Similar Datasets
Project description:Determination of accessible chromatin regions in the 8-cell stage mouse embryo after Suv39h2 knockdown The study aimed to address a potential function of H3K9me3 in early mouse development by assessing its impact on chromatin compaction. The histone methyltransferase responsible for de novo H3K9me3 at fertilization Suv39h2, was knocked down by microinjection of dsRNA targeting Suv39h2 in the early zygote. Embryos were then cultured until the 8-cell stage of development. They were then fixed and chromatin compaction was assessed by NicE-seq in pools of 10 8-cell stage embryos.
2020-03-31 | GSE138686 | GEO
Project description:NicE-seq in Suv39h2 knockdown 8-cell stage
| PRJNA576800 | ENA
Project description:RNA-seq 2-cell Suv392 knockdown
| PRJNA522081 | ENA
Project description:The placenta is constructed through the orchestration of trophoblast stem (TS) cell expansion and differentiation along a multi-lineage pathway. Dynamic regulation of histone H3K9 methylation is pivotal to cell differentiation for many cell lineages, but little is known about its involvement in trophoblast development. Among the twelve-known histone H3K9 methyltransferases, only SUV39H2 exhibited robust differential expression in stem versus differentiated rat TS cells. SUV39H2 transcript and protein expression were high in the stem state and rapidly declined as TS cells differentiated. Disruption of SUV39H2 expression in TS cells led to prominent phenotypic changes. Suv39h2-specific shRNA knockdown resulted in an arrest in TS cell proliferation and activation of trophoblast cell differentiation. These observations were reinforced by flow cytometry and transcript profiling. Histone H3K9 methylation status at specific loci exhibiting differentiation-dependent gene expression were regulated by SUV39H2 and also represented sites for SUV39H2 occupancy. Analyses of SUV39H2 on ex vivo rat blastocyst development supported its role in regulating TS cell expansion and differentiation. Finally, we identified SUV39H2 as a downstream target of CDX2, a master regulator of trophoblast lineage development. In summary, our findings indicate that SUV39H2 contributes to the maintenance of the TS cell stem state and restrains trophoblast cell differentiation and thus serves as a contributor to the epigenetic regulation of hemochorial placental development.
2021-07-15 | GSE154701 | GEO
Project description:RNA-seq of ERINA knockdown T47D cell lines
| PRJNA622513 | ENA
Project description:RNA-seq upon PAX8 knockdown in Renal Cell Carcinoma cell lines
| PRJEB31824 | ENA
Project description:RNA-seq of Myla cell line after FOXM1 knockdown
| PRJNA1174723 | ENA
Project description:RNA-seq for HepG2 cell line with AUF1 knockdown.
| PRJNA682635 | ENA
Project description:BACKGROUND:CCCTC-Binding Factor (CTCF), also known as 11-zinc finger protein, participates in many cellular processes, including insulator activity, transcriptional regulation and organization of chromatin architecture. Based on single cell flow cytometry and single cell RNA-FISH analyses, our previous study showed that deletion of CTCF binding site led to a significantly increase of cellular variation of its target gene. However, the effect of CTCF on genome-wide landscape of cell-to-cell variation remains unclear. RESULTS:We knocked down CTCF in EL4 cells using shRNA, and conducted single cell RNA-seq on both wild type (WT) cells and CTCF-Knockdown (CTCF-KD) cells using Fluidigm C1 system. Principal component analysis of single cell RNA-seq data showed that WT and CTCF-KD cells concentrated in two different clusters on PC1, indicating that gene expression profiles of WT and CTCF-KD cells were systematically different. Interestingly, GO terms including regulation of transcription, DNA binding, zinc finger and transcription factor binding were significantly enriched in CTCF-KD-specific highly variable genes, implying tissue-specific genes such as transcription factors were highly sensitive to CTCF level. The dysregulation of transcription factors potentially explains why knockdown of CTCF leads to systematic change of gene expression. In contrast, housekeeping genes such as rRNA processing, DNA repair and tRNA processing were significantly enriched in WT-specific highly variable genes, potentially due to a higher cellular variation of cell activity in WT cells compared to CTCF-KD cells. We further found that cellular variation-increased genes were significantly enriched in down-regulated genes, indicating CTCF knockdown simultaneously reduced the expression levels and increased the expression noise of its regulated genes. CONCLUSIONS:To our knowledge, this is the first attempt to explore genome-wide landscape of cellular variation after CTCF knockdown. Our study not only advances our understanding of CTCF function in maintaining gene expression and reducing expression noise, but also provides a framework for examining gene function.
| S-EPMC6933653 | biostudies-literature
Project description:Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.
2015-03-11 | E-GEOD-66719 | biostudies-arrayexpress