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Hi-C sequencing analysis of wild-type, β-actin knockout and β-actin hetereozygous mouse embryonic fibroblasts

ABSTRACT: Hi-C sequencing analysis of wild-type, β-actin knockout and β-actin hetereozygous mouse embryonic fibroblasts

PROVIDER: PRJNA630735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11713521_1.fastq.gz	Fastqsanger.gz
	SRR11713521_2.fastq.gz	Fastqsanger.gz
	SRR11713522_1.fastq.gz	Fastqsanger.gz
	SRR11713522_2.fastq.gz	Fastqsanger.gz
	SRR11713523_1.fastq.gz	Fastqsanger.gz

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Hi-C sequencing analysis of wild-type, β-actin knockout and β-actin hetereozygous mouse embryonic fibroblasts

Project description:β-actin is a crucial component of several chromatin remodeling complexes which control chromatin structure and accessibility. The mammalian Brahma-associated factor (BAF) is one such complex that plays essential roles in development and differentiation by regulating the chromatin state of critical genes and opposing the repressive activity of polycomb repressive complexes. While previous work has shown that β-actin loss can lead to extensive changes in gene expression and heterochromatin organization, it is not known if changes in β-actin levels can directly influence chromatin remodeling activities of BAF and polycomb proteins. Here we conduct a comprehensive genomic analysis of β-actin knockout mouse embryonic fibroblasts (MEFs) using ATAC-Seq, HiC-seq, RNA-Seq and ChIP-Seq of various epigenetic marks. We demonstrate that β-actin levels can affect the complex interplay between chromatin remodelers such as BAF/BRG1 and EZH2 in a dosage-dependent manner. Our results show that changes in β-actin levels and associated chromatin remodeling activities can not only impact local chromatin accessibility but also induce reversable changes in 3D genome architecture. Our findings support a novel role for β-actin levels in shaping the chromatin landscape during development and differentiation.

2021-05-01 | GSE149986 | GEO

ATAC-Seq analysis of beta actin knockout mouse embryonic fibroblasts expressing NLS-tagged beta-actin

Project description:ATAC-Seq analysis of beta actin knockout mouse embryonic fibroblasts expressing NLS-tagged beta-actin to study impact of actin levels on chromatin accessibility

2022-09-19 | GSE213431 | GEO

ATAC-Seq analysis of beta actin knockout mouse embryonic fibroblasts expressing NLS-tagged beta-actin

Project description:ATAC-Seq analysis of beta actin knockout mouse embryonic fibroblasts expressing NLS-tagged beta-actin

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Role of beta-actin in mouse embryonic fibroblasts (MEFs)

Project description:Role of beta-actin in mouse embryonic fibroblasts (MEFs)

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RNA-Seq analysis of beta-actin knockout MEFs expressing NLS-tagged beta-actin

Project description:RNA-Seq analysis of beta-actin knockout MEFs expressing NLS-tagged beta-actin to study role of actin in transcription

2022-09-19 | GSE213433 | GEO

In beta-actin knockout mouse embryonic fibroblasts epigenetic reprogramming and chromatin modifications lead to rDNA transcription inactivation and defects in cell growth and proliferation

Project description:Actin and nuclear myosin 1 (NM1) are emerging as regulators of transcription and chromatin organization. Using a genome-wide approach we report here that β-actin binds both intergenic and genic regions across the entire mammalian genome, associated with both protein-coding and rRNA genes. Across the rDNA transcription unit the distribution of β-actin correlated with NM1 and the other subunits of the B-WICH complex, WSTF and SNF2h. In β-actin-/- mouse embryonic fibroblasts (MEFs), we found that rRNA synthesis levels are down-regulated concomitantly with drops in Pol I and NM1 occupancies across the rRNA gene. In knock-in experiments, reintroduction of wild-type β-actin but not mutated forms with polymerization defects, rescued rRNA synthesis underscoring the direct role for β-actin in Pol I transcription and the importance of polymerization during the transcription process. The rRNA defects in the β-actin-/-MEFs are accompanied by epigenetic reprogramming that leads to up-regulation of the repressive mark H3K4me1. In addition, a high resolution chromatin accessibility assay showed that the absence of β-actin leads to a more compact chromatin at specific locations, including promoter-proximal enhancer (T0 sequence) and Sal boxes (T1-T10), disturbing binding of the transcription termination factor 1 (TTF1). We propose a novel mechanism where the polymerase-associated β-actin synergizes with NM1 to coordinate the establishment of permissive chromatin with the correct rDNA topology for Pol I transcription enhancement.

2015-10-04 | GSE68686 | GEO

ATAC-Seq analysis of Mouse Embryonic Fibroblasts (MEFs) to understand the role of β-actin in regulating chromatin states

2020-01-01 | GSE133196 | GEO

RNA-Seq analysis of beta-actin knockout MEFs expressing NLS-tagged beta-actin

Project description:RNA-Seq analysis of beta-actin knockout MEFs expressing NLS-tagged beta-actin

| PRJNA880774 | ENA

Sequencing analysis of beta-actin KO MEFs expressing NLS-beta-actin

Project description:Sequencing analysis of beta-actin KO MEFs expressing NLS-beta-actin

| PRJNA880630 | ENA

β-actin RNA-BioID

Project description:Function and fate of mRNAs is controlled by RNA binding proteins (RBPs) but determining the proteome of a specific mRNA in vivo is still challenging. RNA proximity biotinylation on the transported β-actin mRNA tagged with MS2 aptamers (RNA-BioID) is used to characterize the dynamic proteome of the β-actin mRNP in mouse embryonic fibroblasts (MEFs). We have identified > 60 β-actin associated RBPs including all six previously known as well as novel interactors. By investigating the dynamics of the β-actin mRNP in MEFs, we expand the set of β-actin mRNA associated RBPs and characterize the changes of the interacting proteome upon serum-induced mRNA localization. We report that the KH-domain containing protein FUBP3 represents a new β-actin associated RBP that binds to its 3’-untranslated region outside the known RNA localization element but is required for β-actin RNA localization. RNA-BioID will allow to obtain a dynamic view on the composition of endogenous mRNPs.

2020-03-12 | PXD010694 | Pride

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