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24 publications mentioning dme-mir-9c

Open access articles that are associated with the species Drosophila melanogaster and mention the gene name mir-9c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 50
The number of predicted sites under selection does not appear to correlate with the breadth of miRNA expression, as among the miRNAs with the largest number of predicted target sites we find some that are highly tissue specific (miR-9 and miR-124 that are expressed in the nervous system [5], and miR-155 that is specific to lymphoid cells [5]) as well some that have broad expression (e. g. the families of miR-29 [9, 10, 41, 42] and miR-30 [41, 42]). [score:9]
Additionally, let-7 is predicted to target several kinases and phosphatases in this pathway, and, importantly for the postulated involvement of let-7 in malignancy, the Fas ligand, TGF β receptor I, nerve growth factor and fibroblast growth factor 11. miR-9 has been described as a brain-specific miRNA [5], and recent evidence suggests that its expression is highest in fetal brain and oligodendrogliomas [54]. [score:5]
This is because this conservation pattern corresponds better to the inferred selection pattern of miR-544 than the inferred selection pattern of miR-9. One of the issues that has been extensively discussed in the miRNA literature is the question of the typical number of functional targets per miRNA, and the related question of what fraction of seed matches in 3' UTRs corresponds to functional target sites. [score:5]
This suggests that, whereas the target repertoires of miR-9 and miR-124a have been largely conserved since the common ancestor of the mammals, significant changes have occurred in the target repertoires of miR-544 and miR-205 since that time. [score:5]
Additionally, let-7 is predicted to target several kinases and phosphatases in this pathway, and, importantly for the postulated involvement of let-7 in malignancy, the Fas ligand, TGF β receptor I, nerve growth factor and fibroblast growth factor 11. miR-9 has been described as a brain-specific miRNA [5], and recent evidence suggests that its expression is highest in fetal brain and oligodendrogliomas [54]. [score:5]
This is because this conservation pattern corresponds better to the inferred selection pattern of miR-544 than the inferred selection pattern of miR-9. One of the issues that has been extensively discussed in the miRNA literature is the question of the typical number of functional targets per miRNA, and the related question of what fraction of seed matches in 3' UTRs corresponds to functional target sites. [score:5]
In particular, whereas the target sites for the miRNAs on the right (miR-9 and miR-124a) tend to be shared between all mammals, and to some extent with chicken and opossum, the target sites for the miRNAs on the right (miR-544 and miR-205) are shared mostly among primates, but not with other mammals. [score:5]
These targets suggest that miR-9 may be involved in regulating the intercellular communication in the brain and the function of neural circuits. [score:4]
The top pathway associated with this miRNA is that of glutamate metabolism, in which miR-9 appears to target glutamate decarboxylase, glutamate dehydrogenase, glutamase, glutamate-cysteine ligase, glutamic-oxaloacetic transaminase 1, as well as glucosamine-phosphate N-acetyltransferase 1, 4-aminobutyrate aminotransferase, and phosphoribosyl pyrophosphate amidotransferase. [score:3]
The second most significant association for miR-9 is with with the focal adhesion pathway, in which many more genes appear to be targeted, among which collagen V α1, collagen IV α2, integrin 6, tenascin C, talin, trombospondin 2, and vinculin. [score:3]
For example, in the example above a site for miRNA miR-544 that is only conserved in primates would get considerably higher posterior probability than a site for miR-9 with the same conservation pattern. [score:1]
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2
[+] score: 38
