7 publications mentioning dre-mir-205

Open access articles that are associated with the species Danio rerio and mention the gene name mir-205. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1

Four different morpholinos were designed to inhibit miR-205 biogenesis: two targeting the Drosha cleavage site complementary to either the 5′ or 3′ arm of the stem, and two morpholinos similarly targeting the Dicer cleavage site (Figure S1).

We decided to test this strategy on miR-205, since it is expressed relatively early, and there are only two, but identical, copies in the fish genome.

Again, we could not detect mature miR-205 derived from this construct after targeting by morpholinos (Figure 2D).

Together, this indicates that these morpholinos inhibit primary miRNA processing and result in primary miRNA accumulation, as we described for miR-205.

Design of Morpholinos Targeting the miR-205 Precursor.

These morpholinos were injected under similar conditions as described for miR-206 and compared to the morpholino targeting mature miR-205.

Therefore, we injected a miR-205 precursor in the one-cell–stage embryo.

After incubation for 8 h, RNA was isolated and subjected to Northern blot analysis to probe for injected miR-206 and injected miR-205.

After isolation, samples were analyzed by Northern blotting for the presence of miR-206 and miR-205.

Pri-miR-205 is positioned just upstream of the polyA signal in the 3′ UTR of the GFP mRNA.

miR-205 serves as a loading control.

A construct containing pri-miR-205 was made by amplifying a genomic region (801 base pairs) containing the miR-205 precursor (miR-205-hairpinF ggcattgaattcataaCCTCTTACCTGCATGACCTG; miR-205-hairpinR ggcatttctagaGTGTGTGCGTGTATTCAACC).

Therefore, we injected a mature miR-206 and a control duplex (miR-205) together with a morpholino against miR-206 in the embryo.

Interestingly, the miR-205 precursor also could not be detected in the embryos co -injected with morpholinos, whereas pre-miR-205 could be detected in the absence of morpholinos (Figure 2D).

Interestingly, all five morpholinos induced complete or near-complete loss of miR-205 (Figure 2B).

Because pri-miR-205 was cloned in the 3′ UTR of GFP, we monitored GFP fluorescence after injection of this construct.

To examine the effect of a morpholino on the isolation of a mature miRNA, we incubated a mature miR-206 duplex and a control duplex (miR-205) with a morpholino against miR-206 in vitro.

Therefore, we performed reverse transcriptase PCR (RT-PCR) on 8-h-old embryos injected with GFP-pri-miR-205 and a control mRNA (luciferase) (Figure 2F).

2

This network visualization shows that (1) all modules contain at least 2 genes that are predicted targets of a deregulated miRNA identified in this study, except the module “Apoptosis and NAFLD”; (2) dre-miR-2189, the only DE miRNA that was downregulated, targets many genes in modules that are predominantly upregulated such as Cell cycle (4 target mRNAs), Apoptosis and Autophagy (19 targets), Epigenetics and Apoptosis/Autophagy (2 targets) and Receptors (4 targets); (3) certain miRNAs have only 1 target gene in the selected modules, including dre-miR-184 (“Oxidative phosphorylation”), dre-miR-430a and dre-miR-430b (“Apoptosis and Autophagy”); (4) while other miRNAs have common target genes in the same modules, i. e., dre-miR-725/dre-miR-724/dre-miR-193a, dre-miR-202, dre-miR-205 and dre-miR-133a that have several common target genes in modules “Oxidative phosphorylation and NAFLD”, “Apoptosis/Autophagy”, “NAFLD” and “Cell cycle”.

3

Given that recent studies have reported that the microRNA-200 family and miR-205 regulate EMT by targeting ZEB-1 and SIP-1, we examined whether the expression of members of the microRNA-200 family and miR-205 were up-regulated prior to repression of ZEB-1 and SIP-1 expression in ERβ1 -expressing cells [16].

In contrast to the cluster of miR-200b-200a-429, the cluster miR-200c-141 and the miR-205 were unchanged in ERβ1 -expressing MDA-MB-231 cells (Additional file 9, Figure S5).

Regulation of miR-200c, miR-141 and miR-205 by ERβ1.

The figure shows the regulation of miR-200c, miR-141 and miR-205 by ERβ1.

4

By contrast, we identified 12 miRNAs corresponding to 9 families (miR-199, miR-140, miR-152, miR-214, miR-205, miR-200, miR-183, miR-182, miR-96) that displayed highly enriched expression in the olfactory system (Figure 1A).

Five of 24 probes, including miR-449 and miR-205, displayed expression limited to the nonneural respiratory epithelium (Figure 2A, left column, and Table S3).

5

The mutated miR-184 antagonizes miR-205 to maintain the expression of the inositol polyphosphate phosphatase-like 1 (INPPL1) gene, which generates the disease phenotype [19].

6

Venn diagrams depicting the distribution of miR-205/181c, miR-725, miR16/138, miR-203a/b predicted targets (middle panel).

7

The most abundant miRs expressed in the developing mouse OE are: the miR-200-class (- 200a, - 200b, - 200c, - 141 and - 429), miR-199, miR-152, miR-214, miR-205, miR-183, miR-182 and miR-96 (Choi et al., 2008).