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CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (CLIP-Seq dataset)

ABSTRACT: CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (CLIP-Seq dataset)

PROVIDER: PRJNA613063 | ENA |

REPOSITORIES: ENA

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CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (TRAP-Seq dataset)

Project description:Quaking RNA binding protein(QKI) is essential for oligodendrocyte development as myelination requires MBP mRNA regulation and localization to distal processes by its cytoplasmic isoforms(e.g. QKI-6). QKI-6 is also highly expressed in astrocytes, which we and others recently demonstrated have regulated mRNA localization. Here, we show via CLIPseq that QKI-6 binds 3’UTRs of a subset of astrocytic mRNAs, including many enriched in peripheral processes. Binding is enriched near stop codons, which is mediated partially by QKI binding motifs(QBMs) yet spreads to adjacent sequences. We developed CRISPR TRAPseq: a viral approach for mosaic, cell-type specific gene mutation with simultaneous translational profiling. This enabled study of QKI-6 CLIP targets in QKI-deleted astrocytes in an otherwise normal brain. Astrocyte-targeted QKI deletion altered translation and maturation, while also increasing synaptic density within the astrocyte's territory. Overall, our data indicate QKI is required for astrocyte maturation and demonstrate an approach for a highly targeted translational assessment of gene knockout in specific cell-types in vivo.

2021-01-21 | GSE146935 | GEO

CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses

Project description:CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses

| PRJNA613058 | ENA

CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (TRAP-Seq dataset)

Project description:CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (TRAP-Seq dataset)

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Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

Project description:To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor. The RBP QKI was depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.

2010-05-27 | E-GEOD-21574 | biostudies-arrayexpress

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

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Transcriptome-wide HITS-CLIP of Quaking (QKI) in TGF-Beta-treated HMLE (Mesenchymal-like) cells

Project description:Members of the miR-200 family are critical gatekeepers of the epithelial state, restraining expression of pro-mesenchymal genes that drive epithelial-mesenchymal transition (EMT) and contribute to metastatic cancer progression. Here, we show that miR-200c and another epithelial-enriched miRNA, miR-375, exert widespread control of alternative splicing in cancer cells. This is achieved by their strong suppression of the RNA binding protein Quaking (QKI), which is required to mediate the splicing changes regulated by these miRNAs. During EMT, QKI-5 directly binds to and regulates hundreds of alternative splicing events and exerts pleiotropic effects, such as increasing cell migration and invasion and restraining tumour growth, without appreciably affecting mRNA levels. QKI-5 is both necessary and sufficient to direct EMT alternative splicing changes, and this splicing signature is broadly conserved across many epithelial-derived cancer types. Importantly, several actin cytoskeleton-associated genes are directly targeted both by QKI and miR-200c, revealing coordinated control of alternative splicing and mRNA abundance during EMT. These findings demonstrate the existence of a miR-200/miR-375/QKI axis that impacts cancer-associated epithelial cell plasticity through widespread control of alternative splicing. The purpose of the CLIP experiment was to determine direct targets of QKI.

2018-03-15 | GSE111188 | GEO

CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (CLIP-Seq dataset)

Project description:We immunoprecipitated QK-6 from P21 mouse brains to identify which mRNAs QK-6 binds to in vivo.

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Sequencing data of Photoactivatable Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation (PAR-CLIP) of QKI-5 and QKI-6

Project description:This study was designed to look for the RNAs that directly bind with QKI

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QKI and miR-155 in inflammation and leukemogenesis

Project description:Transcription profiling by array of siRNA against Quaking (QKI) transcripts to identify transcripts that are modulated by QKI activity. MiR-155 is an oncogene and we report here that it targets QKI transcripts. Therefore, we believe that QKI acts as a tumor suppressor gene in different leukemias. We ablated the expression of QKI transcripts using siRNAs in order to further elucidate the effects of QKI in leukemogenesis, and how miR-155 and QKI functionally interact with each other.

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CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses

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

2021-01-21 | GSE147121 | GEO