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3 publications mentioning cel-mir-52

Open access articles that are associated with the species Caenorhabditis elegans and mention the gene name mir-52. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 152
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]
0037185.g005 Figure 5Loss of mir-52 does not enhance the ability of ectopically-expressed to regulate its target, cog-1. (A–E) Effect of mir-52 on mediated regulation of cog-1::gfp::cog-1 expression. [score:9]
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]
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]
Loss of mir-52 partially suppressed mutant lim-6::gfp expression in (ot149lf)/lsy-6(ot150rf): 85% of rf/lsy-6lf worms displayed mutant lim-6::gfp expression compared to 61% of mir-52;rf/lsy-6lf (Figure 3B). [score:6]
Loss of mir-52 does not enhance the ability of ectopically-expressed lsy-6 to regulate its target, cog-1.. [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]
One hypothesis to account for the observed suppression of multiple miRNA-regulated pathways is that the loss of an abundant miRNA such as miR-52 frees up miRNA -induced silencing complex (miRISC) so that it is available for binding by other miRNAs in a cell. [score:4]
mir-52/53/54/55/56 mutant worms display impenetrant embryonic lethality, slow growth, and mating defects [13], [25] indicating that mir-51 family targets are sufficiently misregulated to result in severe, penetrant mutant phenotypes. [score:4]
We used a lin-28::gfp::lin-28 transgene to determine whether mir-52 suppression is the result of a misregulation of lin-28. [score:4]
To account for the observation that the loss of mir-52 suppressed multiple miRNA -dependent phenotypes, we proposed that mir-52 may act to broadly regulate miRNA biogenesis or activity. [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]
Loss of mir-51 family members does not broadly enhance miRNA biogenesis or activityTo account for the observation that the loss of mir-52 suppressed multiple miRNA -dependent phenotypes, we proposed that mir-52 may act to broadly regulate miRNA biogenesis or activity. [score:4]
0037185.g001 Figure 1Loss of mir-52 suppresses hbl-1 misregulation in mir-48/84/241 mutants. [score:4]
mir-51 family members function upstream of hbl-1, but not lin-28, to suppress developmental timing defects in let-7 family mutantsGenetic interactions between mir-52 and let-7 family members as well as hbl-1(ve18) suggest that mir-52 may act upstream of hbl-1 to promote its activity. [score:4]
We found that loss of mir-52 weakly suppressed the levamisole resistance phenotype of worms (Figure 3H). [score:3]
This indicates that mir-52 acts upstream of hbl-1 expression in opposition to let-7 family activity. [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]
Loss of mir-52 did not suppress the puf-9 alae defects (Table 1). [score:3]
Loss of the mir-51 family member, mir-52, partially suppressed the vulva cell fate defects of let-60gf mutants, the ASEL cell fate defects of mutants, the defecation defects of mutants, and the levamisole resistance of mutants. [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]
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]
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]
0037185.g002 Figure 2Loss of mir-52 does not result in increased expression of lin-28::gfp::lin-28. [score:3]
Loss of mir-52 partially suppressed lin-46 developmental timing defects: mir-52; lin-46 double mutant worms had fewer seam cells and displayed weaker alae defects compared to lin-46 mutant worms (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]
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]
In order to determine if loss of mir-52 can act to enhance miRNA activity, we analyzed the activity of ectopically expressed in the repression of a cog-1::gfp reporter [14]. [score:3]
0037185.g003 Figure 3The mir-51 family members, mir-52 and mir-54/55/56, function in multiple miRNA -dependent developmental pathways. [score:2]
These data indicate that activity is not enhanced in the absence of mir-52, thereby suggesting that the mir-51 family does not function broadly to regulate the activity of miRNAs. [score:2]
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]
This suggests that the developmental timing pathway is the most sensitive to the loss of mir-52 in the L2 stage. [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 enhances precocious developmental timing phenotypes. [score:2]
Loss of mir-52. [score:1]
In addition, loss of mir-52 did not result in an enhancement of ectopic activity in uterine cells as would be predicted by the limiting miRISC mo del. [score:1]
We found that loss of mir-52 had no effect on the activity of ectopic repression of cog-1 (Figure 5). [score:1]
Further, worms that are multiply mutant for 5 out of 6 members of the mir-51 family, mir-52/53/54/55/56, also do not display alae formation defects (Table 1 and Table 2), despite displaying other mutant phenotypes including slow growth and larval lethality [13], [25]. [score:1]
We found that the levels of these miRNAs are unchanged in mir-52 mutants as well as in mir-52/53/54/55/56 mutants (Figure 4). [score:1]
Loss of mir-52 significantly enhanced this precocious alae formation in the mir-48(ve33) background (Table 2). [score:1]
However, no such elevation in the mature miRNA levels was observed for the four miRNAs that were analyzed in the absence of mir-52 or mir-52/53/54/55/56 activities. [score:1]
We found that loss of mir-52 significantly reduced the average defecation cycle time of worms (Figure 3F). [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]
A mix of 1000 late L4 and L4 molt worms were collected for wild type, mir-52, and mir-52/53/54/55/56 mutant worms. [score:1]
dindicates significant difference between strains of same genotype +/− mir-52 (χ2, p<0.05). [score:1]
Loss of mir-52 enhances precocious developmental timing phenotypesWe next characterized genetic interactions between mir-52 and a set of precocious developmental timing genes. [score:1]
First, it is expected that overall levels of all mature miRNAs would be elevated in mutants that lack the abundant miR-52 due to increased loading into miRISC. [score:1]
Genetic interactions between mir-52 and let-7 family members as well as hbl-1(ve18) suggest that mir-52 may act upstream of hbl-1 to promote its activity. [score:1]
mir-52 mutants show weakly enhanced sensitivity to levamisole. [score:1]
lsy-6. The mir-51 family members, mir-52 and mir-54/55/56. [score:1]
This is observed in mir-52;let-60gf worms (Figure 3E). [score:1]
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2
[+] score: 8
Hypoxia N2: For the hypoxia -treated samples, we selected mir-52-5p as highly expressed (19899,848 reads), mir-241-3p as intermediately expressed (1086,805 reads) and mir-254 as lowly expressed (585,136 reads) to validate by qPCR (Figure 4). [score:7]
mir-58-3p, mir-230-3p and mir-357-3p are stable upon hypoxia regardless of HIF-1 presence, V. mir-241-3p, mir-254 and mir-52-5p are stable upon hypoxia. [score:1]
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3
[+] score: 7
Other miRNAs from this paper: cel-let-7, cel-mir-1, cel-mir-35, cel-mir-58a, dme-mir-1, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, dme-bantam, mmu-let-7d, dme-let-7, 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-16-1, mmu-mir-16-2, mmu-mir-1a-2, cel-lsy-6, 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-16a, dre-mir-16b, dre-mir-16c, 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-1b, cel-mir-58b, mmu-let-7j, mmu-let-7k, cel-mir-58c
Translational activity was monitored through measurement of RL activity in the presence of miR-52 2′- O-Me inhibitor or a non-cognate miR-58 2′- O-Me inhibitor. [score:5]
Deadenylation of a similarly structured reporter encoding six binding sites for the zygotic miR-51-56 family was affected in a comparable manner by PAB-1/2 depletion (Figure 3C; 6× miR-52). [score:1]
The constructs harboring 3 or 6× miR-35 sites or miR-52 sites and a 161 nt linker were previously generated in (9). [score:1]
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