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8 publications mentioning dme-mir-31a

Open access articles that are associated with the species Drosophila melanogaster and mention the gene name mir-31a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 73
The mechanism by which mir-31a expression in the progenitor cell is regulated and in turn CG16947 expression is regulated, has yet to be uncovered, however, I provide evidence that misregulation of this fine balance between mir-31a with CG16947 in the progenitor cells and subsequent excessive degradation of cdk9 in the progeny can alter the number of glia in the adult Drosophila brain. [score:8]
In Drosophila melanogaster, it has been shown that glia are still being produced in early adulthood by progenitor cells that persist into adulthood 2– 4. A subset of these predominantly glial progenitor cells express the microRNA, mir-31a, which inhibits the expression of a RING finger and CHY zinc finger domain containing 1, E3 ubiquitin ligase, CG16947. [score:7]
In mir-31a mutants, where the inhibition of CG16947 translation is lifted by the absence of mir-31a, there is excessive expression of CG16947 in the progenitor cells. [score:7]
CG16947 is expressed in the progenitor cells and mir-31a serves to limit its expression in the progenitor cells. [score:5]
This study does not exclude the possibility that cdk9 can be regulated in a mir-31a-CG16947-independent manner, but illustrates one way in which cdk9 expression can be regulated in glia. [score:5]
Thus, knocking down the interacting partner of CG16947 should mimic the loss of glia observed in both mir-31a mutants and when CG16947 is overexpressed. [score:4]
If cdk9 is the interacting partner of CG16947 and that its depletion is the cause of glial cell death in the adult, then overexpressing cdk9 only in the mir-31a mutant background should be sufficient to prevent glial loss. [score:3]
Indeed, overexpression of cdk9 in adult glia using Repo-Gal4 under the control of tubGal80 [ts] was able to prevent the glial loss observed in mir-31a mutants. [score:3]
The number of glia generated upon eclosion was not significantly different between the mir-31a mutants, the otherwise wildtype controls of Repo-Gal4 >  UAS-GFP and the conditions were UAS-CG16947 and UAS-cdk9 RNAi was overexpressed at this age (Supplemental Fig.   1b–f). [score:3]
Additionally, I show that in the condition where there are fewer glia in the brain; as in the mir-31a mutants, the adult-specific overexpression of cdk9 in glia prevents glial loss. [score:3]
In mir-31a mutants, the absence of mir-31a leads to the overexpression of CG16947. [score:3]
CG16947 expression in a subset of progenitor cells in the adult brain is controlled by the microRNA, mir-31a. [score:3]
As I did not observe an increase in glial number in the brain when cdk9 was overexpressed in adult glia, it suggests that cdk9 is not sufficient to generate more glial cells unless in aberrant conditions where glia number is reduced, as is in the case of the mir-31a mutants [4]. [score:3]
Cdk9 was able to restore the number of glia in mir-31a mutant brains to levels observed in an otherwise wildtype control animal, where Repo-Gal4 was used to drive the expression of UAS-GFP. [score:3]
I also show that the expression of cdk9 in adult glia can prevent the glial loss observed in mir-31a mutants. [score:3]
There was no significant difference in the number of glia between mir-31a mutants and in the genotype where cdk9 was knocked down. [score:2]
In the mir-31a mutants, flies eclose with the same number of glia but suffer significant glial loss by 7d post-eclosion [4]. [score:1]
The mir-31a mutant used was generated as described in ref. [score:1]
This shows that it is loss of cdk9 in adult glia that is the likely reason for the glial loss observed in mir-31a mutants. [score:1]
mir-31a mutants have fewer glia in the 7d old adult brains due to aberrant inheritance of CG16947 by the progeny [4]. [score:1]
The flies were processed 1d post-eclosion as it had previously been shown that the mir-31a mutant animals eclose with the same number of glia but lose their glia by 7d of age. [score:1]
Taken together, the genetic results and the biochemistry suggest that the subsequent ubiquitination and degradation of cdk9 due to excessive inheritance of CG16947 by the progeny in mir-31a mutants, is the likely cause for glial cell death in these mutants. [score:1]
