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24 publications mentioning cel-mir-48

Open access articles that are associated with the species Caenorhabditis elegans and mention the gene name mir-48. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 91
Indeed, loss of mir-52 partially suppressed the hbl-1 misexpression phenotype of mir-48/84/241 mutant worms: in 91% of mir-48/84/241 worms hbl-1::gfp::hbl-1 transgene expression remained high in L3, whereas only 62% of mir-52; mir-48/84/241 displayed high hbl-1::gfp::hbl-1 expression (Figure 1). [score:9]
We therefore determined whether the observed suppression of developmental timing defects in mir-52; mir-48/84/241 reflects a suppression of hbl-1 misregulation. [score:7]
This likely reflects a partial suppression of mir-48/84/241 phenotypes, rather than an inability to suppress molting since loss of mir-52 strongly suppresses the ectopic molting phenotype of alg-1 worms [17] as well as mir-48/84 double mutant worms (Table 1). [score:7]
The let-7 family members, mir-48, mir-84, and mir-241, function together to control the timing of the L3 stage program through down-regulation of their target, hbl-1 [12]. [score:6]
Thus, misregulation of lin-28 does not account for the observed suppression of developmental timing defects in mir-52; mir-48/84/241 worms. [score:5]
0037185.g001 Figure 1Loss of mir-52 suppresses hbl-1 misregulation in mir-48/84/241 mutants. [score:4]
To determine if puf-9 is necessary for mir-52 -mediated suppression of the let-7 family developmental timing defects, we examined worms multiply mutant for mir-52, puf-9, and let-7 family miRNAs, mir-48 and mir-241 (mir-48/241). [score:4]
Next, we examined the effect of elevated expression of mir-51 family members on the retarded development of mir-48 mir-241 (mir-48/241) mutant worms. [score:4]
suppresses hbl-1 misregulation in mir-48/84/241 mutants. [score:4]
The down-regulation of hbl-1 in the hypodermis requires the let-7 family members, mir-48, mir-84, and mir-241 [12]. [score:4]
However, no suppression of alae formation defects was observed in mir-52; mir-48/241; puf-9 worms relative to mir-52; mir-48/241 (Table 1). [score:3]
Loss of mir-52 suppressed the seam cell and alae formation defects in mir-48/241 mutants (Table 1). [score:3]
mir-52; mir-48/84/241 had fewer seam cells than mir-48/84/241 worms, indicating a suppression of the L2 reiteration phenotype (Table 1). [score:3]
Representative fluorescent micrographs of hbl-1::gfp::hbl-1 transgene expression in (A) mir-48/84/241 and (B) mir-52; mir-48/84/241 mutant worms in the L3 stage with corresponding DIC images (C and D, respectively). [score:3]
Loss of puf-9 did not affect the mir-52 mediated suppression of the extra seam cell phenotype of mir-48/241 mutant worms (Table 1). [score:3]
We observed that loss of the mir-51 family member, mir-52, strongly suppressed the L2 stage reiteration phenotype of mir-48/84/241 mutants and lin-46 mutants. [score:3]
However, no difference was observed in lin-28::gfp::lin-28 expression between mir-48/84/241 and mir-52; mir-48/84/241 in L2 molt stage worms (Figure 2). [score:3]
The enhancement of the precocious developmental timing defects observed in mir-48(ve33), hbl-1(ve18), and lin-14(n179ts) mutant worms is consistent with a role for the mir-51 family in the regulation of L2 versus L3 cell fate decisions. [score:3]
Additionally, loss of mir-52 suppressed the alae formation defects and bursting phenotypes of mir-48/84/241: 100% of mir-48/84/241 displayed incomplete alae formation and 56% of mir-48/84/241 worms burst at the L4 to adult transition compared to 51% and 3% of mir-52;mir-48/84/241 mutants, respectively (Table 1). [score:2]
mjEx160 enhanced developmental timing defects of mir-48/241 mutant worms (Table 1). [score:2]
Loss of mir-52 enhanced the developmental timing defects observed in three precocious mutants: mir-48(ve33), hbl-1(ve18), and lin-14(n179). [score:2]