These results support the hypothesis that the sNPFR1 and NPY2R mRNAs are legitimate targets of miR-9a/miR-9. To further support our hypothesis that miR-9a inhibits growth and suppresses insulin signalling via its target sNPFR1, we simultaneously overexpressed both miR-9a and sNPFR1 in the Drosophila IPCs. [score:11]
These results support the hypothesis that the sNPFR1 and NPY2R mRNAs are legitimate targets of miR-9a/miR-9. To further support our hypothesis that miR-9a inhibits growth and suppresses insulin signalling via its target sNPFR1, we simultaneously overexpressed both miR-9a and sNPFR1 in the Drosophila IPCs. [score:11]
miR-9 in mammals is expressed in both the brain and the pancreatic beta cells where it has been shown to regulate glucose levels via its targets onecut2 and sirt1 (refs 18, 19). [score:6]
Similar to the known miR-9a/miR-9 targets senseless 13 and Foxg1 (ref. [score:3]
The largest and most significant reductions in wing length are induced by overexpression of miR-9a, miR-9b and miR-79, which are all members of the conserved miR-9 miRNA family (Fig. 1c). [score:3]
Here we show that both fly sNPFR1 and mammalian NPY2R are targets of miR-9a/miR-9 by demonstrating direct binding of miR-9a/miR-9 to the sNPFR1 and NPY2R 3′-UTRs using an in vitro binding assay and a CLIP assay (Fig. 6). [score:2]
It will thus be interesting to see if the relationship we have uncovered between the miR-9, NPY, insulin signalling and body growth extends to in vivo mammalian mo dels despite the differences in anatomical location and embryonic origin of the IPCs. [score:1]
Our results suggest an evolutionarily conserved relationship between the miR-9 family and the sNPF/NPY receptors (Fig. 9). [score:1]
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3
[+] score: 21
mir-995 cdc2c Yes mir-11/998 E2f Yes mir-92a jigr1 Yes mir-999 CASK Yes mir-281-1/281-2 Oda Yes mir-970 Tomosyn Yes mir-2b-2/2a-1/2a-2 spi Yes mir-13b-2 CG7033 Yes mir-9c/306/79/9b grpYes [a] mir-33 HLH106 No expression information mir-1012 Lerp No expression information mir-1010 SKIP No a Detected in the oocyte. [score:5]
Here I show that mir-9c-5p targets more unstable transcript during the MZT than expected by chance (Table 3), which indicates that mir-9c-5p may have a role during maternal transcript clearance during the initial steps of development. [score:4]
Members of the mir-9 family, particularly mir-9c, are particularly abundant in unfertilized eggs but lower expressed in early embryos (Figure 1). [score:3]
Last, the microRNA-9 family also targets unstable maternal transcripts. [score:3]
Another maternal microRNA gene, mir-9c, is necessary to regulate the number of germ cells (Kugler et al. 2013). [score:2]
Indeed, is the maternal loss of mir-9c what produces this phenotype (Kugler et al. 2013). [score:1]
Although the microRNA level varies substantially across biological replicates, the presence of seven of the maternal microRNAs here described is validated (bantam-3p, mir-311-3p, mir-92b-3p, mir-184-3p, mir-14-3p, mir-995-3p, and mir-9c-5p), although the levels of the latter two were relatively low. [score:1]
This indicates that mir-9 may be the first case of a maternal microRNA contributing to the degradation of maternal transcripts during MZT. [score:1]
Additionally, I suggest that mir-9c may be involved in maternal transcript clearance during MZT. [score:1]
[1 to 20 of 9 sentences]
4
[+] score: 21
Other miRNAs from this paper: dme-mir-9a, dme-mir-9b
Taurine -upregulated gene-1 (TUG1) negatively regulates miR-9 in a human cancer cell line (Zhao and Ren 2016). [score:5]
Since miR-9a is capable of regulating TnT levels in Drosophila, it is possible that the human miR-9 may also play a role in regulating TNNT levels. [score:3]
Incidentally, bioinformatic analysis failed to find a miR-9 target site in the mRNA sequence of mouse TNNT. [score:3]
It would be interesting to know if the increase in cardiac TNNT that occurs in response to hypertrophic stimulus is mediated by miR-9. Many mutations of the human cardiac TnT give rise to the hypertrophic condition (Di Pasquale et al. 2012). [score:2]
