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10 publications mentioning cel-mir-81

Open access articles that are associated with the species Caenorhabditis elegans and mention the gene name mir-81. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 24
On the other hand, miR-81 is much less expressed than miR-58 and -80 (21), and then this may restrict its potential to act as a dauer inhibitor in the company of the other members of the family. [score:5]
Also, in support of the above, we know that miR-81, in contrast to miR-58, -80 and -82, is the only one that is not able to rescue the dauer defective phenotype of mir-58f(-) when expressed by itself (5). [score:3]
However, the two less abundant members of mir-58f, miR-81 and -82 (21), do not significantly change their expression depending on the TGF-β Sma/Mab pathway (Figure 9A). [score:3]
In contrast to the previous three miRNAs, miR-81 has only been weakly detected in head neurons from L1 (22, 23). [score:1]
Wild-type C. elegans N2 strain (Bristol) and the following mutant strains were obtained from Caenorhabditis Genetics Centre (CGC): BW1940 ctIs40 X [ZC421 (dbl-1(+)) + pTG96(sur-5::gfp)], CB1370 daf-2(e1370) III, DR63 daf-4(m63) III, DR609 daf-1(m213) IV, LT186 sma-6(wk7) II, MT13949 mir-80(nDf53) III, MT13954 mir-81&mir-82(nDf54) X, MT15024 mir-58(n4640) IV, MT15563 mir-80(nDf53) III; mir-58(n4640) IV; mir-81&mir-82(nDf54) X, NU3 dbl-1(nk3) V, RB1739 sma-10(ok2224) IV, and RB2589 daf-3(ok3610) X. DR2490 mIs27 [P [daf-8]::daf-8::gfp, rol-6(su1006)], EUB0032 P [mir-58]::gfp and pwIs922 [P [vha-6]::daf-4::gfp] were kindly provided by Drs D. Riddle, M. Isik and R. Padgett, respectively. [score:1]
All these miRNAs belong to the mir-58 family, having small differences among themselves (miR-81 and -82 differ only in one nucleotide, and therefore we only used miR-81). [score:1]
In accordance with this hypothesis, a recent paper by Than et al. suggests that mir-81, in contrast with the rest of its family, is a dauer repressor acting through the cyclic guanosine monophosphate signalling (cGMP) (60). [score:1]
Cells were transfected in triplicate 24/48 h later with Lipofectamine 2000 (Invitrogen), 150 ng of a 3′UTR luciferase vector (see below), and 50 nmol of test miRNA mimic (miR-58, miR-80, miR-81 and miR-1834; miRIDIAN, Dharmacon) or the standard control miRNA mimic miR-67 provided by the manufacturer. [score:1]
The normalization of miRNA real-time PCRs was performed with geNorm (38) and NormFinder (39) algorithms, whereby the two most stable miRNAs across samples were miR-47 and miR-81 for TGF-β Sma/Mab genes, and miR-81 and miR-82 for the TGF-β Dauer pathway. [score:1]
Human HeLa cells were transiently transfected with psiCHECK-2 vector containing either wild-type (white) or mutated (grey) 3′UTRs from TGF-β genes dbl-1, sma-6, daf-4, daf-1 and daf-7, along with miR-58 family mimics of miR-58, miR-80, miR-81 and miR-1834, or the unrelated miR-67 as negative control. [score:1]
This family is made of five members, mir-58 (chromosome IV), mir-80 (III), mir-81 and mir-82 (approximately 4 kb apart from each other in chromosome X), and mir-1834, although this last one has not been fully validated as a functional miRNA (chromosome IV; >3 Mb apart from mir-58) (18). [score:1]
In relation to the overall effect on growth of each miR-58 family member, we have shown that their contribution to body length is highest for miR-58, intermediate for miR-80 and lowest for miR-81 & -82 (Table 1). [score:1]
[b]Referred to the length of mir-58(n4640);mir-80(nDf53);mir-81&mir-82(nDf54) treated with RNAi empty vector. [score:1]
However, mir-58(n4640) showed such a reduction (P < 0.001), which was even more pronounced in the company of mir-80(nDf53) (P < 0.001) but not of mir-81&mir-82(nDf54) (P = 0.2). [score:1]
We conclude that miR-58 is the miRNA that contributes the most on body size, followed by miR-80 and the tandem miR-81/-82 (in that order). [score:1]
We observed that neither mir-80(nDf53), nor mir-81&mir-82(nDf54), or a combination of both, showed any significant reduction in length with respect to N2 (Table 1). [score:1]
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2
[+] score: 22
