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10 publications mentioning dme-mir-263a

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

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[+] score: 315
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]
If Cyclin E over -expression is the cause of the bristle loss in miR-263a mutants, limiting their capacity to express Cyclin E should suppress this phenotype. [score:7]
Therefore over -expression of a biologically important target in miR-263a expressing cells would be expected to result in IOB loss, phenocopying the miR-263a mutant phenotype. [score:7]
Similarly, over -expression of the anti-apoptotic protein DIAP1, a direct target of the proapoptotic protein Hid [23], was able to prevent IOB loss in miR-263a flies (Figure 4A, 4B). [score:6]
To test this possibility, we made use of miR-263a- Gal4 to express the anti-apoptotic protein p35 in miR-263a expressing cells. [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]
Restoring miR-263a expression under the control of miR-263a-Gal4 using a UAS-miR-263a transgene fully suppressed the loss of IOB in miR-263a mutant flies (Figure 2A, 2B). [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]
Expression of UAS-p35 using miR-263a-Gal4 suppressed IOB loss in miR-263a mutant flies (Figure 4A, 4B). [score:5]
Identification of miR-263a Targets miR-263a has several hundred computationally predicted targets [24], [25]. [score:5]
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]
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]
Δ263a denotes the targeted miR-263a deletion, Δ263a-G4 denotes the miR-263a-Gal4 knock-in allele, UAS-263a denotes the UAS-miR-263a transgene, and bft is bft [24]. [score:4]
miR-263a and miR-263b Gal4 knock-in alleles were made using a modified targeting vector [13]. [score:4]
hid downregulation by miR-263a is required for IOB formation. [score:4]
To address whether hid is a direct target of miR-263a, we generated luciferase reporter constructs carrying the full length endogenous hid 3′UTR or mutant versions in which two nucleotides of each predicted miR-263a site were mutated to compromise pairing to the miRNA seed region (Figure 6A, in red). [score:4]
The genetic evidence presented here identifies hid as a key target of the miR-263 family in supporting bristle development. [score:4]
hid Is a Direct Target of miR-263a/b. [score:4]
Although Cyclin E is upregulated in the miR-263a mutant, this does not appear to contribute to the bristle loss phenotype. [score:4]
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]
1000396.g005 Figure 5 hid downregulation by miR-263a is required for IOB formation. [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]
We have explored the possibility that miR-263a/b might function in a regulatory feed-forward network to control hid both directly and indirectly. [score:4]
hid Is a Direct Target of miR-263a/b The hid 3′UTR contains four potential miR-263a binding sites (Figure 6A). [score:4]
We report that a pair of related microRNAs, miR-263a/b, protect sense organs during this pruning process by directly acting upon and limiting the expression of the proapoptotic gene hid. [score:4]
RNA was extracted from 30 h pupal eye imaginal discs from flies expressing a GFP reporter carrying the hid 3′UTR or a mutated version of it, in a miR-263a mutant or wild-type control background. [score:3]
Therefore, miR-263b and miR-263a can each act directly via these sites to regulate hid mRNA levels. [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]
To address this we introduced the antimorphic allele of hid, W [1], into miR-263a miRNA mutant flies and found that mechanosensory bristle loss on head and thorax was also significantly suppressed (Figure S3; p<0.001). [score:3]
Identification of miR-263a Targets. [score:3]
Taken together, these data suggest that miR-263a serves to prevent apoptosis in the IOB precursors by limiting hid expression during the wave of interommatidial cell pruning. [score:3]
The absence of the mature miR-263a miRNA was confirmed by Northern blot using total RNA isolated from adult flies homozygous mutant for the targeted allele (Δ263a, Figure 1B). [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]
In this scenario, miR-263a would act directly to repress hid and indirectly via the RAS/MAPK pathway (illustrated in Figure S8). [score:3]
miR-263a inhibits apoptosis in the shaft cells. [score:3]