It would be interesting to determine what represses miR-9 during myofibril assembly. [score:1]
miR-9 is required for maintaining protein stoichiometry and may have implications in the etiology of myopathies. [score:1]
Interestingly, sequence analysis of the human skeletal and cardiac isoforms of TNNT reveals that only the cardiac TNNT possesses the miR-9 binding site (Figure S4C) while the skeletal isoforms lack it. [score:1]
The 3′-UTR of the up gene has the miR-9 binding site sequence (Figure 2D). [score:1]
Drosophila miR-9a is identical to human miR-9 and the human TnT (TNNT) has significant homology to Drosophila TnT (Lagos-Quintana et al. 2001). [score:1]
It is important to note that the initial report of miR-9’s role in muscle hypertrophy were from studies on mice (Wang et al. 2010), so miR-9a could be playing varied roles in different organisms. [score:1]
Generation of UAS-TnT lacking the miR-9 binding site. [score:1]
The present study provides a plausible candidate in the form of miR-9 to explore in the etiology of idiopathic cardiomyopathies. [score:1]
[1 to 20 of 12 sentences]
5
[+] score: 20
Other miRNAs from this paper: dme-mir-7, dme-mir-92a, dme-mir-969
Increased variance also was rescued by restoring maternal expression of the corresponding miRNA in the mutant background (Figure 2, A and B; P < 0.001 for miR-969; P < 0.05 for miR-9c). [score:3]
It is possible miR-969 and miR-9c act through multiple targets on these processes and that, through increased variance, lead to a reduction of PGC production, proliferation, or survival. [score:3]
Maternal expression of a miR-9c transgene restored PGC number to control levels (Figure 1D; P < 0.01). [score:3]
T-9c@Fb is an UAS transgene allowing expression of the miR-9c hairpin (Szuplewski et al. 2012). [score:3]
The miR-9c [KO] mutant allele is a deletion mutation for which the mini-white cassette initially replacing the miRNA was excised by lox-CRE–mediated cis-recombination. [score:2]
We observed that females lacking miR-969 or miR-9c (Figure S1) produced S10 embryos with reduced PGC numbers (henceforth, we refer to embryos by the genotype of their mothers). [score:1]
Quantification of this phenotype showed a clear increase in variance in PGC number (Figure 2, A and B; P < 0.001 for miR-969; P < 0.05 for miR-9c). [score:1]
Genotypes are (d) miR-9c [KO]/ miR-9c [KO];T-9c@Fb/+, (e) miR-9c [KO]/ miR-9c [KO];+/nosGal4, (f) miR-9c [KO]/ miR-9c [KO];T-9c@Fb/nosGal4, (g) miR-9c [KO]/+;T-9c@Fb/+, and (h) +/ miR-9c [KO];+/nosGal4 In addition, we noted that the range of PGC numbers was broader in embryos from the miRNA mutant mothers than from the controls. [score:1]
Figure 2Maternal loss of miR-969 and miR-9c leads to elevated primordial germs cell (PGC) number variance. [score:1]
Figure 1Maternal loss of miR-969 and miR-9c leads to reduced primordial germs cell (PGC) numbers. [score:1]
Similarly, miR-9c embryos had ∼20% fewer PGCs than control embryos (Figure 1D; P < 0.001). [score:1]
[1 to 20 of 11 sentences]
6
[+] score: 20
Expression of miR-9 increases on a timescale equivalent to the down-regulation effects on KCNMA1 mRNA. [score:6]
miR-9 is predicted to target ALCOREX-containing KCNMA1 mRNAs based on the presence of and complementarity with an alternative 3'UTR (called 3'UTR-2.1) that is associated with ALCOREX-containing mRNAs (Pietrzykowski et al., 2008). [score:3]
These data identify miR-9 as a key regulator of BK channel ethanol tolerance although the in vivo consequences of this regulation remains to be tested, particularly in combination with beta subunit effects on sensitivity and tolerance. [score:3]
Very acutely, KCNMA1 expression in rats is decreased by miR-9 in response to ethanol treatment, but induction of KCNMA1 has been observed in mice in separate studies in specific brain regions 4 h after an injection of ethanol. [score:3]
The well-established roles for the microRNA miR-9 and the BK β subunits in altering BK function, and, specifically, in modifying the ethanol responsiveness of BK, make them excellent targets for study. [score:3]
