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Hi-C of the K562 cells with CRISPR-Cas9 KO of either HUB162 or HUB161

ABSTRACT: HUB162 (chr11:42,878,450-42,883,450, hg38) was identified as an essential locus in the quiescent region in the K562 cells, and HUB161 (chr11:42,873,450-42,878,450, hg38) as a nonessential one. We used Arima Hi-C to study chromosomal structure after CRISPR-Cas9 deletion of either HUB162 (Ess) or HUB161 (Noness)

ORGANISM(S): Homo sapiens

PROVIDER: GSE231381 | GEO | 2023/06/01

REPOSITORIES: GEO

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gene profiling at single-cell level of the K562 cells with CRISPR-Cas9 KO of either HUB162 or HUB161

Project description:HUB162 (chr11:42,878,450-42,883,450, hg38) was identified as an essential locus in the quiescent region in the K562 cells, and HUB161 (chr11:42,873,450-42,878,450, hg38) as a nonessential one. We used scRNA-seq of 10x Genomics Chromium to study gene expression after CRISPR-Cas9 deletion of either HUB162 (Ess) or HUB161 (Noness)

2023-06-01 | GSE231382 | GEO

chromatin accessibility assay at single-cell level (scATAC-seq) of the K562 cells with CRISPR-Cas9 KO of either HUB162 or HUB161

Project description:HUB162 (chr11:42,878,450-42,883,450, hg38) was identified as an essential locus in the quiescent region in the K562 cells, and HUB161 (chr11:42,873,450-42,878,450, hg38) as a nonessential one. We used scATAC-seq of 10x Genomics Chromium to study chromatin accessibiliy after CRISPR-Cas9 deletion of either HUB162 (Ess) or HUB161 (Noness)

2023-06-01 | GSE231380 | GEO

RNA-Seq analysis of Harlequin Ichrthyosis skin, HI 3D model ABCA12 CRISPR-Cas9 KO cell line

Project description:The biology of Harlequin Ichthyosis (HI), a devastating skin disorder, caused by loss of function mutations in the gene ABCA12, is poorly understood and to date no satisfactory treatment has been developed. We sought to investigate pathomechanisms of Harlequin Ichthyosis which could lead to the identification of safe and effective treatments to improve patients' quality of life. RNA-Seq analysis using normal skin (n=5) and HI patient skin (n=4) were performed to define the effects of loss of ABCA12. Functional annotation clustering analysis showed changes in three common groups: epidermal differentiation, lipid metabolism and inflammation (innate immunity and IFNγ signalling). In HI patient skin, gene expression of STAT1, STAT3 and Interleukin 36 (IL-36) A and G cytokines was significantly upregulated compared to normal skin, whereas IL-37, an inhibitor of innate immunity, was downregulated. RNA-Seq and functional assays were performed to define the effects of loss of ABCA12, using an engineered CRISPR-Cas9 ABCA12 KO 3D model. Functional annotation clustering analysis showed changes in three common groups: epidermal differentiation, lipid metabolism and inflammation.

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Characterization of two rat models of cystic fibrosis-KO and F508del CFTR-Generated by Crispr-Cas9.

Project description:BackgroundGenetically engineered animals are essential for gaining a proper understanding of the disease mechanisms of cystic fibrosis (CF). The rat is a relevant laboratory model for CF because of its zootechnical capacity, size, and airway characteristics, including the presence of submucosal glands.MethodsWe describe the generation of a CF rat model (F508del) homozygous for the p.Phe508del mutation in the transmembrane conductance regulator (Cftr) gene. This model was compared to new Cftr -/- rats (CFTR KO). Target organs in CF were examined by histological staining of tissue sections and tooth enamel was quantified by micro-computed tomography. The activity of CFTR was evaluated by nasal potential difference (NPD) and short-circuit current measurements. The effect of VX-809 and VX-770 was analyzed on nasal epithelial primary cell cultures from F508del rats.ResultsBoth newborn F508del and Knock out (KO) animals developed intestinal obstruction that could be partly compensated by special diet combined with an osmotic laxative. The two rat models exhibited CF phenotypic anomalies such as vas deferens agenesis and tooth enamel defects. Histology of the intestine, pancreas, liver, and lungs was normal. Absence of CFTR function in KO rats was confirmed ex vivo by short-circuit current measurements on colon mucosae and in vivo by NPD, whereas residual CFTR activity was observed in F508del rats. Exposure of F508del CFTR nasal primary cultures to a combination of VX-809 and VX-770 improved CFTR-mediated Cl- transport.ConclusionsThe F508del rats reproduce the phenotypes observed in CFTR KO animals and represent a novel resource to advance the development of CF therapeutics.

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A C57BL/6J Fancg-KO Mouse Model Generated by CRISPR/Cas9 Partially Captures the Human Phenotype.

Project description:Fanconi anemia (FA) develops due to a mutation in one of the FANC genes that are involved in the repair of interstrand crosslinks (ICLs). FANCG, a member of the FA core complex, is essential for ICL repair. Previous FANCG-deficient mouse models were generated with drug-based selection cassettes in mixed mice backgrounds, leading to a disparity in the interpretation of genotype-related phenotype. We created a Fancg-KO (KO) mouse model using CRISPR/Cas9 to exclude these confounders. The entire Fancg locus was targeted and maintained on the immunological well-characterized C57BL/6J background. The intercrossing of heterozygous mice resulted in sub-Mendelian numbers of homozygous mice, suggesting the loss of FANCG can be embryonically lethal. KO mice displayed infertility and hypogonadism, but no other developmental problems. Bone marrow analysis revealed a defect in various hematopoietic stem and progenitor subsets with a bias towards myelopoiesis. Cell lines derived from Fancg-KO mice were hypersensitive to the crosslinking agents cisplatin and Mitomycin C, and Fancg-KO mouse embryonic fibroblasts (MEFs) displayed increased γ-H2AX upon cisplatin treatment. The reconstitution of these MEFs with Fancg cDNA corrected for the ICL hypersensitivity. This project provides a new, genetically, and immunologically well-defined Fancg-KO mouse model for further in vivo and in vitro studies on FANCG and ICL repair.

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Hi-C of the K562 cells with CRISPR-Cas9 KO of either HUB162 or HUB161

Project description:Hi-C of the K562 cells with CRISPR-Cas9 KO of either HUB162 or HUB161

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RNA-Seq analysis of Harlequin Ichrthyosis skin, HI 3D model ABCA12 CRISPR-Cas9 KO cell line

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CRISPR-Cas9 KO Cell Line Generation and Development of a Cell-Based Potency Assay for rAAV-FKRP Gene Therapy.

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Hi-C and capture Hi-C for HPV16 infected human W12 cervical cell lines and normal cervical tissue

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Project description:We sequenced polyA mRNA from OVCAR8-ADR-Cas9 cells in which one or two of 3 epigenetic regulators (BRD4, KDM4C, KDM6B) had been knocked out to examine how global gene expression was affected and evaluate potential synergistic effects at a molecular level. Gene expression data (RNA-Seq) in OVCAR8-ADR-Cas9 cells infected with control vector or vectors expressing gRNAs targeting one of 4 epigenetic regulators (BRD4, KDM4C, KDM6B) with biological replicates.

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