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9 publications mentioning dme-mir-11

Open access articles that are associated with the species Drosophila melanogaster and mention the gene name mir-11. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 91
Other miRNAs from this paper: dme-mir-1, dme-mir-285, dme-mir-995, dme-mir-998
Comprehensive lists of predicted miR-998 targets and miR-11 targets were compiled from TargetScan [56], MinoTar [57], PITA [58], miRanda [59], and RNAhybrid [60]. [score:7]
This function of miR-11 is explained by its ability to directly regulate the expression of dE2F1-regulated cell death genes, thus highlighting a complex interaction between an intronic miRNA and its host gene [1], [8]. [score:6]
Furthermore, although miR-11 and miR-998 share 170 common targets, cell death GOBP terms were not enriched among them but were overrepresented among genes that are exclusively miR-11 targets. [score:5]
This apoptosis is strongly suppressed by co -expression of miR-11 (Figure S2B and [8]). [score:5]
Figure S2Overexpression of miR-11, but not miR-998 suppresses dE2f1 -induced apoptosis in transgenic animals. [score:5]
We previously showed that mir-11 directly represses a subset of apoptotic genes that are transcriptional targets of the host gene dE2f1, and in doing so, miR-11 limits E2F -dependent cell death induced by DNA damage. [score:4]
In contrast, as it has been shown previously [8], GOBP terms that relate to the induction and positive regulation of cell death were significantly enriched among miR-11 targets (Figure 3B, Table S2). [score:4]
Table S1 The complied list of predicted miR-11, miR-998 and miR-29 targets. [score:3]
The sequence of mature miR-998 is different than that of miR-11, particularly at the 5′ end in the seed sequence (Figure 1A), which is the primary determinant of miRNA target selection. [score:3]
While miR-11 repressed components of the core cell death machinery, including rpr and hid, miR-998 limited E2F -dependent cell death by elevating prosurvival signaling downstream of the Epidermal Growth Factor Receptor (EGFR) through regulation of dCbl, a negative regulator of EGFR. [score:3]
It was essential that the mir-998 loss-of-function allele did not disrupt the expression of mir-11 or dE2f1, such that any observed phenotype could be attributed specifically to the function of miR-998. [score:3]
In contrast, miR-11 suppressed dE2F1 -induced phenotypes but failed to block apoptosis in rbf mutants. [score:3]
miR-11 and miR-998 limit dE2F -dependent cell death through different targets. [score:3]
The last intron of the Drosophila E2F gene dE2f1 harbors a miRNA, mir-11, which is co-expressed with dE2f1 (Figure 1A and Figure S1). [score:3]
Importantly, the expression of dE2f1 and miR-11 were not affected in the mir-998 [exc222] mutant animals (Figure 2B). [score:3]
However, neither miR-11 nor miR-998 modulated dE2F1 -induced proliferation, as the level of E2F1 -induced ectopic BrdU incorporation was largely unchanged by co -expression of miR-11, as was previously shown [8], or miR-998 (Figure S2B). [score:3]
Thus, miR-998 and miR-11 both suppressed E2F -dependent cell death, but did so in mutually exclusive contexts. [score:3]
GFP and miR-998 or miR-11 were expressed in the entire eye disc of rbf1 [120a] hemizygous males using a flip-out technique induced by ey-FLP. [score:3]
Heat map of GOBP enrichment analysis of predicted miR-11 and miR-998 targets (FDR [score:3]
Interestingly, unlike miR-998, miR-11 failed to block apoptosis in rbf mutants as the number of C3 positive cells was similar between rbf [120a], act>mir-11 and rbf [120a] eye discs. [score:1]
A diagram of the dE2f1 exon/intron structure, mutant alleles, and mir-11 gene examined is shown. [score:1]