Cell lysates were obtained from 30 h pupal eye imaginal discs from flies expressing a luciferase reporter carrying the hid 3′UTR, or the mutated version of it, in a miR-263a mutant or wild-type background. [score:3]
In S2 cells, co -expression of the luciferase reporter carrying the intact sites with miR-263a significantly reduced luciferase activity (Figure 6B, p<0.001). [score:3]
Intriguingly, an upstream element of the MAPK pathway, Ras85D, is a predicted target of miR-263a. [score:3]
miR-263a has several hundred computationally predicted targets [24], [25]. [score:3]
A lower level of Gal4-independent expression that results from leakiness of the UAS-miR-263a transgene also conferred partial rescue of IOB loss in the Δ263a/bft background (Figure 2A, 2B). [score:3]
This difference was abolished in miR-263a mutant flies rescued by expression of UAS-miR-263a under miR-263a-Gal4 control. [score:3]
Δ263a denotes the targeted miR-263a deletion, bft denotes the bft [24] allele described in [11]. [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]
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]
The bristle loss on head and thorax observed in miR-263a mutants was also rescued by Gal4 -dependent expression of UAS-miR-263a (Figure S3). [score:3]
Middle and right panels: transgenes were expressed under miR-263a-Gal4 control. [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]
Thus miR-263a/b may have a dedicated antiapoptotic role to ensure the robustness of sense organ development in a fluctuating developmental landscape. [score:3]
Taken together these experiments provide evidence that miR-263a acts directly via the sites identified in the 3′UTR to regulate hid mRNA levels in vivo. [score:3]
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]
To test whether hid over -expression is the cause of bristle loss, we reduced hid activity in the miR-263a mutant background by introducing the hid [05014] loss of function allele [22]. [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]
Through a process of experimental validation we identify hid, among over 50 candidates examined in vivo, as a biologically important target of miR-263a/b in this context. [score:3]
Reducing the dosage of CycE to wild-type levels does not rescue bristle loss, which indicates that over -expression of CycE is not the cause of the miR-263a phenotype. [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]
However, apoptotic Pax2 -expressing nuclei corresponding to bristle shaft cells were seen in miR-263a mutants (arrows, Figure 4D). [score:3]
We also did not find evidence that miR-263a/b act in the context of a gene regulatory network. [score:2]
It is noteworthy that as little as 20% of normal miR-263a levels are sufficient to support IOB development. [score:2]
Loss of IOB by Apoptosis in miR-263a MutantsBecause of the greater dependence of IOB development on miR-263a, we focused on the miR-263a mutant for more in-depth analysis. [score:2]
Figure S7 miR-263a regulates a GFP transgene carrying the hid 3′UTR. [score:2]
Whether there is more than a coincidental similarity to the role of miR-263a/b in support of sensory hair development in Drosophila remains to be determined. [score:2]
However, as shown in Figure 6F, hid primary transcript levels were not significantly affected in the miR-263a mutant, although mature hid mRNA levels increased due to loss of miRNA direct mediated repression. [score:2]
To determine whether hid might be a biologically relevant target of miR-263a in vivo, we compared hid mRNA levels in RNA samples from mutant and control pupal eye discs. [score:2]
Negative regulation of Ras85D by miR-263a would repress MAPK activity and alleviate repression of hid transcription and of Hid protein activity. [score:2]
The available evidence suggests that miR-263a/b may have a dedicated role in controlling hid -induced apoptosis during developmental pruning of interommatidial cells. [score:2]
These findings indicate that miR-263a acts to protect these sense organs from the wave of programmed cell death that sweeps over the retina during early pupal development. [score:2]
In this report we present evidence that the miR-263a/b family of miRNAs contributes to the robustness of sense organ development. [score:2]
Our findings suggest a role for the miR-263a/b miRNAs in conferring robustness of a different sort, ensuring the survival of sense organ cells, after they have been specified by the developmental patterning process. [score:2]
