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Chromatin accessibility changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [ATAC-seq]

ABSTRACT: Chromatin accessibility changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [ATAC-seq]

PROVIDER: PRJNA821880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18560344_1.fastq.gz	Fastqsanger.gz
	SRR18560344_2.fastq.gz	Fastqsanger.gz
	SRR18560345_1.fastq.gz	Fastqsanger.gz
	SRR18560345_2.fastq.gz	Fastqsanger.gz
	SRR18560346_1.fastq.gz	Fastqsanger.gz

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Transcriptomic changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [RNA-seq]

Project description:Long non-coding RNAs (lncRNAs) are molecular switches in cellular differentiation, movement and in the reprogramming of cell states by altering gene expression patterns. However, in endothelial cells their role is not well understood. LINC00607 is an endothelial-enriched lncRNA. In order to uncover the functional relevance of LINC00607, an endothelial lentiCRISPR/Cas9-mediated knock-out was created and subjected to RNA- and ATAC-Seq, which revealed that LINC00607 is important for many pathways, among them VEGF- and TGF-beta-signalling.

2023-01-09 | GSE199877 | GEO

Chromatin accessibility changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [ATAC-seq]

2023-01-09 | GSE199876 | GEO

Transcriptomic changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [RNA-seq]

Project description:Transcriptomic changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [RNA-seq]

| PRJNA821879 | ENA

ATAC-seq and RNA-seq after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC

Project description:ATAC-seq and RNA-seq after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC

| PRJNA821874 | ENA

LINC00607 is essential to maintain the endothelial phenotype through SWI/SNF chromatin remodeler BRG1

Project description:Long non-coding RNAs (lncRNAs) are regulatory RNAs, which by altering gene expression impact on the cellular phenotype and cardiovascular disease development. The pool of endothelial lncRNAs and their vascular function is largely undefined. Deep-endothelial RNA-Seq and FANTOM5 CAGE analysis revealed LINC00607 as a specifically enriched and highly expressed lncRNA in human endothelial cells. LINC00607 was induced in response to hypoxia, arteriosclerosis regression in non-human primates and also in response to propranolol used to induce regression of human arteriovenous malformations. siRNA Knockdown or CRISPR/Cas9 knockout of LINC00607 attenuated VEGF-A-induced angiogenic sprouting. LINC00607 knockout HUVEC also integrated less into newly formed vascular networks in an in vivo assay in SCID mice. Overexpression of LINC00607 in CRISPR knockout cells restored the normal function. RNA- and ATAC-Seq of the LINC00607 knockout revealed changes in transcription of endothelial gene sets particularly linked to the endothelial phenotype. This was most likely the consequence of a reduced chromatin accessibility of the ERG binding motif. Mechanistically, LINC00607 interacts with the SWI/SNF chromatin remodeling protein BRG1. CRISPR/Cas9-mediated knockout of BRG1 in HUVEC followed by CUT&RUN revealed that BRG1 is required to secure a stable chromatin state, mainly on ERG-binding sites. In conclusion, LINC00607 is a highly expressed endothelial-specific lncRNA important for efficient endothelial gene transcription through sustaining ERG target gene transcription by interaction with the chromatin remodeler BRG1.

2023-01-09 | GSE201824 | GEO

METTL21B is a novel human lysine methyltransferase of translation elongation factor 1A: discovery by CRISPR/Cas9 knock out

Project description:Lysine methylation is widespread on human proteins, however the enzymes that catalyse its addition remain largely unknown. This limits our capacity to study the function and regulation of this modification. Here we report that human METTL21B is a protein methyltransferase, which methylates lysine 165 of eukaryotic translation elongation factor 1A (eEF1A). The CRISPR/Cas9 system was used to knock out putative protein methyltransferases METTL21B and METTL23 in K562 cells. The known eEF1A methyltransferase EEF1AKMT1 was also knocked out as a control. Targeted mass spectrometry revealed the loss of lysine 165 methylation upon knock out of METTL21B, and the expected loss of lysine 79 methylation on knock out of EEF1AKMT1. No loss of eEF1A methylation was seen in the METTL23 knock out. Recombinant METTL21B was then shown to catalyse methylation on lysine 165 in eEF1A1 and eEF1A2 in vitro, confirming it as the methyltransferase responsible for this methylation site. Stable isotope labelling by amino acids in cell culture (SILAC) proteomic analysis revealed dysregulation of processes related to eEF1A function in knock outs of METTL21B and EEF1AKMT1, but specific dysregulation of ribosomal proteins in the knock out of METTL21B. This indicates a specific function for lysine 165 methylation of eEF1A in human. METTL21B is specific to vertebrates, with its target lysine showing similar evolutionary conservation. We suggest METTL21B be renamed eEF1A-KMT3. This is the first study to specifically generate CRISPR/Cas9 knock outs of the genes encoding putative protein methyltransferases, for the purpose of substrate discovery and site mapping. Our approach should prove useful for the discovery of further novel methyltransferases, and more generally for the discovery of sites for other protein-modifying enzymes.

2017-07-03 | PXD005497 | Pride

ATAC-seq and RNA-seq after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC

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

2023-01-09 | GSE199878 | GEO

Transcriptome network analysis of Smug1 knock-out cells by using CRISPR/Cas9 system

Project description:Transcriptome network analysis of Smug1 knock-out cells by using CRISPR/Cas9 system

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High-throughput screens of PAM-flexible Cas9 variants for gene knock-out and transcriptional modulation

Project description:A key limitation of the commonly-used CRISPR enzyme S. pyogenes Cas9 is the strict requirement of an NGG protospacer-adjacent motif (PAM) at the target site, which reduces the number of accessible genomic loci. This constraint can be limiting for genome editing applications that require precise Cas9 positioning. Recently, two Cas9 variants with a relaxed PAM requirement (NG) have been developed (xCas9 and Cas9-NG) but their activity has been measured at only a small number of endogenous sites. Here we devised a high-throughput Cas9 pooled competition screen to compare the performance of both PAM-flexible Cas9 variants and wild-type Cas9 at thousands of genomic loci and across 3 modalities (gene knock-out, transcriptional activation and suppression). We show that PAM flexibility comes at a substantial cost of decreased DNA targeting and cutting. Of the PAM-flexible variants, we found that Cas9-NG outperforms xCas9 regardless of genome engineering modality or PAM. Finally, we combined xCas9 mutations with those of Cas9-NG, creating a stronger transcriptional modulator than existing PAM-flexible Cas9 variants.

2020-01-26 | GSE143892 | GEO

CRISPR/Cas9 knock down line

Project description:CRISPR/Cas9 knock down line

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