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12 publications mentioning cel-mir-124

Open access articles that are associated with the species Caenorhabditis elegans and mention the gene name mir-124. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 120
As miR-124 will affect protein expression by destabilizing RNA levels of target genes or by inhibiting translation of target mRNAs, the next step is to perform large scale proteomic analyses to identify proteins in our Mus musculus and C. elegans animal mo dels involved in the insulin signaling pathway, redox balance, energy homeostasis, and healthy aging. [score:11]
We next validated the differential expression of the seven miRNAs listed in Table 1 using the liver tissues of four different Wrn [Dhel/Dhel]mutant and four wild type mice (three months of age) Of the seven miRNAs tested, only miR-375 and miR-124 showed significant differential expressions in Wrn [Dhel/Dhel] mutant compared to wild type animals (Figure 1A and Supplementary Figure S1). [score:4]
These results indicate that miR-124 expression is decreased in both Mus musculus and C. elegans during aging and in animals with a mutation in the WRN helicase ortholog. [score:4]
To our knowledge, this is the first study showing a significant altered expression of miR-124 in the liver of aging mice. [score:3]
These results indicate that the expression of miR-124 correlates inversely with age in the liver of mice (Figure 1B). [score:3]
The impact of the Wrn helicase on miR-124 expression is conserved in C. elegansWe next determine whether the observed alteration of the miRNAs in mice could be a global phenomenon during aging by studying these miRNAs in the nematode C. elegans. [score:3]
miR-124 has a role in premature aging through the loss of a functional WRN ortholog helicase activity, although the mechanism by which the loss of WRN affects miR-124 expression remains somewhat unknown. [score:3]
More precisely, the expression of miR-124 in the mouse brain is associated with the differentiation status of neuronal cells [38]. [score:3]
The impact of the Wrn helicase on miR-124 expression is conserved in C. elegans. [score:3]
Expression of mir-124 in C. elegans. [score:3]
Of relevance to our study, miR-124 is also expressed in the normal human liver [42]. [score:3]
These results indicate that the miR-124 expression signature in the liver of young Wrn [Δ] [hel/] [Δ] [hel] mice corresponds to the miR-124 signature in old wild type animals. [score:3]
Expression of mir-124 in C. elegansThree hundred 7-days old adult worms (post-larval L4 stage) were sorted by size to exclude remaining larvae using a COPAS BIOSORT instrument (Union Biometrica, Inc. [score:3]
Furthermore, the loss of miR-124 expression is associated with the lack of WRN helicase function in both species. [score:3]
However, miR-124 is expressed in cell types other than neurons [40, 41]. [score:3]
Furthermore, we found that mir-124 expression is also reduced in older wild type worms (seven days after L4 stage) compared to young worms (at the L4-larvae developmental stage) (Figure 1D). [score:3]
To determine whether miR-375 and miR-124 were also differentially expressed during aging, quantitative RT-PCR was performed on the liver tissues of four young (three months) and four old (21 months) wild type mice. [score:3]
As miR-124 is a regulator of several proteins involved in insulin exocytosis and intracellular signaling in pancreatic beta cell lines [40, 41], it is possible that miR-124 may alter insulin action in vivo directly impacting on organismal homeostasis and aging. [score:3]
The liver of Wrn [Δ] [hel/] [Δ] [hel] mice show differential expression of miR-375 and miR-124. [score:3]
All these phenotypes could be reversed in mir-124 mutation strains after vitamin C treatment. [score:2]
miR-375 was up regulated more than three-fold and miR-124 was down regulated by ten-fold in the liver of Wrn [Dhel/Dhel] mutant mice compared to the liver of wild type animals (Figure 1A). [score:2]
Among them, one conserved miRNA in animals (miR-124) was down regulated in both the liver of Wrn [Dhel/Dhel] mice and in whole wrn-1 C. elegans mutants. [score:2]
Finally, the progeroid phenotypes associated with either WRN or miR-124 mutations can be reversed by vitamin C treatment. [score:2]