Because of the greater dependence of IOB development on miR-263a, we focused on the miR-263a mutant for more in-depth analysis. [score:2]
To ask whether miR-263a/b might be responsible for this activity, we compared the effects of reducing miR-263a/b activity in animals expressing the constitutively active form of Hid, hid(Ala5), in the eye. [score:2]
miR-263a limits Hid activity during eye development. [score:2]
In this report we examine the role of miR-263a/b in conferring robustness to sensory organ survival during a developmental pruning process. [score:2]
miR-263a and miR-263b differ in sequence, with the seed region being shifted by one residue (Figure S2A). [score:1]
Although miR-263b showed little effect alone, the miR-263a miR-263b double mutant showed a stronger viability phenotype (Figure S4). [score:1]
miR-263a acts on binding sites in the hid 3′UTR. [score:1]
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]
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]
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]
In miR-263a homozygous mutants and in Δ263a/bereft [24] flies ∼80% of IOB were missing (Figure 1C, 1D). [score:1]
Finally, we asked whether the loss of the other mechanosensory bristles in miR-263a mutant flies was also a consequence of apoptosis due to elevated Hid activity. [score:1]
1000396.g004 Figure 4(A) SEM of adult eyes from miR-263a mutant flies carrying UAS-p35 or UAS-DIAP1 transgenes. [score:1]
Cyclin E mRNA levels were elevated by ∼2.5-fold in RNA samples from miR-263a mutants (Figure S5). [score:1]
The extent of the 2.8 Kb deletion in the bereft [24] allele and that of the 350 nt deletion in the miR-263a deletion allele (Δ263a) are indicated. [score:1]
To address this, ends-out homologous recombination was used to generate a small deletion removing miR-263a. [score:1]
The hid 3′UTR contains four potential miR-263a binding sites (Figure 6A). [score:1]
WT: wild-type; Δ263a/bft: trans-heterozygous miR-263a mutant; Δ263a,CycE [AR95]/bft: miR-263a mutant carrying one copy of CycE [AR95], a null allele of CycE. [score:1]
1000396.g001 Figure 1 miR-263a and miR-263b mutants. [score:1]
miR-263a is located near the bereft locus on chromosome 2L (Figure 1A). [score:1]
In the absence of miR-263a/b sensory bristles are lost, like other cells, in a stochastic manner. [score:1]
Flies carrying the miR-263a-Gal4 allele in trans to bereft [24] or Δ263a displayed IOB loss (Figure 2A, 2B; unpublished data). [score:1]
Figure S3 Absence of miR-263 causes loss of bristles on head and thorax. [score:1]
Based on the observations of Li et al. [7], we examined whether the severity of the miR-263a/b mutant phenotype would be affected by environmental fluctuation to increase noise but found no effect (unpublished data). [score:1]
1000396.g006 Figure 6 miR-263a acts on binding sites in the hid 3′UTR. [score:1]
In each of the single mutants we observed a variable loss of IOB, suggesting that the chance of any given nascent IOB cell succumbing to apoptosis has increased in the absence of the protective effect of miR-263a/b. [score:1]
Instead, miR-263a/b appears to function in a different context, acting as a buffer in a biological process that is inherently stochastic. [score:1]
There was no difference in luciferase activity for the transgene carrying the mutant form of the hid reporter, but the reporter with the intact sites clearly showed increased luciferase activity in the miR-263a mutant (Figure 6D). [score:1]
Figure S1 miR-263a is absent in bft lines. [score:1]
Figure S4 Viability of miR-263a and miR-263b mutants. [score:1]
In miR-263a mutant retinas many of the larger Pax2 positive nuclei were missing, consistent with bristle shaft cell loss (Figure 3H). [score:1]
Loss of IOB by Apoptosis in miR-263a Mutants. [score:1]
The most abundant product of miR-263a detected by sequencing is 24 nt in length [25]. [score:1]
[*] and [**] =  p<0.001 using two-tailed unpaired Student's t test comparing to the miR-263a/+ control [*] or the miR-263a single mutant [**]. [score:1]
Measurement of mature miR-263a by quantitative PCR showed that less than 20% of the normal expression level was sufficient to achieve a full rescue (Figure 2B, green bars). [score:1]
Viability of different miR-263a and miR-263b mutant lines. [score:1]
In miR-263a mutant retinas, the majority of these cells were missing at 40 h APF (arrowheads, Figure 3E, 3F). [score:1]