This data suggests that cdk9 acts downstream of mir-31a in the progeny to control glial cell survival. [score:1]
This demonstrates that knocking down of cdk9 in glia is detrimental not to gliogenesis, but to the survival of glia in the adult, just as what was shown in Foo et al. 2017 where fewer glia were seen in 7d old mir-31a mutant adults, but no difference was observed in 2d old animals when compared to age-matched control animals [4]. [score:1]
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2
[+] score: 19
Other miRNAs from this paper: cel-let-7, dme-mir-31b, dme-let-7
In addition to the transcription regulators, such as CREM (cAMP-responsive element modulator), CREB1 (CREM -binding protein 1) and NFAT (NFκB, AP1 and nuclear factor of activated T-cells), it was shown that miR-31, downregulated in SLE T-cells, could repress the expression of RhoA, a negative regulator of NFAT, and was responsible for impaired IL2 expression [79, 80]. [score:10]
miRNA Target Regulated Process let-7a IL6 IL6 induction[65] let-7c Blimp1, SOCS1 Activation of DCs[64] miR-125a KLF13 CCL5 induction in T-cells[81] miR-126 DNMT1 DNA methylation in T-cells[73] miR-146a TRAF6, IRAK1 NFκB mediated inflammatory response[53] TRAF6, IRAK1, IRAK2 RIG-I -dependent anti-viral pathway[54] IRF5, STAT1 Type I IFN induction and signaling[55] miR-148a DNMT1 DNA methylation in T-cells[71] miR-150 SOCS1 Renal fibrosis[94] miR-155 MyD88, TAB2 TLR/IL1 inflammatory pathway[57, 58] SOCS1 Type I IFN signaling[59] PP2Ac IL2 induction[110] miR-155* IRAKM Type I IFN induction[60] miR-17~92 PTEN, Bim Proliferation of lymphocytes[84] Rora, PHLPP2 Differentiation and function of Tfh cells[85, 86] miR-21 RASGRP1 DNA methylation in T-cells[71] miR-23b TAB2, TAB3, IKKα IL17, TNFα, IL1β signaling[91] miR-29b Sp1 DNA methylation in T-cells[74] miR-30a Lyn Activation of B-cells[87] miR-31 RhoA IL2 induction in T-cells[80] miR-3148 TLR7 TLR7 inflammatory pathway[63] As we are still at the early stage of the exploration of miRNA’s essential roles in SLE pathogenesis, there are many unresolved questions. [score:4]
Moreover, the expression of miR-31 was inversely correlated with RhoA in SLE patients [80]. [score:3]
Fan W. Liang D. Tang Y. Qu B. Cui H. Luo X. Huang X. Chen S. Higgs B. W. Jallal B. Identification of microRNA-31 as a novel regulator contributing to impaired interleukin-2 production in t cells from patients with systemic lupus erythematosus Arthritis Rheumatol. [score:2]
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3
[+] score: 4
These included miR-SPs targeting bantam, miR-1, the K-box family (miR-2b, miR-2c and miR-13b displayed strong phenotypes; miR-2a and miR-13a were flight impaired but fell below our stringent cutoff; ), miR-7, the miR-31 family, miR-34, miR-190, miR-957, miR-986, miR-987 and miR-1001. [score:3]
Recent studies suggest that vertebrate orthologues for several of the conserved miRNAs required for muscle maintenance in our screen (miR-1, miR-7, miR-31 and miR-34, and the K-box orthologue miR-23) are associated with muscle physiology in vertebrate species (Supplementary Table 1). [score:1]
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4
[+] score: 4
The final wave, represented by CoMod-C, is expressed in late embryos and post-embryonic development and involves bantam, Mir-1, Mir-8, Mir-278, Mir- 281, Mir-252 and Mir-31. [score:4]
[1 to 20 of 1 sentences]
5
[+] score: 3
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]
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6
[+] score: 1
In the 15 missed reference pre-miRNAs, 4 did not pass the pre-processing filter due to their predicted double-loop structures (mir-2c, mir-31a, mir-31b, mir-286) and another 2 due to their low predicted free energy (mir-309, mir-311). [score:1]
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7
[+] score: 1
We did not find mir-242 and mir-216, which are also lost in other arthropods, nor mir-31, which is not found in the chelicerate family of Ixodidae, or the mandibulate-specific mir-282 or mir-965 (Rota-Stabelli et al. 2011; Tarver et al. 2013). [score:1]
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8
[+] score: 1
Likewise, miR-31a (Fig. 3F) might also exhibit low amplitude cycling similar to that of miR-124. [score:1]
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