The following stocks were previously published: UAS-miR-11 (Brennecke et al. 2005), Act88F-Gal4 and Act88F-Gal4, UAS-dE2f1 (from Erick Morris and Teiichi Tanimura), Cbl [F165], FRT 80B, UAS-Cbl-L (A18) and UAS-Cbl-S (A1) (from Trudi Schupbach), rbf1 [120a], ey-FLP; act5c>CD2>GAL4, UAS-GFP/CyO, GFP [Act], and rbf1 [120a], ey-FLP/FM7, GFP [Act];; FRT 82B, GFP [Ubi], and rbf1 [120a], ey-FLP/FM7, GFP [Act];; GFP [Ubi], FRT 80B (from Nam Sung Moon). [score:1]
Here we show that miR-998 limits dE2F -dependent cell death, but it does so in a different context and by a different mechanism than miR-11. [score:1]
Therefore, the physiological role of mir-11 was revealed only when examined in the sensitized background of its host gene. [score:1]
The expression of mir-11 and mir-998, were measured using qPCR, and normalized to β-tubulin and rp49 levels. [score:1]
miR-11 and miR-998 have different functions. [score:1]
RNA was extracted from third instar larval eye discs, and miR-998, miR-11, dE2f1, β-tubulin, and rp49 expression was measured by quantitative RT-PCR. [score:1]
We used one piggyBac element and two P elements inserted near the dE2f1 gene and screened for local transpositions of these transposons into intron 5, which harbors miR-11 and miR-998. [score:1]
In addition to mir-11, the last intron of the dE2f1 gene contains another miRNA, mir-998. [score:1]
Differences in suppression of cell death in rbf mutant cells by miR-11 and miR-998 prompted us to investigate the impact of the two miRNAs on dE2F1 -dependent apoptosis in other settings. [score:1]
Two miRNAs are in the last intron: mir-11 and mir-998, and are co-transcribed with dE2f1. [score:1]
Therefore it is not surprising that both the mir-11 and mir-998 mutant alleles were viable, and exhibited no phenotypes on their own. [score:1]
This cell death phenotype is strongly rescued by miR-11 (Figure S2A and [8]). [score:1]
This insert contained the de2f1 intron 5′ sequence flanking two mir-1 chimeras: mir1/mCherry shmiR [55] replaced the mir-11 gene, and mir-1/998 replaced the mir-998 gene, which was designed as in Haley et al. (2008) and was synthesized by GenScript USA. [score:1]
The loss of mir-11 was shown to strongly enhance dE2F1 -dependent DNA damage -induced apoptosis even though it was insufficient to cause cell death in unprovoked settings. [score:1]
Full genotypes are: rbf1 [120a], ey-FLP; +/+ (top), rbf1 [120a], ey-FLP; act5c>CD2>GAL4, UAS-GFP/UAS-mir-998 (middle), and rbf1 [120a], ey-FLP; act5c>CD2>GAL4, UAS-GFP/UAS-mir-11 (bottom). [score:1]
The aligned sequences of mature miR-11 and miR-998 are shown, with the seed sequence highlighted. [score:1]
The potential for complex interactions between intronic miRNAs and their host is illustrated by the Drosophila dE2f1 gene, and the two miRNAs embedded in its last intron: mir-11 and mir-998. [score:1]
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[+] score: 19
As a member of the miR-2 seed family, miR-11 is expected to regulate the same targets as miR-2. Regulation of reaper by miR-11 has been confirmed in the embryo by Leaman et al. and Ge et al. (Leaman et al., 2005; Ge et al., 2012). [score:5]
Coexpression of a miR-2a/2b cluster transgene or a miR-11 transgene suppressed the undergrowth of yki -depleted tissue caused by elevated reaper mRNA (Fig.  4A,B; P<0.001). [score:5]
*** indicates statistically significant increase in the width of the ptc-Gal4 expression domain when miR-11 level was increased (P<0.001). [score:3]
Expression of miR-2a/2b or miR-11 on their own had no effect on growth. [score:3]
Histogram shows quantification of the effects of the UAS-miR-11 transgene alone and together with UAS-yki [RNAi]. [score:1]
miR-11 was not significantly changed. [score:1]
UAS-miR-11 transgene was described by Szuplewski et al. (Szuplewski et al., 2012). [score:1]