Posttranscriptional regulation of BK channel splice variant stability by miR-9 underlies neuroadaptation to alcohol. [score:2]
[1 to 20 of 6 sentences]
7
[+] score: 11
To verify these results in a more physiological setting we used human neuroblastoma SH-SY5Y cells, since both miR-124 and miR-9 are highly expressed in neural cells [45], [46]. [score:3]
Interestingly, two of the most prominent miRNAs found associated to hStau1 during screening were miR-124 and miR-9, which have been described as highly relevant for neural development [24], [47]– [49]. [score:2]
Furthermore, the association of both miR-124 and miR-9 to hStau1 complexes was verified in non -transfected SH-SY5Y human neuroblastoma cells (Figs. 4, 5). [score:1]
All miRNAs tested were detected in the hStau1-containing F1 pool and, interestingly, miR-124 and miR-9 were preferentially found in this fraction. [score:1]
Particularly interesting were miR-124 and miR-9, that showed the highest hStau1 vs TAP ratio, using as a control miR-147a, that was not present among those detected in the initial screening (Fig. 3C). [score:1]
We show the association of hStau1 with the Ago components of the RISC and identify miR-124 and miR-9 as the miRNAs preferentially associated to hStau1 RNA granules. [score:1]
Here we identify miR-124 and miR-9 as miRNAs specifically associated to hStau1, one of these proteins, and show that hStau1 is important for the proper differentiation of human neuroblastoma to neuron-like cells. [score:1]
These results were verified for miR-124 and miR-9 in three independent filtration experiments and the data are presented in Fig. 4C. [score:1]
[1 to 20 of 8 sentences]
8
[+] score: 10
Other miRNAs from this paper: dme-mir-9a, dme-mir-9b
Together, these results suggest that increased miRNA‐9 levels alter the equilibrium of the miR9/CBX7 regulatory loop resulting in upregulation of p16 [INK4a] and senescence. [score:5]
Expression of miR‐9 repressed the luciferase activity of the reporter suggesting that miR9 did indeed target human CBX7 (Fig.   1B). [score:5]
[1 to 20 of 2 sentences]
9
[+] score: 9
Phylogenetic analysis, target gene prediction and pathway analysis showed that, among the 13 conserved miRNAs (miR-1, miR-100, miR-10a, miR-124, miR-125, miR-184, miR-33, miR-34, miR-7, miR-9, miR-92a, miR-92b and miR-let7), several highly conserved miRNAs (miR-1, miR-7 and miR-34) targeted the same or similar genes leading to the same pathways in shrimp, fruit fly and human (Figure 3b). [score:5]
Six miRNAs (miR-279, miR-33, miR-79, miR-9, miR-S5 and miR-S12) were significantly down-regulated by more than twofold. [score:4]
[1 to 20 of 2 sentences]
10
[+] score: 9
Other miRNAs from this paper: dme-mir-9a, dme-mir-9b
In a GBM mo del, miR-9 -mediated downregulation of PTCH1 resulted in the upregulation of Hh signaling and resistance to the standard-of-care drug, temozolomide that was reversed by treatment with the Smo inhibitor, vismodegib [141]. [score:9]
[1 to 20 of 1 sentences]
11
[+] score: 8
Other miRNAs from this paper: dme-mir-9a, dme-mir-9b, dme-let-7
In support of miR-9a as a negative regulator of adhesion are the findings that it represses two functionally orthologues of N-cad: in Drosophila the cadherin protein Flamingo (Fmi) and in mammals E-cad 22, 23, suggesting that miR-9 plays a broad role in regulating cell–cell adhesion. [score:3]
In contrast, the levels of Epithelial-cadherin (E-cad), an N-cad family member that is not a predicted miR-9 target, were unchanged (Table  1). [score:3]
Ma L miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasisNat. [score:2]
[1 to 20 of 3 sentences]
12
[+] score: 8
In D. melanogaster, maternal mRNA clearing has been associated with the Mir-309 cluster, which includes Mir-9/4/79, Mir-5/6/2944, Mir-3/309 and Mir-279/286, which are mainly expressed between 9 and 12% of embryo development [21]. [score:3]
The first two waves of miRNA expression, represented by CoMod-A1 and CoMod-A2, involve Mir-279, which is associated with multiple biological processes [24], and let-7 and Mir-9, which are related with neural differentiation and function [25– 27]. [score:3]
