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6 publications mentioning dme-mir-263b

Open access articles that are associated with the species Drosophila melanogaster and mention the gene name mir-263b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 123
We made use of the Gal4 knock-in alleles to direct UAS-GFP reporter expression in the endogenous miR-263a and miR-263b expression domains. [score:7]
The miR-263a phenotype is rescued by expression of a miR-263a or overexpression of a miR-263b transgene. [score:5]
Apical focal planes of the same cells, left to right: cell outlines and IOB labelled with anti-DE-cadherin (red in merged image); miR-263a (I) and miR-263b (J) expressing cells visualized by GFP expression (green in merged image). [score:5]
Cells were cotransfected to express miR-263a or miR-263b or with a vector-only control, and with a plasmid expressing Renilla luciferase as a transfection control. [score:5]
miR-263b-Gal4 was used to drive over -expression of target genes in this series of experiments because it has higher Gal4 activity than miR-263a-Gal4. [score:5]
Similarly, reducing hid levels by expression of a UAS-hid -RNAi transgene under the control of miR-263b-Gal4 produced a strong suppression of the miR-263a mutant phenotype (Figure 5C, 5D). [score:5]
1000396.g002 Figure 2The miR-263a phenotype is rescued by expression of a miR-263a or overexpression of a miR-263b transgene. [score:5]
To this end, we produced Gal4 “knock-in” alleles of miR-263a and miR-263b, in which the miRNA hairpin sequences were replaced by Gal4 and mini-white (using a modified targeting vector; [13]). [score:4]
The genetic evidence presented here identifies hid as a key target of the miR-263 family in supporting bristle development. [score:4]
In light of the observation that loss of miR-263b has a milder impact than loss of miR-263a, these results imply that the two miRNAs have targets in common in their role during IOB development. [score:4]
miR-263a and miR-263b Gal4 knock-in alleles were made using a modified targeting vector [13]. [score:4]
Nonetheless, expression of UAS-miR-263b under miR-263b-Gal4 control was able to rescue the miR-263a mutant phenotype (Figure 2C, 2D). [score:3]
Drosophila miR-263a and miR-263b are expressed in sense organ precursors in embryos [11], [56] and in mechanosensory organs of the eye, antenna, and haltere ([11], [50], this report). [score:3]
Basal focal planes, left to right: DAPI labelled nuclei (blue in merged image); GFP whose expression was driven with miR-263a-Gal4 (I) or miR-263b-Gal4 (J) (green in merged image); Pax2 labelled IOB sheath (small nuclei) and bristle shaft cells (large nuclei; red in merged image). [score:3]
Left panel: miR-263a mutant with one copy of hid [05014]; middle panel: miR-263a mutant with one copy of the antimorphic hid allele W [1]; right panel: miR-263a mutant expressing a UAS-hid -RNAi transgene under control of miR-263b-Gal4. [score:3]
Only two of the candidates caused bristle loss when expressed under control of miR-263b-Gal4: Cyclin E and head involution defective (hid). [score:3]
Predicted miR-263b target sites in the hid 3′UTR. [score:3]
Quantification of macrochaetae on head and thorax of adult flies: wild-type (WT), miR-263a mutant (Δ263a/bft), miR-263a mutant expressing an UAS-miR-263a transgene (rescue flies: Δ263a-G4/bft; UAS-263a/+), miR-263a miR-263b double mutant (Δ263a/bft; Δ263b/Def, where Def represents the genomic deficiency Df(3L)X-21.2), miR-263a mutant with one copy of the antimorphic hid allele W [1] (Δ263a/bft; W [1]/+). [score:3]
hid expression under miR-263b-Gal4 control caused loss of IOB (Figure 5A). [score:3]
Δ263b: miR-263b knockout allele, Δ263b-G4/Def: miR-263b-Gal4 knock-in allele in trans with the genomic deficiency Df(3L)X-21.2. [score:3]
Ras85D is on the list of predicted miR-263a targets (but not on the miR-263b list due to differences in the seed sequence). [score:3]
Although miR-263b differs from miR-263a by three residues, including position 1 of the seed region, hid is also a predicted target of miR-263b (Figure S6; [24], [25]). [score:3]
Therefore, miR-263b and miR-263a can each act directly via these sites to regulate hid mRNA levels. [score:3]
Figure S6 miR-263b target sites in the hid 3′UTR. [score:3]
Table S1 List of tested candidate genes, with the corresponding EP lines and results (IOB loss: yes or no) when expression is driven with miR-263b-Gal4. [score:3]
Rescue occurred at levels of miR-263b several-fold above normal (Figure 2D, green bars), suggesting that miR-263b can replace miR-263a when over-expressed. [score:3]
Coexpression of miR-263b also significantly reduced luciferase activity from the reporter carrying the intact hid 3′UTR but not from the reporter in which the miRNA sites were mutated (Figure 6B). [score:3]
Although miR-263b showed little effect alone, the miR-263a miR-263b double mutant showed a stronger viability phenotype (Figure S4). [score:1]
Figure S2 miR-263b contributes to IOB formation. [score:1]
Viability of different miR-263a and miR-263b mutant lines. [score:1]
1000396.g001 Figure 1 miR-263a and miR-263b mutants. [score:1]
We generated a miR-263b deletion allele (Δ263b) by homologous recombination and confirmed that mature miR-263b was absent in the mutant (Figure S2B). [score:1]