[1 to 20 of 7 sentences]
[+] score: 5
Furthermore, many targets of Notch signaling were also predicted as targets of the Bearded-box microRNAs miR-4 and miR-79 (E(spl)m5, Bearded, E(spl)mγ, and Tom) and of the K-box microRNAs miR-2 and miR-11 (E(spl)m5, E(spl)m2, E(spl)mδ, and E(spl)m3), consistent with previous observations [27]. [score:5]
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[+] score: 5
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]
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[+] score: 5
For instance, Frolov and colleagues recently demonstrated that a micro -RNA, mir-11, which is located within the last intron of the Drosophila E2f1 gene, acts to dampen expression of pro-apoptotic E2f1 target genes following DNA damage [28]. [score:5]
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[+] score: 5
Likewise, although unstable PGC transcripts are enriched for miR-1, miR-2a-2 cluster, miR-8, miR-10, miR-11, miR-13b-1 cluster, miR-92a, miR-274, and miR-283 target sites, all of these miRs are expressed in the soma but not in the PGCs [73]. [score:5]
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[+] score: 4
The miRNAs miR-309clus, miR-10, and iab-4 (which all reside between annotated mRNA genes on the genome), and miR-11, miR-274, and miR-281clus (which all reside within introns of annotated genes) are all expressed in a graded fashion along the anterior–posterior axis of the blastoderm embryo [14, 60]. [score:3]
gov/Genbank/) GeneIDs for the genes discussed in this paper are arf3 (817014), eve (36039), hb (41032), hoxb8 (15416), iab-4 (3772110), lbl1 (100037819), miR-10 (3772568), miR-11 (3771987), miR-196 (387191), miR-274 (3771876), miR-281–1 (3772402), miR-281–2 (3772497), miR-309 (3772613), scr (40833), tas3 (3768766), and ubx (42034). [score:1]
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[+] score: 2
Importantly, sequences derived from several pri-miRNAs, including Bantam, miR-2 family, miR-11, miR- 33 and miR- 34 were also recovered, thus demonstrating direct interactions between SmD1 and pri-miRNAs (Figs 3C, 5C, 5D and S9; S6 Table). [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, dme-mir-1, dme-mir-8, hsa-mir-34a, hsa-mir-210, dme-mir-184, dme-mir-275, dme-mir-92a, dme-mir-276a, dme-mir-277, dme-mir-33, dme-mir-281-1, dme-mir-281-2, dme-mir-34, dme-mir-276b, dme-mir-210, dme-mir-92b, dme-bantam, dme-mir-309, dme-mir-317, hsa-mir-1-2, hsa-mir-184, hsa-mir-190a, hsa-mir-1-1, hsa-mir-34b, hsa-mir-34c, aga-bantam, aga-mir-1, aga-mir-184, aga-mir-210, aga-mir-275, aga-mir-276, aga-mir-277, aga-mir-281, aga-mir-317, aga-mir-8, aga-mir-92a, aga-mir-92b, hsa-mir-92b, hsa-mir-33b, hsa-mir-190b, dme-mir-190, dme-mir-957, dme-mir-970, dme-mir-980, dme-mir-981, dme-mir-927, dme-mir-989, dme-mir-252, dme-mir-1000, aga-mir-1174, aga-mir-1175, aga-mir-34, aga-mir-989, aga-mir-11, aga-mir-981, aga-mir-1889, aga-mir-1890, aga-mir-1891, aga-mir-190, aga-mir-927, aga-mir-970, aga-mir-957, aga-mir-1000, aga-mir-309, cqu-mir-1174, cqu-mir-281-1, cqu-mir-1, cqu-mir-275, cqu-mir-957, cqu-mir-277, cqu-mir-252-1, cqu-mir-970, cqu-mir-317-1, cqu-mir-981, cqu-mir-989, cqu-mir-1175, cqu-mir-276-1, cqu-mir-276-2, cqu-mir-276-3, cqu-mir-210, cqu-mir-92, cqu-mir-190-2, cqu-mir-190-1, cqu-mir-1000, cqu-mir-11, cqu-mir-8, cqu-bantam, cqu-mir-1891, cqu-mir-184, cqu-mir-1890, cqu-mir-980, cqu-mir-33, cqu-mir-2951, cqu-mir-2941-1, cqu-mir-2941-2, cqu-mir-2952, cqu-mir-1889, cqu-mir-309, cqu-mir-252-2, cqu-mir-281-2, cqu-mir-317-2, aga-mir-2944a-1, aga-mir-2944a-2, aga-mir-2944b, aga-mir-2945, aga-mir-33, aga-mir-980
miR-11 and miR-989 map to the plus strand in the Ae. [score:1]
quinquefasciatus since (i) miR-11 and miR-989 are located on the plus strand in An. [score:1]
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