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Human Microglial State Dynamics in Alzheimer's Disease Progression [scRNA-seq]

ABSTRACT: In this study, we derived iPS-derived microglia-like cells (iMGLs) from a healthy donor (Sample: Control) CRISPR engineered to carry a dead CAS9 fused to the transcriptional repressor KRAB (dCAS9-KRAB) and treated these cultures with the pro-inflammatory stimulant LPS (Sample: LPS).

ORGANISM(S): Homo sapiens

PROVIDER: GSE227222 | GEO | 2023/09/28

REPOSITORIES: GEO

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Human Microglial State Dynamics in Alzheimer's Disease Progression [RNA-seq]

Project description:In this study, we derived iPS-derived microglia-like cells (iMGLs) from a healthy donor (Sample: Control) CRISPR engineered to carry a dead CAS9 fused to the transcriptional repressor KRAB (dCAS9-KRAB) and treated these cultures with pre-formed amyloid beta 1-42 fibrils. We then performed gene expression profiling analysis using data obtained from RNA-seq of treated and untreated cells at 4 different time points.

2023-09-28 | GSE227221 | GEO

RNA-seq of CSMD1 enhancer CRISPRi in LUHMES cells and differentiated neurons

Project description:we performed lentiviral CRISPR interference (CRISPRi) by recruiting dCas9 fused with the KRAB domain to the CSMD1 enhancer (fam3) in the neuronal precursor cell line – Lund human mesencephalic (LUHMES). Given that the expression of CSMD1 was not detectable in LUHMES cells we differentiated these cells into neurons. Differentiated neurons with CRISPRi of CSMD1 enhancer showed significantly higher expression of CSMD1 than control.

2022-06-30 | E-MTAB-8027 | biostudies-arrayexpress

Identification of a novel enhancer of CEBPE essential for granulocytic differentiation

Project description:RNA-Seq of Control, dCas9-KRAB-EV, dCas9-KRAB-sg2 and dCas9-KRAB-sg5

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Single-cell profiling of cell cultures during endoMT induction.

Project description:Single-cell RNA sequencing (scRNAseq) data from EndoMT Day 1 dcas9-KRAB-MeCP2 (KRAB Control Day1), EndoMT Day 3 dcas9-KRAB-MeCP2 (KRAB Control Day3), and EndoMT Day 3 dcas9-KRAB-MeCP2 + rs117430032 gRNA (rs117430032i) cells.

2022-12-16 | GSE193206 | GEO

RNA-seq following enhancer repression

Project description:Using RNA-seq to identify genes regulated by dCas9-KRAB mediated enhancer repression in NCI-H2009 lung adenocarcinoma cells NCI-H2009 cells were first transfected with dCas9-KRAB fusion and subsequently transfected with no guide RNA (Empty), a guide RNA that has no target in the human genome (Dummy), and two separate guide RNAs (e3 #1 and e3 #2) recognizing the enhancer region of our study.

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A novel role of CDK2 inhibition in restraining microglial overactivation

Project description:Neuroinflammation driven by microglial overactivation is a significant contributor across a diverse range of neurological disorders. While MEF2C mutations have been associated with a syndromic form of autism spectrum disorder (ASD) and various other neurological disorders in humans, the role of MEF2C as a key immune checkpoint to restrain microglial overactivation remains elusive. In this study, we established MEF2C-knockout (KO) induced microglia-like cells (iMGLs) via differentiation of corresponding human pluripotent stem cells, and subsequently treated with LPS, as a disease model of overactivated microglia. Through high-throughput screening, we identified BMS265246, a CDK2 inhibitor, which effectively normalized overactivated phenotypes in LPS-stimulated MEF2C-KO iMGLs, nearing levels seen in WT counterparts. Mechanistically, absence of MEF2C instigated a sequential cascade encompassing p21 downregulation, CDK2 activation, RB phosphorylation and degradation, and NF-κB p65 subunit nuclear translocation, thereby intensifying inflammatory responses. Remarkably, BMS265246 treatment significantly rectified microglial overactivation and ASD behavioral defects in both global and microglia-specific Mef2C heterozygous mice. Overall, our findings elucidate a novel protective mechanism governed by MEF2C, and unveil CDK2 as a promising therapeutic target for treating various diseases influenced by overactivated microglia with aberrant MEF2C expression and/or CDK2 activation.

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Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

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2024-03-07 | GSE222689 | GEO

CUT&RUN-seq of H3K9me3, H4K20me3 or H3K4me3 in mESC after epigenetic editing and upon release of the trigger

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2021-11-23 | E-MTAB-10525 | biostudies-arrayexpress

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 | GSE70671 | GEO

Highly specific epigenome editing by CRISPR-Cas9 repressors for silencing of distal regulatory elements

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