Loss of mir-52 significantly enhanced this precocious alae formation in the mir-48(ve33) background (Table 2). [score:1]
mir-48/241 worms have 19.1 seam cells on average. [score:1]
First, mir-48(ve33) worms display early accumulation of miR-48 and precocious formation of adult-specific alae one stage early at the L3 to L4 transition [32]. [score:1]
mir-48/84/241 mutant worms often display defects in alae formation at the L4 to adult transition. [score:1]
This is increased to 22.1 in mir-48/241; mjEx160 worms (Table 1). [score:1]
However, 77% of mir-52; mir-48/84/241 worms showed the bag of worms phenotype, indicating an extra adult-stage molt. [score:1]
In mutants lacking mir-48, mir-84 and mir-241 (hereafter referred to as mir-48/84/241), the L3 stage program is not executed properly and the L2 stage program is reiterated. [score:1]
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2
[+] score: 68
Other miRNAs from this paper: cel-let-7, cel-lin-4, cel-mir-84, cel-mir-241
These results suggest that elt-1 normally contributes to developmental timing, at least in part, by promoting the down-regulation of lin-41 expression during L4, and that it may do so by promoting the expression of LET -7. elt-1/GATA normally promotes the expression of the developmental timing miRNAs LET-7, miR-48, miR-84, and miR-241The LET-7 family of miRNAs (miR-48, miR-84, and miR-241) have previously been shown to be expressed during or near the L2 molt to promote developmental progression [27, 28], while LET-7 is expressed primarily during L4 and required for the L4-to-Adult transition, largely by down -regulating lin-41 mRNA [3, 13]. [score:18]
This suggests that both daf-12 and elt-1 promote the expression of miR-48, miR-84, and miR-241, but that this regulation is highly redundant, so that either transcription factor alone is sufficient to promote sufficient expression of the miRs to prevent a gross phenotype in the single-mutant strains, despite defective expression of LET-7 in those single-mutant animals. [score:8]
The LET-7 family of miRNAs (miR-48, miR-84, and miR-241) have previously been shown to be expressed during or near the L2 molt to promote developmental progression [27, 28], while LET-7 is expressed primarily during L4 and required for the L4-to-Adult transition, largely by down -regulating lin-41 mRNA [3, 13]. [score:7]
In this study, we used a genetic enhancer screen to identify the GATA transcription factor ELT-1 as a new heterochronic gene and have shown that it contributes to developmental timing by providing positive regulation of the expression of the developmental timing miRNAs LET-7, miR-48, miR-84, and miR-241. [score:6]
These data are also consistent with previous studies showing that daf-12 regulates developmental progression [25, 26] and the expression of miR-48, miR-84, miR-241 and LET-7 at the L2 molt [28] and L3 stages [27]. [score:5]
A recent study of transcription factor binding sites in C. elegans included ELT-1 [45], and analysis of their data (Table 3) shows that the ELT-1 protein binds the likely promoter region of the DNA sequences encoding all members of the LET-7 miRNA family (mir-48, mir-84, mir-241, let-7), supporting the idea that ELT-1 directly regulates the transcription of the let-7 family miRNAs during late larval development. [score:4]
elt-1/GATA normally promotes the expression of the developmental timing miRNAs LET-7, miR-48, miR-84, and miR-241. [score:4]
However, the three LET-7 family miRNAs (miR-48, miR-84, and miR-241) all have a statistically-significant decrease in their expression during the L4 stage in the elt-1(ku491); daf-12(rh61rh411) double-mutant animals but not in either single-mutant, which likely accounts for the differences in the phenotypes and data. [score:3]
The expression of the LET-7, miR-48, miR-84, and miR-241 miRNAs was therefore examined during the L4 stage in elt-1(ku491); daf-12(rh61rh411) double-mutant animals using RT-qPCR. [score:3]