Interestingly, we observed that the expression of the conserved miR-124 is significantly reduced by 20% in the wrn-1(gk99) animals (unpaired Student's t-test: P = 0.048) compared to the wild type strain (Figure 1C). [score:2]
Both wrn-1(gk99) and mir-124(n4255) strains obtained from the C. elegans Genetics Center (University of Minnesota, St Paul, MN) were out-crossed four times with the wild type N2 strain to remove possible unrelated mutations. [score:2]
However, the amount of ATP in vitamin C treated wrn-1;mir-124 double mutant worms was still lower than untreated wild type animals (P = 0.0440). [score:1]
The loss of wrn-1 and mir-124 lead to an increase of the aging marker lipofuscinTo determine whether the reduced life span observed in mir-124(n4255) worms was due to a progeroid phenotype, accumulation of the aging marker lipofuscin was examined. [score:1]
Thus, vitamin C did not normalized the amount of ATP in mir-124(n4255) worms to the wild type levels. [score:1]
To conclude, our data indicate that miR-124 is a conserved miRNA that is involved in the aging phenotype across mouse and worm species. [score:1]
The miR-124 has been shown to be involved in neurogenesis not only in mouse but also in C. elegans [38, 39]. [score:1]
Finally, we determined the life span of double mutant wrn-1;mir-124 worms treated with vitamin C. While vitamin C did extend the lifespan of these double mutant worms from 6.6 days to 8.4 days (Figure 5C, P = 3.1 × 10 [−6]), it was not as a dramatic effect as observed for the single mutant worms. [score:1]
The expression of miR-124 was not only reduced in the livers of young Wrn [Δ] [hel/] [Δ] [hel] mice compared to age-matched wild type mice, but it was also reduced in the livers of old wild type mice compared to young wild type mice. [score:1]
In this study, we show that vitamin C also rescued the shorter life span of both wrn-1(gk99) and the mir-124(n4255) mutant animals. [score:1]
We first determined if the modulation of miR-124 is also conserved in C. elegans animals carrying a loss-of-function deletion of the wrn-1 gene (wrn-1(gk99) allele) that encodes the human WRN helicase ortholog [32]. [score:1]
Similarly, the lipofuscin fluorescence observed in mir-124(n4255) mutant worms was also stronger than in the wild type animals. [score:1]
To determine whether the reduced life span observed in mir-124(n4255) worms was due to a progeroid phenotype, accumulation of the aging marker lipofuscin was examined. [score:1]
Deletion of mir-124 in C. elegans resulted in a decrease in life span, an increase in reactive oxygen species (ROS) production, a decrease in ATP levels, and an increase in the aging marker lipofuscin. [score:1]
wild type; **P = 0.00222 for mir-124(n4255) vs. [score:1]
The median life span of mir-124(n4255) mutant worms was also significantly increased to a level similar to wild type animals upon vitamin C supplementation (Figure 5B; log-rank test: P = 3.0 × 10 [−9]). [score:1]
wild type; and *** P = 0.00078 for wrn-1;mir-124 vs. [score:1]
The loss of mir-124, in return, led to a significant increase in overall ROS levels (16% increase; P = 0.0442). [score:1]
In this study, we identified miR-124 as a conserved miRNA in both mouse and worm animal mo dels. [score:1]
Finally, there was a synergic effect on the accumulation of lipofuscin in the double mutant wrn-1;mir-124 worms (Figure 4). [score:1]
Previous studies have not shown an alteration of miR-124 during normal hepatic aging in mice or rats, or in the long-lived Ames dwarf mice [24, 27, 36]. [score:1]
untreated mir-124(n4255) worms: P = 3.0 × 10 [−9]; vitamin C treated wrn-1(gk99) vs. [score:1]
Nevertheless, we demonstrate that a deletion of the mir-124 gene ortholog in C. elegans results in reduced life span, increased whole body ROS levels, and reduced ATP levels. [score:1]
These results indicate that the animals lacking either wrn-1 or mir-124 exhibit a progeroid phenotype that is exacerbated by the loss of both genes. [score:1]
org) revealed that miR-124 is conserved in the short-lived C. elegans but not the miR-375. [score:1]
The loss of mir-124 causes a reduction of life span in C. elegans. [score:1]
The loss of wrn-1 and mir-124 leads to an increase in reactive oxygen species (ROS) generation and a reduction in ATP levels. [score:1]
