 in the retina is a relevant approach (Jin et al., 2009), though not yet exploited in the inner ear. [score:1]
This conserved miRNA triad, composed of miR-183, miR-182, and miR-96, is transcribed in one polycistronic transcript. [score:1]
The mutated 3′UTR could not bind miR-182 and the decrease in luciferase activity that was observed in the wild-type construct was lost. [score:1]
Patel et al. (2013) Early growth response 1 (Egr1) Insulin receptor substrate 1 (Irs1) miR-182 SRY-box containing transcription factor (Sox2) In situ hybridization; luciferase assay in HEK293 cells Weston et al. (2011) miR-182 T-box 1 (Tbx1) Luciferase assay in COS1 cells; overexpression of miR in cultured otic progenitor/stem cells. [score:1]
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3
[+] score: 35
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-15a, hsa-mir-18a, hsa-mir-21, hsa-mir-27a, hsa-mir-96, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30b, mmu-mir-99a, mmu-mir-124-3, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-181a-2, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, 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-15a, mmu-mir-18a, mmu-mir-21a, mmu-mir-27a, mmu-mir-96, mmu-mir-135b, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, hsa-mir-200a, hsa-mir-135b, dre-mir-183, dre-mir-181a-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-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-15a-1, dre-mir-15a-2, dre-mir-18a, dre-mir-21-1, dre-mir-21-2, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30b, 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-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-135c-1, dre-mir-135c-2, dre-mir-200a, dre-mir-200b, dre-let-7j, dre-mir-135b, dre-mir-181a-2, dre-mir-135a, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
In order to address the essential question of the effect of miRNAs throughout development, a study was conducted examining the expression pattern of the mir-183, mir-182 and mir-96 cluster (Sacheli et al, 2009). [score:4]
Over -expression of miR-182 in a miR-96 knockdown embryo demonstrated a partial rescue effect, and the number of hair cells was increased, as compared to the knockdown. [score:4]
These analyses revealed that the conserved cluster of mir-183, mir-182 and mir-96 have a restricted expression to the mouse inner ear, as compared to brain, heart and whole embryo expression. [score:4]
A conserved miRNA cluster, which includes miR-183, miR-182 and miR-96, was shown to be expressed in the zebrafish in the hair cells, otic neurons and other primary sensory cells. [score:3]
Embryos with miR-182 and miR-96 over -expression exhibited body malformations and produced ectopic hair cells. [score:3]
However, the expression of miR-183 and miR-182 continued in the hair cells, but ceased to be present in hair cells from P11-15, and was only found in the spiral limbus and the inner sulcus. [score:3]
provides another example of the involvement of miRNAs in regeneration, as over -expression of miR-182 and miR-96 resulted in production of ectopic hair cells (Li et al, 2010). [score:3]
In situ hybridization revealed the unique expression pattern of mir-182, mir-183 and mir-96 in inner and outer hair cells of the cochlea, hair cells of the vestibular organs and spiral and vestibular ganglia. [score:3]
By P0, miR-183, miR-182 and miR-96 were strongly expressed in hair cells of the cochlea and the vestibular system, and in the spiral ganglia. [score:3]
Since this report, several studies have focused on the mir-96, mir-182 and mir-183 genes as a source for more deafness mutations. [score:2]
In a different mo del system, zebrafish were used to understand the role of the miR-96, miR-182 and miR-183 cluster in inner ear development (Li et al, 2010). [score:2]
miR-183 and miR-182, but not miR-96, were detected in the otic vesicle in the embryonic early inner ear. [score:1]
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4
[+] score: 13
The miR-182 forms a part of miR-183/96/182 cluster, whose expression is considerably enriched in the pineal gland and up-regulated by light [23], [24]. [score:6]
MiR-181a and miR-182 were the highly expressed miRNAs in the brain and pineal gland of zebrafish. [score:3]
It is also reported that over -expression of miR-182 results in production of ectopic hair cells [21]. [score:3]
The maximum read count was observed for miR-181a and miR-182 in the brain and pineal gland, respectively. [score:1]
[1 to 20 of 4 sentences]
5
[+] score: 13
Other miRNAs from this paper: dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-183, dre-mir-181a-1, 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-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-92b, dre-mir-96, dre-mir-100-1, dre-mir-100-2, 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-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-135c-1, dre-mir-135c-2, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-153a, dre-mir-181c, dre-mir-200a, dre-mir-218a-1, dre-mir-218a-2, dre-mir-219-3, dre-mir-375-1, dre-mir-375-2, dre-mir-454a, 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-34b, dre-mir-34c, dre-mir-222b, dre-mir-138-2, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-128-3
miR-182 and miR-96 show almost identical expression patterns to miR-183 (Figure 2f,g; and Table E in7), although expression is not as robust. [score:5]
The expression of these miRNAs in peripheral sensory neural cells overlaps with miR-200a (Additional data file 16), although miR-200a lacks the CNS and cranial ganglia expression sites common to miR-183, miR-182 and miR-96 (Table E in7). [score:5]
Thus, predominant sites of miR-183, miR-182 and miR-96 expression are sensory cells with modified apical structures. [score:3]
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6
[+] score: 9
Other miRNAs from this paper: dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-183, dre-mir-205, dre-mir-214, 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
Therefore, we analyzed embryos injected with morpholinos against miR-182, miR-183, or miR-140 in more detail, because we could easily stain the tissues that express these miRNAs (Figure 4B). [score:3]
Embryos injected with morpholinos against miR-182 or miR-183, which are expressed in the lateral line neuromasts and hair cells of the inner ear, were treated with DASPEI, which stains hair cells. [score:3]
In addition, many miRNAs reside in families of related sequence (e. g., let-7 and miR-182), and these should possibly be targeted simultaneously by different morpholinos to obtain a biological effect. [score:3]
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7
[+] score: 8
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-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, 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
Finally, 8 of 24 miRNA probes, including miR-200a and miR-200b, as well as miR-96, miR-141, miR-182, miR-183, miR-191, and miR-429, revealed robust expression in the MOE and VNO neuroepithelium, with weaker expression in the adjacent respiratory epithelium (Figure 2A, right column, and Table S3). [score:5]
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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8
[+] score: 6
miRNA name Fold△ Molecular Function Biological process dre-mir-30d-5p 2.667 (↑) ND Phosphoinositide metabolic process miR_46 2.352 (↑) ribonucleotide binding, ATP binding ND dre-mir-146a-5p 2.145 (↑) protein tyrosine/serine/threonine phosphatase activity ND dre-mir-182-5p 4.783 (↓) ND glucose metabolic process dre-mir-458-3p 2.601 (↓) ND regulation of developmental process miR_8 7.956 (↓) aminoacyl-tRNA ligase activity tRNA aminoacylation for protein translation dre-mir-133a-2-3p 2.199 (↓) receptor signaling protein activity ND dre-mir-183-5p 3.294 (↓) cytoskeletal protein binding ND ND: Not determined. [score:5]
In total, we found 4 (dre-mir-30d-5p, dre-mir-182-5p, dre-mir-458-3p, and miR_8) and 5 miRNAs (miR_46, dre-mir-133a-2-3p, dre-mir-146a-5p, dre-mir-183-5p, and miR_8) with overrepresented biological process and molecular function GO terms, respectively (Table 3). [score:1]
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9
[+] score: 4
Expression patterns of miR-96, miR-182 and miR-183 in the development inner ear. [score:4]
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10
[+] 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-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, 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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