They stimulate the nuclear hormone receptor (NHR) DAF-12, the vitamin D NHR ortholog, to promote progression from the 2 [nd] larval stage (L2) to the 3 [rd] larval stage (L3) [24– 26] by, in part, initiating expression of the LET -7 family of miRNAs, miR-48, miR-84, and miR-241, during or near the L2-to-L3 molt [27, 28]. [score:3]
As shown in Fig. 4A, elt-1(ku491); daf-12(rh61rh411) double-mutant animals have deficient expression of LET-7 and each of the LET-7 family of miRNAs (miR-48, miR-84, and Mir-241). [score:3]
In addition, the double-mutants have an L4-stage bursting vulva phenotype (Table 1), similar to that caused by mutation of delayed heterochronic genes, including let-7 and the three other let-7 family miR genes (mir-48, mir-84, and mir-241) [3, 30]. [score:2]
A. ELT-1 and DAF-12 redundantly regulate LET-7, miR-48, miR-84, and miR-241. [score:2]
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3
[+] score: 44
LIN-14, LIN-28, HBL-1 and LIN-41 are expressed at the start of larval development and are eventually repressed by the microRNAs lin-4, let-7 and the three let-7 family members miR-48, miR-84, and miR-241 (3 let-7s). [score:4]
Given the redundancy of the three let-7 paralogs mir-48, mir-84, and mir-241 in regulating L2 fates, two alternatives seem likely: either lin-28 inhibits the accumulation of multiple let-7 family members, including these three let-7s known to control the L2-to-L3 transition, or let-7 is at least partially redundant with its relatives in controlling this early fate transition. [score:4]
Animals lacking mir-48, mir-84, and mir-241 (3 let-7s), or animals carrying a transgene constitutively expressing lin-28 (lin-28(gf)) [62]. [score:3]
1002588.g001 Figure 1Histograms depicting the temporal expression profiles of (A) let-7, (B) miR-84, (C) miR-48 and (D) miR-241 levels in wild type (grey bars) and lin-28(n719) (blue bars). [score:3]
Histograms depicting the temporal expression profiles of (A) let-7, (B) miR-84, (C) miR-48 and (D) miR-241 levels in wild type (grey bars) and lin-28(n719) (blue bars). [score:3]
hbl-1 has been shown to be the primary target of let-7's relatives mir-48, mir-84; and mir-241 [6]. [score:3]
Also as seen previously [6], in a strain lacking mir-48, mir-84, and mir-241, the reporter was constitutively expressed from L1 to L4 (Figure 2B, Table S4). [score:3]
Curr Opin Genet Dev 6 Abbott AL Alvarez-Saavedra E Miska EA Lau NC Bartel DP 2005 The let-7 MicroRNA family members mir-48, mir-84, and mir-241 function together to regulate developmental timing in Caenorhabditis elegans. [score:3]
To construct mir-48 mir241; mir-84 let-7 quadruple mutants, animals of the genotype mir-48 mir-241; mir-84 unc-3 let-7/+ were cultured on hbl-1(low RNAi) (see below) to suppress the lethality characteristic of these mutations. [score:2]
Seven C. elegans microRNAs—let-7, miR-48, miR-84, miR-241, miR-793, miR-794, and miR-795—belong to the let-7 family based on 5′-end sequence identity of the mature microRNAs [41]– [43]. [score:1]
Significantly, Abbott and colleagues discovered that three let-7 relatives—miR-48, miR-84 and miR-241—function redundantly to repress the transcription factor gene hbl-1 and cause the succession of L2 to L3 cell fates [6]. [score:1]
D, lin-28; mir-48 mir-241; let-7 mir-84 (lin-28; 4 let-7s). [score:1]
Comparable to lin-28 null mutants alone, 21% of the seam cells in animals that also lack mir-48, mir-84, and mir-241 displayed adult alae at the L2 molt (Table 3). [score:1]
C. elegans LIN-28 protein interacted with pre-let-7, pre-miR-48, pre-miR-84 and pre-miR-241, but not with the other let-7 family pre-microRNA sequences (Table 1; Figure S1). [score:1]
The removal of lin-28 caused no change in the levels of mature miR-48 and -241 in the early stages (Figure 1C and 1D, blue bars). [score:1]
In contrast to removing let-7, which had no effect, removing ain-1 from a strain lacking mir-48, mir-84, and mir-241 nearly doubled its seam cell nuclei number (Table 2, line 10). [score:1]
We demonstrate by using null alleles that lin-28 does not require let-7, mir-48, mir-84, and mir-241 for its control of L2 cell fates (Table 2). [score:1]
Control experiments using the mir-48 mir-241; mir-241 mutant strain showed that this procedure caused no attenuation of the progeny's retarded phenotype. [score:1]
Given that mir-48, mir-84, and mir-241 act redundantly and are related in sequence to let-7, we first wished to test whether let-7 might also be redundant with them in controlling L2 seam cell behavior. [score:1]
B, mir-48 mir-241; mir-84 (3 let-7s). [score:1]
C, lin-28; mir-48 mir-241; mir-84 (lin-28; 3 let-7s). [score:1]
The miR-48, -84, and -241 levels were all relatively low but detectable at the L1 molt and peaked by the L2 molt (Figure 1B–1D, grey bars). [score:1]
The three let-7 family members mir-48, mir-84, and mir-241 act redundantly to control seam cell fates: when they are deleted together, the L2-specific symmetric cell division is reiterated, resulting in supernumerary seam cells [6]. [score:1]
E, a hbl-1::GFP::unc-54 3′UTR reporter in lin-28; mir-48 mir-241; let-7 mir-84 (lin-28; 4 let-7s). [score:1]
D, a hbl-1::GFP::unc-54 3′UTR reporter in lin-28; mir-48 mir-241; mir-84 (lin-28; 3 let-7s). [score:1]
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4
[+] score: 39
Other miRNAs from this paper: cel-let-7, cel-lin-4, cel-mir-84, cel-mir-237, cel-mir-241, cel-lsy-6
Three of the let-7 family miRNAs (mir-48, mir-84, and mir-241) are expressed starting at the L2 stage and function to regulate the L2 stage proliferative seam cell division, while the let-7 miRNA is strongly upregulated from the L3 stage to control the larval-to-adult transition of seam cells (Reinhart et al. 2000; Abbott et al. 2005). [score:7]
Besides suppressing the heterochronic phenotypes of mir-48 mir-241(nDf51) animals, stau-1(tm2266) also exerts significant suppression of the heterochronic adult alae phenotype of let-7(n2853) animals (Figure 1B). [score:5]
Interestingly, loss of function of eri-1 enhanced the adult alae and seam cell defects of mir-48 mir-241(nDf51) animals (Figure 5), which is opposite to the suppression caused by stau-1 mutation. [score:4]
Although the stau-1 loss-of-function mutant does not exhibit any developmental timing defects in an otherwise wild-type genetic background, we observed that both stau-1(tm2266) and stau-1(q798) significantly suppresses the heterochronic phenotypes of the mir-48 mir-241(nDf51) mutant (Figure 1, B and C). [score:4]
Surprisingly, the eri-1(mg366); mir-48 mir-241(nDf51) mutant exhibited enhanced heterochronic phenotypes, which is the opposite from the effect of stau-1. First of all, this finding indicates that the modulation of miRNA activity by STAU-1 is unlikely to stem simply from an enhanced exogenous RNAi pathway; otherwise, we would have expected that eri-1(mg366), like stau-1(loss-of-function), should suppress mir-48 mir-241(nDf51) mutant phenotypes. [score:3]
As expected, both of these null alleles significantly suppressed the adult alae and seam cell phenotypes of mir-48 mir-241(nDf51) animals (Figure 2, D and E). [score:3]
Furthermore, to test if the stau-1 null mutants also suppress phenotypes of miRNA mutants, we crossed the null alleles into the let-7 family mutant mir-48 mir-241(nDf51). [score:3]
This work was funded by a NIH grant (R01 GM34028) to V. A. and a Leukemia and Lymphoma society postdoctoral fellowship to I. V-L. Abbott A. L. Alvarez-Saavedra E. Miska E. A. Lau N. C. Bartel D. P., 2005 The let-7 microRNA family members mir-48, mir-84, and mir-241 function together to regulate developmental timing in Caenorhabditis elegans. [score:3]
