Dataset Information

Quantitative ChIP-MS analysis of proteins associated with H3K4me1- and H3K4me3-enriched mono-nucleosomes purified from crosslinked IMR-90 cells

ABSTRACT: Here we used ChIP-MS to quantitatively profile chromatin-associated proteins that are specifically associated with H3K4me1- and H3K4me3-modified nucleosomes in IMR-90 chromatin.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Andrey Tvardovskiy

LAB HEAD: Till Bartke

PROVIDER: PXD042826 | Pride | 2023-12-10

REPOSITORIES: Pride

ACCESS DATA

Publications

Decoding chromatin states by proteomic profiling of nucleosome readers.

Lukauskas Saulius S Tvardovskiy Andrey A Nguyen Nhuong V NV Stadler Mara M Faull Peter P Ravnsborg Tina T Özdemir Aygenli Bihter B Dornauer Scarlett S Flynn Helen H Lindeboom Rik G H RGH Barth Teresa K TK Brockers Kevin K Hauck Stefanie M SM Vermeulen Michiel M Snijders Ambrosius P AP Müller Christian L CL DiMaggio Peter A PA Jensen Ole N ON Schneider Robert R Bartke Till T

Nature 20240306 8004

DNA and histone modifications combine into characteristic patterns that demarcate functional regions of the genome1,2. While many 'readers' of individual modifications have been described3-5, how chromatin states comprising composite modification signatures, histone variants and internucleosomal linker DNA are interpreted is a major open question. Here we use a multidimensional proteomics strategy to systematically examine the interaction of around 2,000 nuclear proteins wi ...[more]

PMID: 38448585

Similar Datasets

Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. In response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expression (Xu J, et al. 2009) Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. In order to investigate changes in histone variant H2A.Z occupancy associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed H2A.Z ChIP-Seq in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. Please note that RNA-seq data generated in conjunction to this ChIP-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5628 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5628 ).

Dataset Information

Quantitative ChIP-MS analysis of proteins associated with H3K4me1- and H3K4me3-enriched mono-nucleosomes purified from crosslinked IMR-90 cells

Publications

Decoding chromatin states by proteomic profiling of nucleosome readers.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure