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Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Bulk ATAC-seq]

ABSTRACT: Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Bulk ATAC-seq]

PROVIDER: PRJNA478036 | ENA |

REPOSITORIES: ENA

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Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [scATAC-seq]

Project description:Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [scATAC-seq]

| PRJNA478037 | ENA

Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Perturb-ATAC (ATAC)]

Project description:Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Perturb-ATAC (ATAC)]

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Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Bulk ATAC-seq]

Project description:Here we present Perturb-ATAC, a method which combines multiplexed CRISPR interference or knockout with genome-wide chromatin accessibility profiling in single cells, based on the simultaneous detection of CRISPR guide RNAs and open chromatin sites by Assay of Transposase-accessible Chromatin with sequencing (ATAC-seq). We applied Perturb-ATAC to transcription factors (TFs), chromatin-modifying factors, and noncoding RNAs (ncRNAs) in ~3,700 single cells, encompassing more than 75 unique genotype-phenotype relationships.

2018-12-20 | GSE116247 | GEO

Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [scATAC-seq]

2018-12-20 | GSE116248 | GEO

Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Perturb-ATAC (ATAC)]

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Coupled single-cell CRISPR screening and epigenomic profiling reveals causal gene regulatory networks

Project description:Coupled single-cell CRISPR screening and epigenomic profiling reveals causal gene regulatory networks

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Coupled single-cell epigenome editing and profiling reveals causal gene regulatory networks [Perturb-ATAC (GBC/sgRNA)]

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Improving disease resistance in plants by editing the epigenome

Project description:Pathogens rely on expression of host susceptibility (S) genes to promote infection and disease. DNA methylation is an epigenetic modification that affects gene expression. Theoretically, blocking access to S genes through targeted methylation could increase disease resistance. Xanthomonas axonopodis pv. manihotis, the causal agent of cassava bacterial blight (CBB), uses transcription activator-like20 (TAL20) to induce expression of the S gene MeSWEET10a. We directed methylation to the TAL20 effector binding element within the MeSWEET10a promoter using a synthetic zinc-finger DNA binding domain fused to a component of the RNA-directed DNA methylation pathway. We demonstrate that this methylation prevents TAL20 binding, blocks transcriptional activation of MeSWEET10a and that these plants display increased resistance to CBB. This work establishes epigenome editing as a new strategy for crop improvement.

2022-12-08 | GSE187022 | GEO

Epigenome Editing by CRISPR/Cas9 Repressors for Silencing of Distal Regulatory Elements

Project description:Epigenome editing with the CRISPR/Cas9 platform is a promising technology to modulate gene expression to direct cell phenotype and to dissect the causal epigenetic mechanisms that direct gene regulation. Fusions of the nuclease-inactive dCas9 to the KRAB repressor domain (dCas9-KRAB) can effectively silence target gene expression. We targeted dCas9-KRAB to the HS2 enhancer, a distal regulatory element that orchestrates the expression of multiple globin genes. Genome-wide analyses demonstrated that localization of dCas9-KRAB to HS2 specifically induced H3K9 tri-methylation (H3K9me3) at that enhancer and reduced the chromatin accessibility of both the enhancer and its promoter targets. Targeted epigenetic modification of HS2 silenced the expression of multiple globin genes, with minimal off-target changes in gene expression. These results demonstrate that repression mediated by dCas9-KRAB is sufficiently specific to disrupt the activity of individual enhancers via local modification of the epigenome. This approach enables precise modulation of epigenetic function without modifying the underlying genome sequence.

2015-10-19 | GSE71557 | GEO

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