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Expression data from HeLa cells transfected with 3'-mivaRNAII-138 mimic.

ABSTRACT: The adenovirus (Ad) serotype 5 genome encodes two non-coding small RNAs (virus-associated RNAs: VA-RNAI and II), which are approximately 160nt-long RNAs transcribed by RNA polymerase III. Recent studies revealed that VA-RNAs are processed into VA-RNA-derived microRNAs (miRNAs) (mivaRNAI, II); however, we and another group recently demonstrated that mivaRNAI does not promote Ad replication. On the other hand, roles of VA-RNAII and VA-RNAII-derived miRNA (mivaRNAII) in Ad replication have remained to be clarified. In this study, we showed mivaRNAII-mediated promotion of Ad replication. Transfection with chemically synthesized 3'-mivaRNAII-138, one of the most abundant mivaRNAII, significantly enhanced Ad replication, while the other species of mivaRNAII did not. We used microarrays to detail gene expression profiles in HeLa cells transfected with 3'-miaRNAII-138 mimic and demonstarted that expression levels of various genes were down- or up-regulated following transfection with 3'-mivaRNAII-138 mimic.

ORGANISM(S): Homo sapiens

PROVIDER: GSE96531 | GEO | 2018/10/11

REPOSITORIES: GEO

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Project description:MicroRNAs (miRNAs) play roles in diverse developmental and disease processes. Distinct miRNAs have hundreds to thousands of conserved mRNA binding sites, but typically direct only modest repression via single sites. Cotargeting of individual mRNAs by different miRNAs could potentially achieve stronger and more complex patterns of repression. Comparing target sets of different miRNAs, we identified hundreds of pairs of miRNAs that share more mRNA targets than expected (often by two-fold or more) relative to stringent controls, with particularly high levels of cotargeting among brain-enriched miRNAs. We profiled miRNA expression changes over a cell culture model of neuronal differentiation, and selected the non-homologous cotargeting miRNA pair miR-138 and miR-137 to study functionally. We generated a CRISPR-mediated mir-138 double knockout (DKO) cell line in the murine CAD cell culture model of neuronal differentiation. mir-138 DKO cells lacking both mir-138 loci were unable to differentiate and project neurites following serum withdrawal. Further characterization of the DKO cells by RNA-seq showed that loss of miR-138 resulted in a de-differentiated state compared to WT cells. Specificity of the mir-138 DKO was confirmed by the rescue of neurite growth upon addition of a miR-138 mimic. Interestingly, addition of a miR-137 mimic, but not mimics of other neuronal miRNAs, could also rescue the neurite growth phenotype and allow mir-138 DKO cells to differentiate, and transcriptome profiling revealed similar gene expression changes. Clustering of all cotargeting pairs revealed a group of 9 predominantly brain-enriched miRNAs that share many targets. In reporter assays, subsets of these miRNAs together repressed gene expression by 5- to 10-fold, often exhibiting cooperative repression. Together, our results uncover an unexpected pattern in which combinations of miRNAs collaborate to robustly repress cotargets, and suggest important developmental roles for cotargeting.

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Expression data from HeLa cells transfected with 3'-mivaRNAII-138 mimic.

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