cel-miR-81 may regulate apoptosis according to the sequence-similar hsa-miR-143, which has been shown to regulate the apoptotic process by affecting MAPK/Extracellular signal-regulated kinase (ERK) signaling transduction and the expression of Bcl-2, pro-caspase-3 and -9 [56, 57]; the target gene drp-1, encoding dynamin-related protein 1 (DRP-1), regulates distinct cell-death execution pathways downstream of ced-3 and independent of ced-9 [74]; another target gene hsp-1 encodes Hsp70A, which is involved in receptor -mediated endocytosis and apoptosis by GO identification. [score:11]
Hence, we speculated that the apoptotic response to space radiation might be attributable to ced-10 -mediated engulfment regulated by miR-797, while miR-81 might be involved in apoptosis by regulating drp-1 and hsp-1. It has been reported that checkpoints and physiological apoptosis in germ cells proceed normally in space-flown C. elegans by evaluating the expression of apoptotic execution and checkpoint genes [31]. [score:3]
In order to refine the functional miRNA–mRNA relationship, we performed integrated analysis of the miRNA and mRNA expression profiles and found two pairs of significantly anti-correlated miRNA and apoptotic genes, including miR-797 and ced-10 in SC conditions and miR-81 and drp-1, hsp-1 in GC conditions (Fig. 4). [score:3]
By integrated analysis of these 17 miRNA and putative target genes, we found that miR-81 and 797 were anti-correlated to apoptotic genes drp-1, hsp-1 and ced-10 (Fig. 4). [score:3]
The results suggest that there may be a feedback loop for the apoptotic process to promote cell survival, supplied by miRNAs and apoptotic genes [39, 40], e. g. miR-81, or by the different stages of apoptosis, e. g. decision, execution and engulfment. [score:1]
Worth noting is that cel-miR-1/256/796, cel-miR-48/84/795 and cel-miR-81/82 have high homology to hsa-miR-1, hsa-let-7 and hsa-miR-143, which have been demonstrated to function in apoptosis in response to IR or microgravity [63– 68]. [score:1]
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3
[+] score: 17
For example, if miR-81 influences cGMP signaling, which indirectly influences IIS and TGF-β signaling, other miRNA influences on these pathways may be limited. [score:2]
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]
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]
The original unc-3(lf) ain-1(lf) strain was used as a control in miR-81/82 and miR-124 experiments. [score:1]
We found that cGMP could partially decrease the rate of dauer formation of unc-3(lf); mir-81/82(lf) mutants but had a variable effect on the other two mutants (Figure 4E). [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]
Moreover, we found mir-58 to be 19-fold depleted from neuronal miRISC (p = 0.00124) while mir-81 was enriched in neuronal miRISC (Figure 4C). [score:1]
These data suggest that different miRNAs modulate different aspects of dauer signaling and that mir-81/82 has a potential role in cGMP signaling. [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]
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]
Interestingly, they found that restoring mir-81 in this familial deletion did not rescue the Daf-d phenotype, which is consistent with our observation of mir-81 repressing dauer formation. [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]
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]
Because of the effect of mir-81/82 in repressing aberrant dauer formation in an unc-3(lf) mutant background, we tested mir-58, a family member of mir-81/82. [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]
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4
[+] score: 15
mir-80 was shown to be expressed in the posterior intestine, head and body wall muscle, uterus, vulva, distal tip cells, excretory cells, dorsal nerve cord, and amphid neurons; mir-81 was shown to be expressed weakly in head neurons; and mir-82 was observed to be expressed in pharyngeal muscle, spermatheca, and a subset of both the ventral nerve cord and the amphid neurons [21]. [score:7]
While the pmk-2 gene is broadly transcribed, its tissue-specific expression is established by the redundant activities of miR-58, miR-80, miR-81, and miR-82, which switch off expression of PMK-2 through destabilization of pmk-2 mRNA in non-neuronal tissues. [score:5]