A prediction of this mo del is that hid transcription should decrease in the miR-263a mutant due to elevation of MAPK activity. [score:1]
In this light, we asked if miR-263a might be the functional product of the bereft locus. [score:1]
Comparable results were obtained comparing GFP reporter transgenes with intact and mutated sites in control and miR-263a mutants (Figure S7). [score:1]
These observations suggest that miR-263a/b play a protective role, preventing the loss of mechanosensory cells due to hid -induced apoptosis. [score:1]
Therefore, miR-263a must act at a later stage, after the asymmetric division of the SOP. [score:1]
The absence of mature miR-263a in these flies suggests that miR-263a is the functional product of the bereft locus. [score:1]
Loss of Sense Organs in Flies Lacking miR-263a and miR-263b. [score:1]
The Drosophila genome encodes a second miRNA closely related in sequence to miR-263a (Figure S2A). [score:1]
There was no significant enhancement of this phenotype in the miR-263a miR-263b double mutant (Figure S3). [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]
miR-263a is located 2.7 Kb downstream of the 3′ end of the annotated bereft transcript. [score:1]
At this stage, miR-263a mutant retinas were indistinguishable from the controls and bristle shaft progenitor cells were present in normal numbers (Figure 3B). [score:1]
Mature miR-263a was also missing in flies carrying the bereft [24] allele in trans to the Δ263a deletion allele (Δ263a/bft, Figure 1B), as well as in other bereft mutants (Figure S1). [score:1]
Reducing miR-263a levels by removing one copy of the miR-263a gene led to fewer IOB, producing a more sparse appearance in the tuft of bristles (Figure 7A, 7B). [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]
RNA was extracted from pupal eye imaginal discs from control and miR-263a mutants at 30 h APF. [score:1]
These data confirm that absence of miR-263a is responsible for the loss of mechanosensory bristles observed in bereft mutants. [score:1]
In addition to the IOB phenotype, the miR-263a and miR-263b mutants exhibit other milder defects. [score:1]
Total apoptotic nuclei as well as apoptotic shaft cell nuclei were counted in control flies and miR-263a mutants and normalized to the total number of ommatidia analyzed. [score:1]
In the fly, the mechanosensory cells are lost due to apoptosis in the miR-263a/b mutants. [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]
Northern blot showing mature miR-263a in total RNA extracted from adult control flies (WT) and the three bft homozygous mutants described in Hardiman et al. 2002 [11]. [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]
However in miR-263a/b mutants sporadic bristle loss was seen and was attributable to elevated hid activity. [score:1]
In the miR-263a mutant (illustrated at right), the predicted elevation of MAPK activity should lower hid activity, acting in opposition to the increase in hid mRNA levels caused by the miR-263a mutant. [score:1]
[*] p<0.001, Student's t test comparing to the miR-263a mutant. [score:1]
CycE is elevated in miR-263a mutants. [score:1]
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For example, CLK-CYC might stimulate the rhythmic expression of a transcriptional inhibitor that blocks expression of miR-263a and -263b during the day. [score:7]
The daily patterns of changes in the levels of miR-263a and -263b are somewhat reminiscent of mRNA targets directly regulated by CLK-CYC. [score:5]
However, whereas the levels of bona-fide direct targets of CLK-CYC, such as dper and tim, are reduced in cyc [01 ]flies [19, 24], the abundance of miR-263a and -263b are pegged at peak amounts (Fig. 2). [score:4]
These considerations raise the possibility that the circadian expression of miR-263a and -263b is not directly driven by core clock transcription factors. [score:4]
Of the 78 miRNAs that we probed by expression profiling only dme-miR263a and -263b displayed strong evidence of circadian regulation (with possible weak cycling for dme-miR-124). [score:4]
Other possible targets of miR-263a and miR-263b include doubletime (dbt) and twins (tws), respectively. [score:3]
Using this more limited search, we noted that Clk might be a target of both miR-263a and -263b (Table 1). [score:3]
Possible circadian-relevant targets of dme-miR-263a and 263b. [score:3]
