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Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (RNA-seq)

ABSTRACT: Ribosomal-depleted total RNA was isolated from neuronal cultures transduced with different shRNA constructs direct against shNogoA with and without mismatches in the seed region

ORGANISM(S): Mus musculus

PROVIDER: GSE156878 | GEO | 2020/12/31

REPOSITORIES: GEO

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Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (miRNA-seq)

Project description:Small RNA was isolated from neuronal cultures transduced with different shRNA constructs direct against shNogoA with and without mismatches in the seed region

2020-12-31 | GSE156879 | GEO

Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-31 | GSE156880 | GEO

Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes

Project description:Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes

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Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (RNA-seq)

Project description:Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (RNA-seq)

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Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (miRNA-seq)

Project description:Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (miRNA-seq)

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Transcriptomic effects of forced expression of FOXO3, PRDM1⍺ and PRDM1β in pre-B ALL cell line 697 [exp1]

Project description:Lentiviral constructs expressing candidate tumoure suppressor genes were transduced into 697 cells. Of the candidates FOXO3, two isoforms of PRDM1 (⍺ and β) suppressed growth in-vitro and in-vivo. To indentify tumour suppressor mechanisms we extracted RNA from triplicate 697 cultures four days after transduced with empty vector (SIN-SIEW) or constructs expressing FOXO3, PRDM1⍺ or PRDM1β. Approximately 90 million 100bp paired-end reads were generated per sample by illumina sequencing.

2022-10-01 | GSE193347 | GEO

Asymmetric bulges within hairpin RNA transgenes influence small RNA size, secondary siRNA production and viral defence II

Project description:Small RNAs (sRNAs) are essential for normal plant development and range in size classes of 21-24 nucleotides. The 22nt small interfering RNAs (siRNAs) and miRNAs are processed by Dicer-like 2 (DCL2) and DCL1 respectively and can initiate secondary siRNA production from the target transcript amplifying the silencing signal in plants. 22nt siRNAs are under-represented due to competition with DCL4, while only a small number of 22nt miRNAs exist due to the rare occurrence of an asymmetric bulge in the precursor miRNA stem. Here we report a strategy to produce abundant 22nt siRNAs and other desired siRNA size classes using long hairpin RNA (hpRNA) transgenes. By introducing asymmetric bulges periodically into the antisense strand of hpRNA, we successfully shifted the dominant siRNA size class from 21nt of the traditional hpRNA to 22, 23 and 24nt of the asymmetric hpRNAs. We showed that the asymmetric hpRNA constructs effectively silenced a β-glucuronidase (GUS) reporter transgene and the endogenous ethylene insensitive-2 (EIN2) and chalcone synthase (CHS) genes. Furthermore, plants containing the asymmetric hpRNA transgenes targeting both GUS and EIN2 showed increased amount of 21nt siRNAs downstream of the hpRNA target site compared to plants with the traditional hpRNA transgenes. This indicates that these asymmetric hpRNAs are more effective at inducing secondary siRNA production to amplify silencing signals. Consistent with the production of secondary siRNAs, the 22nt asymmetric hpRNA constructs increased gene silencing phenotypes and enhanced virus resistance in plants compared to the traditional hpRNA constructs.

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Asymmetric bulges within hairpin RNA transgenes influence small RNA size, secondary siRNA production and viral defence I

2024-06-27 | GSE243255 | GEO

Proteomic and Phosphoproteomic Landscapes of Acute Myeloid Leukemia

Project description:Mass spectrometry results from TurboID experiments using constructs expressing TurboID only, NPM1wt-Turbo ID (N- and C-terminal fusions) and NPMc-Turbo ID fusions (N- and C-terminal fusions) transduced in primary mouse hematopoietic stem/progenitor cells from lineage-depleted mouse bone marrow.

2022-03-09 | MSV000089028 | MassIVE

DAAM2 Variants Cause Nephrotic Syndrome via Actin Dysregulation.

Project description:The discovery of >60 monogenic causes of nephrotic syndrome (NS) has revealed a central role for the actin regulators RhoA/Rac1/Cdc42 and their effectors, including the formin INF2. By whole-exome sequencing (WES), we here discovered bi-allelic variants in the formin DAAM2 in four unrelated families with steroid-resistant NS. We show that DAAM2 localizes to the cytoplasm in podocytes and in kidney sections. Further, the variants impair DAAM2-dependent actin remodeling processes: wild-type DAAM2 cDNA, but not cDNA representing missense variants found in individuals with NS, rescued reduced podocyte migration rate (PMR) and restored reduced filopodia formation in shRNA-induced DAAM2-knockdown podocytes. Filopodia restoration was also induced by the formin-activating molecule IMM-01. DAAM2 also co-localizes and co-immunoprecipitates with INF2, which is intriguing since variants in both formins cause NS. Using in vitro bulk and TIRF microscopy assays, we find that DAAM2 variants alter actin assembly activities of the formin. In a Xenopus daam2-CRISPR knockout model, we demonstrate actin dysregulation in vivo and glomerular maldevelopment that is rescued by WT-DAAM2 mRNA. We conclude that DAAM2 variants are a likely cause of monogenic human SRNS due to actin dysregulation in podocytes. Further, we provide evidence that DAAM2-associated SRNS may be amenable to treatment using actin regulating compounds.

| S-EPMC7820625 | biostudies-literature

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