C. elegans let-7 family miRNAs (including let-7, mir-48, mir-84, and mir-241) function semiredundantly in controlling the developmental timing of certain stage-specific hypodermal seam cell fates. [score:2]
mir-48 mir-241(nDf51) mutant has two let-7 family miRNAs removed while let-7(n2853) is a strong loss-of-function mutation at the seed region of let-7 mature miRNA (Reinhart et al. 2000). [score:2]
Since stau-1(tm2266) and stau-1(q798) have similar effects on the phenotypes of mir-48 mir-241(nDf51) animals, we focused only on stau-1(tm2266) for further analysis. [score:1]
Because stau-1 mutants had been shown to interact genetically with eri-1 (LeGendre et al. 2013), we tested whether eri-1 loss-of-function could affect the heterochronic phenotypes of mir-48 mir-241(nDf51) animals. [score:1]
To test if STAU-1 modulates let-7 family miRNA activity, we used two mutant strains [mir-48 mir-241(nDf51) and let-7(n2853)], which both have partially penetrant heterochronic phenotypes with gaps in adult alae and increased number of seam cells at the young adult stage. [score:1]
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5
[+] score: 35
We also see that miR-48, a miRNA we identified to be suppressed by HSF-1 upon HS, may result in upregulation of aip-1, a known SKN-1 and HSF-1 target gene [8, 40]. [score:8]
We next determined the top biological processes upregulated in response to suppression of miR-48 and miR-228 by HSF-1 during HS (S7B Fig). [score:6]
Thus, HSF-1 may normally suppress miR-228 and miR-48 expression during HS to promote longevity and stress resistance, and to control developmental timing events during stress conditions. [score:6]
Through this method of data analysis, we found that miR-48 and miR-228 are normally downregulated by HSF-1 upon HS. [score:4]
miR-48 belongs to the let-7 miRNA family that is well-known to control developmental timing events at the larval-to-adult transition, and mutations in miR-48 can result in developmental timing defects [32, 33]. [score:4]
Regulatory mutations of mir-48, a C. elegans let-7 family MicroRNA, cause developmental timing defects. [score:4]
miR-48 can act with other let-7 family members to control developmental timing events. [score:2]
miR-48 -0.13 miR-48 belongs to the let-7 family of microRNAs. [score:1]
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6
[+] score: 28
In wild type animals, hbl-1 is down-regulated by let-7-sisters (mir-48, mir-84, and mir-241) between the L2 and L3 stages of larval development [2]. [score:5]
However, previous findings showed that the precocious L3 fate phenotype of lin-28(lf) larvae cannot be entirely attributed to let-7-Family hyperactivity: mutations that simultaneously remove three (mir-48, mir-84, mir-241), or even all four (mir-48, mir-84, mir-241, let-7) of the major let-7-Family microRNAs did not suppress the precocious L3 fates of lin-28(lf) [2], [20]. [score:4]
This is noteworthy in light of previous work showing that simultaneous loss of four of seven let-7-Family genes (mir-84, mir-48, mir-241, and let-7) was not sufficient to suppress the reduced seam cell number of lin-28(lf) [20]. [score:3]
These data, in combination with our observation that lin-28(lf) seam cell lineage defects are suppressed by alg-1(anti) are consistent with the idea that other microRNAs in addition to mir-48, mir-84, mir-241, and let-7 may be hyperactive in lin-28(lf) and may contribute to controlling the L2-L3 transition. [score:3]
These data might suggest that LIN-28 may function to inhibit processing of not only let-7 (as previously shown [22]), but also miR-48. [score:3]
In particular, the let-7-Family microRNAs, let-7, mir-241, mir-48, and mir-84, are key players in the heterochronic genetic network that controls progression through the C. elegans larval development [1]– [3]. [score:2]