Importantly, the levels of miR-263a and -263b were constant throughout a daily cycle in the cyc [01 ]mutant, indicative of bona-fide circadian regulation (Fig. 2A and 2B). [score:2]
Although it is not clear why the daily profiles are slightly different when comparing results obtained using the microarray platform or qRT-PCR, the combined results clearly indicate circadian regulation in the levels of dme-miR-263a and -263b. [score:2]
Intriguingly, the mature forms of dme-miR-263a and -263b are very similar in sequence to several miRNAs recently shown to be under circadian regulation in the mouse retina, suggesting conserved functions. [score:2]
A common mechanism likely underlies daily changes in the levels of dme-miR-263a and -263b. [score:1]
We find two miRNAs (dme-miR-263a and -263b) that exhibit robust daily changes in abundance in wildtype flies that are abolished in the cyc [01 ]mutant. [score:1]
Of these, only two miRNAs (dme-miR-263a and -263b) in wildtype control flies exhibited daily abundance changes that were statistically significant using the ANOVA with 5% FDR test (Fig. 2A and 2B). [score:1]
These results indicate that changes in the amounts of miR-263a and -263b are not merely driven by daily light-dark cycle but are dependent on a functional clock. [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]
We confirmed that both dme-miR-263a and -263b cycle using quantitative RT-PCR (qRT-PCR) and also showed that these oscillations persist in constant dark conditions (Fig. 2C and 2D). [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]
Of these, dme-miR-124 showed a pattern very similar to that of dme-miR-263a and -263b, exhibiting trough levels during the mid-day that were followed by increases during the early to late-night in wildtype flies and constantly elevated levels in the cyc [0 ]mutant (Fig. 3B). [score:1]
The values for miR-263a and miR-263b were normalized to the relative copy number of rp49 or cbp20 cDNAs. [score:1]
This could be especially relevant to this study as evolutionary evidence suggests a different 5' end for miR-263a [51]. [score:1]
dme-miR-263a and -263b reach trough levels during the daytime, peak during the night and their levels are constitutively elevated in cyc [01 ]flies. [score:1]
Importantly, the daily cycles in dme-miR263a and -263b were abolished in the cyc [01 ]mutant, and persisted in constant dark conditions (Fig. 2). [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]
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bmo-let-7b, bmo-let-7c, bmo-miR-9, bmo-miR-9*, bmo-miR-100-like, bmo-miR-263a, bmo-miR-31 and bmo-bantam were expressed in larva and pupa, but were not detected in moth; of these miRNAs, bmo-miR-9 and bmo-miR-9* are also complementary miRNAs. [score:3]
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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The most expressed miRNA corresponded to aga-miR-263a (Additional file 4). [score:3]
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Combined we identified seven miRNA lines (Pictured: miR-263a, miR-2a-2, and miR-2491; Not shown: bantam, miR-33, miR-308, and miR-973/974) that reduce the expression of the Or47b reporter. [score:3]
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But the predicted 5'-ends of miR-263a, miR-274, miR-282 and miR-283 are very different with current annotations. [score:1]
MiR-133, miR-219, miR-263a, miR-274, miR-281-2*, miR-282, miR-283 and miR-310 which are also collected in miRBase without cloning evidence, are also identified. [score:1]
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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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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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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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One copy lost in Drosophila Duplication mir-137Clustered with mir-2682 in Homo sapiens New hairpin mir-184Tandem duplication in Capitella teleta Duplication mir-193 Clustered with mir-365 in vertebrates New hairpin mir-219 Clustered with mir-2964 in vertebrates New hairpin mir-252Tandem duplication in Acyrthosiphon pisum Duplication mir-252Tandem duplication and novel mir-2001 in Lottia gigantea and C. teleta Duplication/new hairpin mir-263a/bClustered together in Daphnia pulex. [score:1]
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