untreated wrn-1;mir-124 worms: P = 3.1 × 10 [−6]; vitamin C treated wrn-1;mir-124 vs. [score:1]
Because total inactivation of both wrn-1 and mir-124 genes had a greater negative impact on ROS and ATP levels than inactivating wrn-1 alone, these results suggest that the decrease of the miR-124 miRNA can contribute to several key biological processes affected in Wrn [Dhel/Dhel] mice [15, 16, 34]. [score:1]
The mir-124(n4255) strain contains a 212 bps deletion that spans the entire mir-124 sequence. [score:1]
Vitamin C restores the normal life span of wrn-1(gk99) and mir-124(n4255) mutant strainsPreviously, we reported that vitamin C restored the normal life span of Wrn [Dhel/Dhel] mice [16]. [score:1]
The loss of wrn-1 and mir-124 lead to an increase of the aging marker lipofuscin. [score:1]
In addition, the deletion of mir-124 accelerated the accumulation of the aging marker lipofuscin in C. elegans and thus highlights the importance of this miRNA in the progeroid phenotype. [score:1]
Interestingly, the level of miR-124 has also been reported to be down regulated in skeletal muscle of old mice compared to young mice [25]. [score:1]
These results indicate that vitamin C normalized lipofuscin accumulation in wrn-1(gk99), mir-124(n4255), and wrn-1;mir-124 worms. [score:1]
Representative photographs of wild type (N2), wrn-1(gk99), mir-124(n4255), and wrn-1;mir-124 double mutant worms at three days into adulthood. [score:1]
The mir-124 sequence is localized in an intron of the trpa-1 gene. [score:1]
Vitamin C normalizes the life span of mutant wrn-1 and mir-124 strains We recently found that Vitamin C supplementation rescued the shorter mean life span of Wrn [Dhel/Dhel] mice and reversed several age-related abnormalities in adipose, cardiac, and liver tissues [16]. [score:1]
These results implicate a role for the conserved miR-124 in aging in C. elegans. [score:1]
Our observation of a significant decrease in miR-124 levels in aging C. elegans further supports the role of this conserved miRNA in the molecular signature of aging in different animal species. [score:1]
These results indicate that the loss of both wrn-1 and mir-124 functions significantly affect ATP levels in C. elegans. [score:1]
Vitamin C restores the normal life span of wrn-1(gk99) and mir-124(n4255) mutant strains. [score:1]
These results indicate that vitamin C significantly increased the life span of animals lacking the wrn-1 or mir-124 genes. [score:1]
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[+] score: 26
The down regulation of brain mRNAs by mir-124 in transfected HeLa cells suggests that this miRNA confers tissue specific expression. [score:4]
Mir-1 is known to have high expression levels in mammalian heart and muscle cells while mir-124 contributes to the cells of the nervous system [24]. [score:3]
Mir-124 has also been shown to promote neuronal differentiation by down regulating the general splice regulator PTB1 [25]. [score:2]
This motif was also found to be especially abundant in the upstream sequences of two old and biologically important miRNAs, mir-1 and mir-124, thus suggesting a connection between the number of motif instances in the upstream sequence close to a miRNA start site and a globally conserved function of the miRNA. [score:1]
The abundance and conservation of this motif in the upstream of two old and important miRNAs, mir-1 and mir-124 suggest a connection to miRNAs with global specialized function. [score:1]
Similar results were observed when looking at the occurrences of GANNNNGA in the mir-124 -family, where the putative promoter sequence of mir-124a-1 is the only one that includes a significant number of the motif in both species, 37 and 19, respectively. [score:1]
Figure 4The frequency diagrams of the motif GANNNNGA occurrences in sequences 1000 bp upstream of mir-1 (panel a) and mir-124 (panel b) family members in C. elegans, C. briggsae, human and mouse. [score:1]
The mir-1-1 and mir-124-a1 1000 bp upstream sequences of human and mouse contain similar number of occurrences of the motif GANNNNGA as the corresponding sequences in C. elegans and C. briggsae. [score:1]
In both cases, we chose mir-1-1 as the representative of mir-1 -family and mir-124a-1 for the representative of mir-124 -family for human and mouse. [score:1]