Therefore the potent suppression that we observe in lin-28(lf) carrying alg-1 mutations suggests that the lin-28(lf) phenotype results from hyperactivity of microRNAs in addition to mir-84, mir-48, mir-241, and let-7. Although the newly isolated missense alleles of alg-1 do not all appear to affect the same domain of ALG-1 (Figure 2A), all four mutants displayed similar phenotypic and genetic characteristics (Table 1, Table 2). [score:2]
The absence of lin-28 dampens the effects of alg-1 mutations on the levels of let-7 and miR-48 microRNAs. [score:2]
This would indicate that in the presence of lin-28 these microRNAs are more vulnerable to the absence of functional ALG-1, suggesting that alg-1 opposes the destabilizing activity of lin-28 upon let-7 and mir-48. [score:1]
Both let-7 and miR-48 levels are reduced at best two-fold in the absence of lin-28 (Figure 7A), but 5–10 fold when lin-28 is intact (Figure 7B). [score:1]
By contrast, loss of let-7-sisters (mir-241, mir-48, and mir-84) results in the reiteration of L2 fates [1], [2], and loss of let-7 causes the reiteration of L3 fates [1]– [3], [20]. [score:1]
Deletion of the let-7 microRNA or its sisters miR-48, miR-241 and miR-84 results in reiteration of larval stage-specific cell fates, delaying the adoption of adult cell fates [1]– [3]. [score:1]
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7
[+] score: 26
The six target miRNAs included three miRNAs (lin-4, mir-48, and mir-84) whose expression levels are known to vary depending on the developmental timing and three constantly expressed tissue-specific miRNAs in C. elegans. [score:8]
lsy-6, mir-55, and mir-56 showed no significant changes in their expression levels, whereas lin-4, mir-48, and mir-84 were upregulated. [score:6]
Similar expression levels for lsy-6, mir-55, and mir-56 were observed between the two stages; on the other hand, lin-4, mir-48, and mir-84 were upregulated in the L4 stage. [score:6]
Abbott AL The let-7 MicroRNA family members mir-48, mir-84, and mir-241 function together to regulate developmental timing in Caenorhabditis elegansDev. [score:3]
Development -associated miRNAs in C. elegans (lin-4, mir-48, mir-84, lsy-6, mir-55, and mir-56) and two controls (snoRNA U18 and mir-159a) were detected via CE-SSCP analysis after the dye-labeling reaction. [score:2]
Product sizes of extended and singly nicked products for mir-48 in each cycle were analyzed via denaturing CE, in which FAM-dCTP was added to label the reaction products in the test reactions. [score:1]
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8
[+] score: 21
Other miRNAs from this paper: cel-let-7, cel-lin-4, cel-mir-1, cel-mir-84, cel-mir-241, cel-lsy-6
The let-7 family members miR-48, miR-84 and miR-241 redundantly regulate the expression of their target gene hbl-1 during the L2-to-L3 larval stage transition [26], [28]. [score:6]
The seam cell developmental program is controlled at different larval stages by the miRNA lin-4 [25] and those of the let-7 family (miR-48, miR-84, miR-241 and let-7) [26], [27] and their targets lin-14, lin-28, hbl-1, daf-12 and lin-41 [26]– [33]. [score:4]
Moreover, this reduced miR-48 and miR-241 abundance was rescued to the levels found in the single alg-1(0) mutant upon expression of a vps-52 rescue transgene (Figure 5). [score:3]
This effect likely underpins the enhanced defects in the developmental program of the seam cells observed with the alg-1(0) and mir-48(0) mutants. [score:2]
It was therefore possible that the altered seam cell development observed in alg-1 mutant and enhanced by loss of vps-52 resulted from impaired miR-48, miR-84 and miR-241 miRNAs function. [score:2]
B) Abundance of miR-48 and miR-241 miRNAs in ain-1 mutant animals. [score:1]
In vps-52 mutant, the abundance of three other miRNAs tested was also significantly reduced as observed for miR-48 and miR-241 (Figure S5C). [score:1]
Alae defects for the vps-52, hbl-1 and mir-48 mutant animals. [score:1]
While in the single vps-52 mutant, we observed a significant decrease of the let-7 family miRNA members miR-48 and miR-241, their levels were further reduced in vps-52 alg-1(0) double mutant (Figure 5). [score:1]