Finally, Mir-9 and Mir-279, which are associated with maternal mRNA clearance in D. melanogaster [21], belong to CoMod-A2 and show high levels of expression in ED2. [score:2]
[1 to 20 of 3 sentences]
13
[+] score: 7
The bifunctional microRNA miR-9/miR-9* regulates REST and CoREST and is downregulated in Huntington’s disease. [score:7]
[1 to 20 of 1 sentences]
14
[+] score: 7
Other miRNAs from this paper: dme-mir-92a, dme-mir-34, dme-mir-92b, dme-let-7, dme-mir-312
However, by relaxing these constraints to require a maximum free energy of miRNA/target hybridization of -12 kcal/mole at room temperature and a minimum of 6 out of 8 consecutive base pairs in the miRNA 5' end, MovingTargets predicts that mir-9c, mir-92a, mir-92b, and mir-312 (the latter three are closely related miRNAs) target ttk. [score:7]
[1 to 20 of 1 sentences]
15
[+] score: 4
bmo-let-7b, bmo-let-7c, bmo-miR-9, bmo-miR-9*, bmo-miR-100-like, bmo-miR-263a, bmo-miR-31 and bmo-bantam were expressed in larva and pupa, but were not detected in moth; of these miRNAs, bmo-miR-9 and bmo-miR-9* are also complementary miRNAs. [score:3]
miRNAs having the most orthologs are mir-133 and mir-9, which are found in 25 and 23 animal species, including D. melanogaster and C. elegans. [score:1]
[1 to 20 of 2 sentences]
16
[+] score: 3
Other miRNAs from this paper: dme-mir-9a, dme-mir-9b
The shift to the production of ethanol-resistant BK channels has been documented in both the hypothalamo-neurohypophysial and medium spiny neurons of rats and is caused by the activation of a microRNA (mir9) that targets slo transcripts encoding ethanol-sensitive channels [31]. [score:3]
[1 to 20 of 1 sentences]
17
[+] score: 2
The analysis of female mutants also reveals that mir-9c (present in ovaries; figure 2) is somewhat involved in the control of the number of germ cells [51]. [score:1]
Among the old microRNAs, we have the mir-92, mir-184 and mir-9 families, which are conserved even in chordates. [score:1]
[1 to 20 of 2 sentences]
18
[+] score: 2
Interestingly, among miR-9 family members tested (miR-9bSP and miR-9cSP), only miR-9cSP was strongly uncovered by Df (Supplementary Fig. 1a), suggesting some degree of specialization for endogenous miRNA functions within the conserved family. [score:1]
Supporting this argument, several hits in the viability screen belonged to the K-box family (miR-2a, miR-2b and miR-2c, and miR-13a and miR-13b) and the miR-9 family (miR-9b and miR-9c). [score:1]
[1 to 20 of 2 sentences]
19
[+] score: 2
However, the evolution of the mir-9 family is particularly complex and will be better understood as new genome sequences become available. [score:1]
We also observed that mir-9 and mir-279 microRNAs appear clustered in some insects (Apis mellifera and Tribolium castaneum according to miRBase), suggesting that an original cluster may have split in Drosophila. [score:1]
[1 to 20 of 2 sentences]
20
[+] score: 1
miR-9 is the most abundant human brain miRNA (Mattick and Makunin, 2005) and a recurring candidate from several AD profiling studies. [score:1]
[1 to 20 of 1 sentences]
21
[+] score: 1
For example, members of the microRNA family mir-1 are characteristic of muscle cells, while mir-9 sequences are expressed in the nervous system in both protostomes and deuterostomes (Christodoulou et al. 2010). [score:1]
[1 to 20 of 1 sentences]
22
[+] score: 1
For instance, dme-miR-9c-5p makes up of 11.5 and 4.1% of miRNAs in 0–1 h and 7–8 h embryos, respectively. [score:1]
[1 to 20 of 1 sentences]
23
[+] score: 1
For the remaining 44 predicted pre-miRNAs, 3 are mapped to the minus strand of reference pre-miRNAs (mir-5, mir-9c, mir-iab-4), and the other 41 are new pre-miRNA candidates which we named as "dme-pmir-1" to "dme-pmir-41" (Additional file 7). [score:1]
[1 to 20 of 1 sentences]
24
[+] score: 1
Other miRNAs from this paper: dme-mir-14, dme-mir-34, dme-mir-989
Quantification was done relative to miR-9c and normalized to sibling ovaries with no miRNA sponge (error bars represent the S. D. of three biological replicates). [score:1]
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