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

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

PROVIDER: PRJNA550354 | ENA |

REPOSITORIES: ENA

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

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.

2020-01-01 | GSE133196 | GEO

ChIP-Seq of H3K27ac in Actb-/- MEFs expressing NLS-tagged beta-actin

Project description:Genome-wide ChIP-Seq of H3K27ac in β-actin KO MEFs expressing NLS-tagged beta-actin to assess the role of nulcear actin in regulating histone acetylation

2022-09-19 | GSE213432 | 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 to study role of actin in transcription

2022-09-19 | GSE213433 | GEO

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

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

| PRJNA630727 | ENA

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

2021-05-01 | GSE149986 | GEO

Next Generation Sequencing Analysis of Beta-actin knockout (KO) Mouse Embryonic Fibroblast (MEFs) Transcriptomes Stimulated by Viral Mimics

Project description:mRNA profiles of beta-actin knockout (KO) MEFs stimulated by viral mimics to study how global transcriptome changes after innate viral immunity activation

2019-05-02 | GSE130596 | GEO

Next Generation Sequencing Analysis of chemically reprogrammed osteoblasts from Beta-actin Wildtype (WT) Heterozygotes (HET) and knockout (KO) Mouse Embryonic Fibroblast (MEFs)

Project description:mRNA profiles of chemically reprogrammed osteoblasts from Beta-actin Wildtype (WT) Heterozygotes (HET) and knockout (KO) Mouse Embryonic Fibroblast (MEFs)

2019-08-06 | GSE135392 | GEO

Next Generation Sequencing Analysis of Beta-actin knockout (KO) and wildtype (WT) Mouse Embryonic Fibroblast (MEFs) Transcriptomes Under Adipogenic Induced Conditions

Project description:mRNA profiles of beta-actin knockout (KO) and wild-type (WT) MEFs induced to adipocyte-like feature to study how global transcriptome changes during differentiation

2019-05-07 | GSE130765 | GEO

ChIP-Seq of H3K27ac in Wild Type (WT), and Actb-/- (KO) Mouse Embryonic Fibroblasts

Project description:Genome-wide ChIP-Seq of H3K27ac in WT and β-actin KO MEFs to assess the role of nulcear actin in regulating histone acetylation

2022-09-01 | GSE196089 | GEO

Actb knockout in primary mouse embryonic fibroblasts LC-MS/MS

Project description:The cytoplasmic actin proteins, beta- and gamma-actin, are 99% identical but perform non-redundant functions. Genes encoding the cytoplasmic actins, Actb and Actg1, respectively, are less similar but still share 89% of their nucleotide sequences. Knockout (KO) of Actb by deletion of first coding exons 2 and 3 in mice is embryonic lethal while KO embryonic fibroblasts (MEFs) fail to proliferate. In contrast, KO of Actg1 is viable but mice lacking Actg1 present with increased perinatal lethality and Actg1 KO MEFs present with a much milder defect in cell proliferation. Recent studies have identified important protein-independent functions for both Actb and Actg1 and demonstrate that deletions within the Actb nucleotide sequence, and not loss of the beta-actin protein, cause the most severe phenotypes in KO mice and cells. Here, we use a multi-omics approach to better understand what drives the phenotypes of Actb KO MEFs. RNA-sequencing and mass spectrometry of Actb KO MEFs reveal largescale changes to the transcriptome, proteome, and phosphoproteome. Pathway analysis of genes and proteins differentially expressed upon Actb KO shows widespread dysregulation of genes involved in the cell cycle. Together, these data suggest novel, protein-independent roles for Actb in regulating gene expression associated with control of cell proliferation.

2024-02-19 | PXD039786 | Pride

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