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9
[+] score: 10
Animals harboring the alg-1(ma192) mutation inappropriately express hbl-1 (the major miRNA target of miR-48, miR-241, and miR-84) in the L3 stage and reiterate L2-specific seam cell division patterns [49]. [score:6]
Consistent with the observation that alg-1(ma192) mutations broadly affect miRNA expression, the abundance of all miRNAs tested (lin-4, miR-48, miR-241, miR-84, let-7, miR-1, miR-46, miR-58 and miR-79) was decreased in alg-1(ma192) mutants (Figure 2B). [score:4]
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10
[+] score: 9
Other miRNAs from this paper: cel-let-7, cel-mir-84, cel-mir-241
Notably, lin-42 negatively regulates expression of mir-48 (McCulloch and Rougvie 2014; Perales et al. 2014; Van Wynsberghe et al. 2014), a miRNA that when overexpressed, results in reduced seam cell number (Li et al. 2005). [score:6]
Abbott A. L. Alvarez-Saavedra E. Miska E. A. Lau N. C. Bartel D. P., 2005 The let-7 microRNA family members mir-48, mir-84, and mir-241 function together to regulate developmental timing in Caenorhabditis elegans. [score:3]
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11
[+] score: 8
Other miRNAs from this paper: cel-let-7, cel-mir-84, cel-mir-241
To further determine the role of let-7s miRNAs in C. elegans innate immunity, we tested the function of mir-48, another let-7 relative, in P. aeruginosa infection and found that the mir-48(n4097) mutant exhibited decreased resistance to P. aeruginosa (Fig. S8A), suggesting that the let-7s miRNAs may target different regulators of C. elegans innate immunity. [score:4]
In C. elegans, the let-7 miRNA homologs mir-48, mir-84 and mir-241 (together referred to as let-7s) regulate developmental timing and promote cellular differentiation pathways [27], [28]. [score:3]
In contrast to the luciferase activity in the 3′-UTR seed region mutants (skn-1 3′-UTR (mut)), which could not bind with and respond to let-7s miRNAs, the luciferase activity of the skn-1 3′-UTR decreased by approximately 30% in response to mir-48 mimics or mir-84 mimics and by approximately 10% in response to mir-241 mimics (Fig. 6B ). [score:1]
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12
[+] score: 7
For instance, miR-48, miR-84, and miR-241 regulate the second larval (L2) to third larval (L3) transition, while let-7 regulates the fourth larval (L4) to adult transition (Fig.   1) (Reinhart et al., 2000; Abbott et al., 2005). [score:3]
During the life cycle of C. elegans, miR-48, miR-84, and miR-241 regulate the L2-to-L3 transition, whereas let-7 regulates the L4-to-adult transition Let-7 miRNAs are found in various animal species, including the human. [score:3]
During the life cycle of C. elegans, miR-48, miR-84, and miR-241 regulate the L2-to-L3 transition, whereas let-7 regulates the L4-to-adult transition Characteristics of the let-7 family Let-7 miRNAs are found in various animal species, including the human. [score:1]
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[+] score: 6
For example, the let-7 miRNA exhibited a major increase in expression around the mid-L4 stage, as did one of the let-7 family members, miR-48, from the mid-L3 stage (Figures 2 and 3a). [score:3]
The founding miRNA genes, lin-4 and let-7, and miR-48, another let-7 family member, are highlighted in color and in bold and are expressed at the times expected from the literature. [score:3]
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[+] score: 6
Three additional C. elegans let-7-like miRNAs, miR-48, miR-84, and miR-241, also act in the control of developmental timing and likely regulate the hbl-1 mRNA, but act earlier in development than the let-7 miRNA [52, 53]. [score:4]
