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

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

PROVIDER: PRJNA478037 | ENA |

REPOSITORIES: ENA

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

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

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

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

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scATAC-seq of mouse Plasmodium-specific CD4+ T cells

Project description:Plasmodium-specific CD4+ T cells from mice infected with Plasmodium chabaudi chabaudi AS parasites were recovered at Days 0, 4, 7, and 32 to undergo processing and to generate scATAC-seq dataset. At Day 7, CXCR5+ and CXCR6+ cells were recovered separately. At Day 32, mice were administered with either saline or artesunate (intermittent artesunate therapy - IAT). scATAC-seq dataset was analysed to investigate epigenomic landscapes of CD4+ T cells from effector to memory states.

2020-10-14 | E-MTAB-9402 | biostudies-arrayexpress

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.

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