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

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

PROVIDER: PRJNA613058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11303716_1.fastq.gz	Fastqsanger.gz
	SRR11303716_2.fastq.gz	Fastqsanger.gz
	SRR11303717_1.fastq.gz	Fastqsanger.gz
	SRR11303717_2.fastq.gz	Fastqsanger.gz
	SRR11303718_1.fastq.gz	Fastqsanger.gz

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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.

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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)

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

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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: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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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.

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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)

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

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Astrocytic EphA4 signaling is important for the elimination of excitatory synapses in Alzheimer’s disease

Project description:Cell surface receptors, including erythropoietin-producing hepatocellular A4 (EphA4), are important in regulating hippocampal synapse loss, which is the key driver of memory decline in Alzheimer’s disease (AD). However, the cellular-specific roles and mechanisms of EphA4 are unclear. Here, we show that EphA4 expression is elevated in hippocampal CA1 astrocytes in AD conditions. Specific knockout of astrocytic EphA4 ameliorates excitatory synapse loss in the hippocampus in AD transgenic mouse models. Single-nucleus RNA sequencing analysis revealed that EphA4 inhibition specifically decreases a reactive astrocyte subpopulation with enriched complement signaling, which are characteristics associated with synapse elimination by astrocytes in AD. Importantly, astrocytic EphA4 knockout in an AD transgenic mouse model decreases complement tagging on excitatory synapses and excitatory synapses within astrocytes. These findings suggest an important role of EphA4 in the astrocyte-mediated elimination of excitatory synapses in AD and highlight the crucial role of astrocytes in hippocampal synapse maintenance in AD.

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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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