However, as we reported previously, mir-84 single mutants or mir-48 mir-241; mir-84 triple mutants do not have a multivulva phenotype [52]. [score:1]
To uncover subtle abnormalities in the miRNA mutant strains will require more detailed analyses, as has been performed for lin-4, let-7, lsy-6, mir-48, mir-84, and mir-241. [score:1]
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This developmental program is controlled at different larval stages by lin-4 miRNA [26], the let-7 family miRNAs (miR-48, miR-84, miR-241 and let-7) [25, 27] and their targets lin-14, lin-28, hbl-1, daf-12 and lin-41 [25, 27– 33]. [score:4]
RNA bounds immunoprecipitated complexes were extracted and the level of let-7 and miR-48 was quantified by quantitative RT-PCR. [score:1]
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Mutants defective in daf-12 or carrying mutations in the microRNAs mir-48, mir-241, and mir-84 exhibit disorganized developmental progression, with specific cell divisions being reiterated or skipped (8). [score:3]
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The penetrance of this phenotype is enhanced by gld-1(op236), with 64% (n = 81, p = 0.013 Fisher's exact test) lethality observed in the gld-1(op236); mir-48 mir-241; mir-84 quadruple mutant. [score:1]
The let-7 family (let-7, mir-48, mir-84, mir-241 and mir-795) miRNAs are much more studied compared with mir-35 family miRNAs during C. elegans development. [score:1]
Forty-two per cent (n = 43) of mir-48 mir-241; mir-84 triple mutants die owing to a burst vulva during the L4 to adult transition reminiscent to the let-7(null) phenotype [44]. [score:1]
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Other miRNAs from this paper: cel-lin-4, cel-mir-84, cel-mir-241
N2 = wild-type, CB1 = dpy-1(e1), VT1207 = lin-4(e912); mir-48 mir-241(nDf51); lin-14(n179) mir-84(n4037). [score:1]
wild-type, CB1370: daf-2(e1370): CB1372, daf-7(e1372), VT2317: daf-16(mgDf50); daf-7(e1372), CB1: dpy-1(e1), VT1207: lin-4(e912); mir-48 mir-241(nDf51); lin-14(n179) mir-84(n4037), GR1395: mgIs49[mlt-10::gfp-pest] (Frand et al. 2005; Hayes et al. 2006). [score:1]
We used a strain with a defective cuticulin, CB1 dpy-1, and a heterochronic mutant with a morphologically abnormal cuticle, VT1207 lin-4; mir-48 mir-241; lin-14 mir-84. [score:1]
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Similarly, C. elegans let-7 and the related miRNAs, mir-48, mir-84 and mir-241, also function to regulate the timing of developmental events [19, 20]. [score:3]
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The third most expressed miRNA was miR-84-5p, that together with other abundant miRNAs like miR-48-5p and let-7-5p, are members of the let-7 family, that also includes miR-7, miR-241, miR-793, miR-794 and miR-795 [65]. [score:3]
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Other miRNAs from this paper: cel-mir-241
In addition to three miRNA genes in this region (cel-mir-48, cel-mir-241, and cel-mir-257), potential plasticity regulators for the transband genes are listed in Table S4. [score:2]
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This family includes a further six miRNAs; miR-48, miR-84, miR-241, miR-793, miR-794, and miR-795 [12]. [score:1]
While let-7 is involved in specifying larval-adult cell fate, miR-48, miR-84 and miR-241 are co-activated at an earlier time point where they co-ordinate the L2-L3 transition [4]. [score:1]
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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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Other miRNAs from this paper: cel-let-7, cel-lin-4, cel-mir-84, cel-mir-232, cel-mir-233, cel-mir-241
Furthermore, Liu et al. [17] have demonstrated that the mir-84(n4037) and mir-241(n4316) mutants exhibit enhanced resistance, whereas the mir-48(n4097) mutant worms exhibit decreased resistance to P. aeruginosa infection. [score:1]
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