We found these motifs also from the mir-1 and mir-124 1000 bp upstream sequences in C. elegans and C. briggsae, thus strengthening the connection of these miRNAs with a muscle specific function in these two worms. [score:1]
To determine whether the motif GANNNGA is conserved in the upstream sequences of mir-1, mir-124 and mir-228 orthologs in other species, we located all its occurrences from 1000 bp upstream sequences of all miRNAs that, according to miRBase [17], belong to mir-1 or mir-124 family in human and mouse genomes. [score:1]
When comparing these results, we found that the motif GANNNNGA is especially abundant in the 1000 bp upstream sequences of miRNAs mir-1, mir-124 and mir-228 in both worms. [score:1]
The multiple sequence alignment of the mir-124 family upstream sequences of C. elegans, C. briggsae, human and mouse. [score:1]
In addition, this motif was observed to be most abundant in the upstream sequences of two important miRNAs, mir-1 and mir-124. [score:1]
We also found the frequency distribution of the motif in the upstream sequences from human and mouse orthologs of mir-1 and mir-124 to approximately follow its corresponding distributions in the two worms, thus confirming the conserved nature of the motif. [score:1]
Mir-228 is not found from these two genomes, and generally it is included in the mir-124 family [18]. [score:1]
The 1000 bp upstream sequences of human and mouse miRNAs that belong to mir-1 and mir-124 families were downloaded from UCSC Genome Browser [40], and the multiple sequence alignments for the mir-1 and mir-124 families upstream sequences were made with ClustalW [37]. [score:1]
Click here for file The multiple sequence alignment of the mir-124 family upstream sequences of C. elegans, C. briggsae, human and mouse. [score:1]
We draw the frequency diagrams of the motif GANNNNGA in the 1000 bp upstream sequences of mir-1 and mir-124 orthologs in these four species (Figure 4), and made the global alignments of mir-1 and mir-124 upstream sequences (Additional files 1 and 2). [score:1]
Prior to and independent from the current study, there has been keen interest in mir-1 and mir-124, two miRNAs with the most abundant GANNNNGA motifs. [score:1]
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[+] score: 13
Promoter regions of several intronic miRNAs show tissue-specific expression: mir-86 and mir-124 are expressed only in neuronal cells and mir-67 is expressed only in muscle cells (Table 1). [score:7]
For mir-67, mir-82, mir-86, mir-87 and mir-124 the relative small RNA cloning frequencies are low (less than 0.2% of total miRNA reads) but detectable at all developmental stages [41] and corroborate temporal expression patterns observed in our study (Figure 2). [score:4]
Regions selected for testing included five miRNAs that were not previously studied (mir-67, mir-71, mir-86, mir-87 and mir-124) and two miRNAs (mir-58 and mir-82) for which GFP fusions were published [36] (Figure 1 and Additional file 2). [score:1]
mir-124 Nervous system [This study]. [score:1]
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[+] score: 12
We found that deletion mutations in mir-81/82, mir-234, or mir-124 significantly enhanced the Daf-c phenotype of unc-3(lf) mutants (Figure 4B and Figure S1E), suggesting that these miRNAs have a role in dauer formation. [score:2]
The original unc-3(lf) ain-1(lf) strain was used as a control in miR-81/82 and miR-124 experiments. [score:1]
However, the absolute rate of dauer formation of the unc-3(lf) ain-1(lf); mir-234(lf) mutant is no different than the other unc-3(lf) ain-1(lf) clones (i. e. the unc-3(lf) ain-1(lf) control for mir-81/82 or mir-124), which may simply be a result of a varying genetic background introduced specifically in the unc-3(lf) ain-1(lf) control clone for mir-234. [score:1]
We also tested cGMP supplementation on unc-3(lf); mir-81/82(lf), unc-3(lf); mir-124(lf), and unc-3(lf); mir-234(lf) mutants. [score:1]
Alleles used are unc-3(e151 lf), ain-1(ku322 lf), miR-58(n4640 lf), miR-81/82(nDf54 lf), miR-124(n4255 lf), miR-234(n4520 lf), and miR-235(n4504 lf). [score:1]
But, a physiological function of miR-124 is revealed within the unc-3(lf) mutant background. [score:1]
