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Systematic discovery of endogenous ribonucleoprotein complexes - RNA DIF-FRAC mouse embryonic stem cell

ABSTRACT: The associated files are mass spec data from size exclusion chromatographic separations of mouse embryonic stem cells with and without RNAse A treatment.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Embryonic Stem Cell

SUBMITTER: Kevin Drew

LAB HEAD: Edward Marcotte

PROVIDER: PXD014607 | Pride | 2019-10-18

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	MES_SEC_Cntl_01a_20180601..comet.pep.xml	Pepxml
	MES_SEC_Cntl_01a_20180601.MSGF.mzid.gz	Mzid
	MES_SEC_Cntl_01a_20180601.mzXML	Mzxml
	MES_SEC_Cntl_01a_20180601.raw	Raw
	MES_SEC_Cntl_01a_20180601.tandemK.out	Other

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Publications

Systematic Discovery of Endogenous Human Ribonucleoprotein Complexes.

Mallam Anna L AL Sae-Lee Wisath W Schaub Jeffrey M JM Tu Fan F Battenhouse Anna A Jang Yu Jin YJ Kim Jonghwan J Wallingford John B JB Finkelstein Ilya J IJ Marcotte Edward M EM Drew Kevin K

Cell reports 20191001 5

RNA-binding proteins (RBPs) play essential roles in biology and are frequently associated with human disease. Although recent studies have systematically identified individual RNA-binding proteins, their higher-order assembly into ribonucleoprotein (RNP) complexes has not been systematically investigated. Here, we describe a proteomics method for systematic identification of RNP complexes in human cells. We identify 1,428 protein complexes that associate with RNA, indicating that more than 20% o ...[more]

PMID: 31665645

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2019-10-18 | PXD015406 | Pride

Systematic discovery of endogenous ribonucleoprotein complexes - RNA DIF-FRAC Human HEK293T Cells Replicate2

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Arid3a modulates the first cell fate decision by direct regulation of both embryonic and extraembryonic gene expression (ChIP-Seq)

Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a ChIP was performed using bioChIP-sequencing. Control ChIP-sequencing was performed using BirA cells. HDAC1 ChIP was performed as native antibody ChIP-sequencing.

2014-10-16 | E-GEOD-56876 | biostudies-arrayexpress

Arid3a modulates the first cell fate decision by direct regulation of both embryonic and extraembryonic gene expression (microarray)

Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a overexpression and Arid3a knockdown Total RNA was isolated from cultured cells using RNeasy plus mini kit (Qiagen). cDNA were synthesized and labelled, followed by hybridization on Affymetrix GeneChip mouse genome 430A 2.0 arrays.

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Genome-wide Regulation of 5hmC, 5mC and Gene Expression by Tet1 Hydroxylase in Mouse Embryonic Stem Cells (expression data)

Project description:DNA methylation of C5-cytosine (5mC) in the mammalian genome is a key epigenetic event that is critical for various cellular processes. However, how the genome-wide 5mC pattern is dynamically regulated remains a fundamental question in epigenetic biology. The TET family of 5mC hydroxylases, which convert 5mC to 5-hydroxymethylcytosine (5hmC), have provided a new potential mechanism for the dynamic regulation of DNA methylation. The extent to which individual Tet family members contribute to the genome-wide 5mC and 5hmC patterns and associated gene network remains largely unknown. Here we report genome-wide mapping of Tet1 and 5hmC in mESCs and reveal a mechanism of action by which Tet1 controls 5hmC and 5mC levels in mESCs. In combination with microarray and mRNA-seq expression profiling, we identify a comprehensive yet intricate gene network influenced by Tet1. We propose a model whereby Tet1 controls DNA methylation both by binding to CpG-rich regions to prevent unwanted DNA methyltransferase activity, and by converting the existing 5mC to 5hmC through its enzymatic activity. This Tet1-mediated antagonism of CpG methylation imparts differential maintenance of DNA methylation status at Tet1 target loci, thereby providing a new regulatory mechanism for establishing the epigenetic landscape of mESCs, which ultimately contributes to mESC differentiation and the onset of embryonic development. Tet1 protein was depleted in J1 or E14 mouse ES cells by siRNA or shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The Tet1-regulated genes were identified by comparing the gene expression profiles of control and Tet1-depleted ES cells.

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Arid3a modulates the first cell fate decision by direct regulation of both embryonic and extraembryonic gene expression

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-16 | E-GEOD-56877 | biostudies-arrayexpress

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