In addition to the IOB phenotype, the miR-263a and miR-263b mutants exhibit other milder defects. [score:1]
UAS-miR-263a and UAS-miR-263b lines were made by cloning a 300 base pair genomic fragment containing the miRNA hairpin into the 3′UTR of dsRed in pUAST, as described in [10]. [score:1]
Figure S3 Absence of miR-263 causes loss of bristles on head and thorax. [score:1]
IOB numbers were only modestly reduced in flies lacking miR-263b alone (Δ263b/Df(3L)X-21.2; Figures S2C, 1D). [score:1]
miR-263a and miR-263b mutants. [score:1]
As miR-263b is located in an intron of CG32150, we removed the intron-containing mini-white gene cassette and confirmed that splicing of CG32150 mRNA was not affected in the ΔmiR-263b mutants by comparing the level of spliced mRNA using qRT-PCR. [score:1]
We also analyzed the effect of miR-263b on the 3′UTR of hid. [score:1]
Figure S4 Viability of miR-263a and miR-263b mutants. [score:1]
Loss of Sense Organs in Flies Lacking miR-263a and miR-263b miR-263a is located near the bereft locus on chromosome 2L (Figure 1A). [score:1]
These observations suggest that both the miR-263a and miR-263b miRNAs contribute to IOB formation, with miR-263a playing the major role. [score:1]
Δ263a/bft: miR-263a mutant, Δ263b/Def: miR-263b mutant, where Def represents the genomic deficiency Df(3L)X-21.2, Δ263a/bft; Δ263b/Def: miR-263a miR-263b double mutant. [score:1]
Drosophila miR-263a and miR-263b are members of a conserved family of miRNAs, including mammalian miR-183, miR-96 and miR-182, and miR-228 in C. elegans. [score:1]
Loss of Sense Organs in Flies Lacking miR-263a and miR-263b. [score:1]
miR-263a and miR-263b differ in sequence, with the seed region being shifted by one residue (Figure S2A). [score:1]
There was no significant enhancement of this phenotype in the miR-263a miR-263b double mutant (Figure S3). [score:1]
Further investigation of the miR-263 family miRNA mutants may lead to identification of targets important for other aspects of the miRNA function, such as the reduced viability observed in the double mutants. [score:1]
Macrochaetae numbers in the miR-263a miR-263b double mutant differed slightly, but not statistically significantly, from those in miR-263a mutants. [score:1]
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[+] score: 20
Intriguingly, miR-263b expression is essentially anti-phase to that of the cycling tws transcript and is constantly high in cyc [01 ]flies (Fig. 2). [score:3]
Two independent search programs (Pictar and EMBL) predict that cwo might be targeted by miR-263b. [score:3]
miR-263b has a similar RNA profile as cwo, raising the possibility that it functions to attenuate translation of cwo transcripts as they accumulate during the night. [score:3]
Thus, miR-263b could amplify daily oscillations in the levels or translational efficiency of tws RNA. [score:3]
Other possible targets of miR-263a and miR-263b include doubletime (dbt) and twins (tws), respectively. [score:3]
The D. melanogaster dme-miR-263b is also similar to the vertebrate miR-182 (three mismatches over the length of 20 aligned nucleotides). [score:1]
The values for miR-263a and miR-263b were normalized to the relative copy number of rp49 or cbp20 cDNAs. [score:1]
However, even though miR-263a and -263b are paralogous genes in the same family (miR-263) with very similar mature sequences (Fig. 4A), they are found on the second and third chromosomes, respectively. [score:1]
Finally, the relative levels of miR-263a and miR-263b at ZT/CT1 were set to 1.0 and the other values normalized. [score:1]
Although potentially coincidental, the mature sequence for miR-183 in vertebrates is very similar to that of both D. melanogaster dme-miR-263a and miR-263b (Figs. 4B and 4C). [score:1]
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[+] score: 2
8 of the 40 Drosophila miRNAs with ≥70% homologous sequences in humans show extensive overall similarity with 5′ mismatches: dme-miR-8 with hsa-miR-141 and hsa-miR-200a, dme-miR-10 with hsa-miR-100 and hsa-miR-99a, dme-miR-100 with hsa-miR-10a and hsa-miR-10b, dme-miR-125 with hsa-miR-10a and hsa-miR-10b, dme-miR263a with hsa-miR-183, dme-miR-263b with hsa-miR-183, dme-miR-306 with hsa-miR-873, and dme-miR-993 with hsa-miR-100*. [score:1]
Most of the fly ≥70% full length homologs exhibit blocks of ≥7 nt identity at the 5′ end except the following 10: dme-miR-10, dme-miR-100, dme-miR-263a, dme-miR-263b, dme-miR-954, dme-miR-966, dme-miR-1009, dme-miR-1010, dme-miR-iab-4-3p and dme-miR-iab4as-3p. [score:1]
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[+] score: 1
elegans, Drosophila,Mouse, Humans miR959-964 – Immunity feeding Peak at ZT12 Trough at ZT0 Drosophila miR263a/b – –Peak at ZT19miR263a trough at ZT1 miR263b trough at ZT7C. [score:1]
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[+] score: 1
These newly identified miRNAs are bmo-miR-2a*, bmo-miR-8*, bmo-miR-13a*, bmo-miR-46*, bmo-miR-263*, bmo-miR-279*, and bmo-miR-305*. [score:1]
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[+] score: 1
For instance, dme-miR-263-5p, 5-5p and 9c-5p are primarily found in the mRNP fraction whereas dme-miR-184-3p is mainly part of polysomal fractions. [score:1]
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