In addition to mir-81, mir-234, mir-235, and mir-240, which were identified in our IPs, we also tested mir-124, which is a highly conserved neuronal miRNA that was not enriched in the IP [30]. [score:1]
Additionally, we found that ablation of mir-81/82, mir-124, or mir-235 in unc-3(lf) ain-1(lf) did not further increase the rate of dauer formation (Figure 4D). [score:1]
Interestingly, we found no robust difference in the rate of dauer formation between the unc-3(lf) mir-81/82(lf) and the unc-3(lf) mir-81/82(lf); mir-124(lf) mutant (Figure S1F). [score:1]
Mutant alleles used were ain-1(ku322)X, ain-1(tm3681)X, unc-3(e151)X, ain-2(tm2432)I, ain-2(tm1863)I, unc-31(e928)IV, daf-5(e1386)II, daf-16(mu86)I, tph-1(mg280)II, lim-4(yz12)X, tax-2(p691)I, unc-119(ed3)III (for single-copy integration), miR-58(n4640)IV, miR-81/82(nDf54)X, miR-124(n4255)IV, miR-234(n4520)II, and miR-235(n4504)I. The transgenic strains used to perform immunoprecipitations were constructed as previously described, with the addition of a 3 kb region upstream of rgef-1 used as a pan-neuronal promoter [4], [10]. [score:1]
For example, a previous study on miR-124 observed no overt phenotypes for the mir-124(lf) mutant [30]. [score:1]
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[+] score: 12
MiR-124 and miR-34a showed similar expression trends in qPCR and deep sequencing data, but we were not able to detect large changes in expression of miR-17 with age using qPCR. [score:5]
While not the predominating miRNA, miR-124 is strongly represented in our set of aging brain-expressed miRNAs. [score:3]
For example, miR-124 was found by Lagos-Quintana and colleagues as dominating the population of brain-expressed miRNAs in young mice [14]. [score:3]
Probes for snRNA U6, miR-124 and miR-155 were used as controls for the qRT-PCR. [score:1]
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[+] score: 9
miR-124 had been found to be involved in regulating macrophages activation and suppressing microglia in CNS (Ponomarev et al., 2011). [score:4]
The miR expression profile showed miR-1, let-7, miR72, miR87 and miR-124 were highly abundant in the muscle larvale, suggesting it’s potential role in growth and metabolism. [score:3]
MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-[alpha]-PU. [score:2]
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[+] score: 6
Indeed, decreased mRNA levels (in human HeLa cells) were observed for dozens of genes upon transfection of two distinct miRNAs, miR-1 and miR-124; it was also shown that the 3′ untranslated regions (UTRs) of these down-regulated mRNAs have significant complementarity to the 5′ extremity of the transfected miRNAs. [score:6]
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[+] score: 4
Other miRNAs from this paper: cel-mir-2, cel-mir-71
miR-2 showed a pattern of neuronal depletion similar to mir-124's pattern, implying that it is also involved in neuronal differentiation; this is consistent with the exclusively neuronal pattern of GFP expressed from the miR-2 promoter [56]. [score:3]
The miR-124 mammalian homolog is known to induce neuronal differentiation [52]. [score:1]
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[+] score: 3
The microarray data from miRNA expression profiling was validated by qRT-PCR for five miRNAs, including miR-55 (GC), miR-56 (SC), miR-73 (SC), miR-84 (SF) and miR-124 (SF) (Table 4). [score:3]
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[+] score: 2
The microinjection of miR-124 was another experiment which further supported the role of RNA -mediated epigenetic inheritance in mice [30]. [score:1]
The miR-124 microinjected mice grew a body size 30–40 percent larger than controls and had a frequent occurrence of twin pregnancies. [score:1]
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[+] score: 1
mir-124 and mir-153 were not identified here as they were originally found from the sequence trace archive [46] with the full precursor sequences not being contained in the reference genome sequence used here. [score:1]
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[+] score: 1
miR-228 belongs to the miR-124 family of microRNAs along with human miR-124a-1, miR-124a-2, miR-124-a-3, m iR-183, and Drosophila miR-268. [score:1]
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