Whereas deletion of miR-58 does not cause any apparent defects, a strain carrying deletions in the miR-58 family, comprised of miR-58 and the homologous microRNAs miR-80, miR-81, and miR-82, exhibits multiple mutant phenotypes, including defects in size, locomotion, and reproductive egg-laying [6]. [score:1]
In addition, our data corroborate prior phenotypic analysis suggestive of redundancy among members of the miR-58 family [5, 6], demonstrating redundant roles for miR-58, miR-80, miR-81, and miR-82 in the destabilization of pmk-2 mRNA and corresponding repression of activated PMK-2 protein levels. [score:1]
The miR-58/80-82 family consists of miR-58, miR-80, miR-81, miR-82, and miR-1834. [score:1]
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5
[+] score: 9
Recently, it was shown that DAF-12 activation in response to germline ablation induces expression of mir-81 and mir-241, which activate DAF-16 by inhibiting the expression of AKT-1 (22). [score:7]
For example, daf-12 -dependent production of the microRNAs mir-81 and mir-241 is required for both the heterochronic pathway during development and lifespan extension in response to germline ablation (8, 22). [score:2]
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6
[+] score: 5
In C. elegans, miR-58-3p is a member of a highly expressed family that also includes miR-80, miR-81, miR-82 and miR-1834 [60]. [score:3]
Comparing the abundances of miR-58-3p to that of miR-81-3p and miR-80-3p, it is clear that the first dominates, contributing more than 90% of the reads assigned to the whole family, as reported by Kato et al. [57]. [score:1]
It is interesting to note that other members of the mir-58 family are also amongst the top 10 most abundant in our analysis, with miR-80-3p and miR-81-3p each contributing about 1% of the miRNA-mapping reads. [score:1]
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7
[+] score: 4
Other miRNAs from this paper: cel-let-7, cel-mir-58a, cel-mir-80, cel-mir-82, cel-mir-58b, cel-mir-58c
The most conserved mir-80 family members encoded in the C. elegans genome are mir-80, mir-58, mir-81 and mir-82 [12], [18]. [score:1]
C. elegans miR-80 familyThe most conserved mir-80 family members encoded in the C. elegans genome are mir-80, mir-58, mir-81 and mir-82 [12], [18]. [score:1]
We did not find an Ex [max] shift in mir-58(Δ) or in the double mir-81(Δ) mir-82(Δ) mutant (data not shown) and thus mir-80 is the sole family member that can be deleted to induce the DR Ex [max] shift. [score:1]
Note that there are 4 close members of the miR-80 family encoded in the C. elegans genome (mir-58, mir-81, mir-82; see [12], 2008, for alignments and discussion). [score:1]
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8
[+] score: 3
In another case, also in worms, the target sites for two coconserved and distinct miRNAs (or miRNA sets) miR-2/miR-43 (CUGUGAU) and miR-80/miR-81/miR-82 (UGAUCUC), were found to overlap more often than expected by chance (p < 10 [−5]) (note that we limited the extent of the overlap to 4 nt in our coconservation analysis). [score:3]
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9
[+] score: 2
Interestingly, in the mir-80 family of miRNAs there is one intergenic (mir-80), one antisense intronic (mir-81) and one sense intronic (mir-82) miRNA; the sense and antisense intronic miRNAs reside in the same host gene but in the different introns. [score:1]
Since intergenic mir-80 and intronic antisense mir-81 should have their own promoters, and we and Martinez et al. [36] show that intronic sense-oriented mir-82 also has an intronic promoter, the most parsimonious explanation of the evolution of the mir-80 family is by the duplication of the locus, which included the promoter region of the ancestral miRNA. [score:1]
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10
[+] score: 1
The homologous C. elegans gene, T07D1.2, contains mir-81 (intron 5, antisense) and mir-82 (intron 1, sense), and the mature sequences for both show only two mismatches to bpa-bantam. [score:1]
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