Mammalian centromere formation is dependent on chromatin that contains centromere protein (CENP)-A, which is the centromere-specific histone H3 variant. Human neocentromeres have acquired CENP-A chromatin epigenetically in ectopic chromosomal locations on low-copy complex DNA. Neocentromeres permit detailed investigation of centromeric chromatin organization that is not possible in the highly repetitive alpha satellite DNA present at endogenous centromeres.We have examined the distribution of CE ...[more]
Project description:Chromatin Immunoprecipitation of Centromeric Proteins, CenpA, CenpC or CenpH from cell line BBB, which contains a neocentromere in band 13q33.1<br><br> Processed data files with additional statistics are available for download from <a href="ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/TABM/E-TABM-245/">ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/TABM/E-TABM-245/</a>
Project description:Chromatin Immunoprecipitation of Centromeric Proteins, CenpA, CenpC or CenpH from cell lines which contain either a neocentromere in band 13q21 or no neocentric chromosomes<br><br> Processed data files with additional statistics are available for download from <a href="ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/TABM/E-TABM-257/">ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/TABM/E-TABM-257/</a>
Project description:Transcription factor-induced reprogramming of somatic cells to pluripotency is a very inefficient process, probably due to the existence of important epigenetic barriers that are imposed during differentiation and that contribute to preserve cell identity. In an effort to decipher the molecular nature of these barriers, we followed a genome-wide approach, in which we identified macro histone variants (macroH2A) as highly expressed in human somatic cells but downregulated after reprogramming to pluripotency, as well as strongly induced during differentiation. Knock down of macro histone variants in human keratinocytes increased the efficiency of reprogramming to pluripotency, while overexpression had opposite effects. Genome-wide occupancy profiles show that in human keratinocytes macroH2A.1 preferentially occupies genes that are expressed at low levels and are marked with H3K27me3, including pluripotency-related genes and bivalent developmental regulators, at which its presence prevents the regain of H3K4me2 during reprogramming, over imposing an additional layer of repression that preserves cell identity. Gemone wide occupancy of HA:macroH2A.1 in human keratinocytes
Project description:ChIP-chip study using Saos-2 cell line infected with adenoviruses encoding GFP (Mock) or GFP together with the p53 H1 helix mutants EL or RE. DNA-protein-complexes were precipitated with monoclonal p53-antibody (clone DO-1). Mock-chromatin was immunoprecipitated in the absence of antibody.<br>Three completely independent biological replicates were performed for each antibody, obtaining the corresponding input as total genomic DNA reference. Hybridizations were performed using Affymetrix GeneChip Human Tiling 2.0R Array set (7 arrays set).<br><br> Affymetrix .BAR files and an additional processed data file containing the coordinates of the identified binding sites can be found in the FTP directory for this experiment. <A HREF="ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/MEXP/E-MEXP-1748">FTP directory</A>
Project description:The mammalian TET dioxygenases contribute to global waves of DNA demethylation in the zygote and in primordial germ cells, but their involvement during de novo DNA methylation at peri/post-implantation development is unknown. Here, we show novel physiological functions of Tet1 in the pre-primitive streak stage mouse embryo, where it is expressed not only in the primed-state epiblast, but also in the extra-embryonic ectoderm. In the epiblast, Tet1 contributes to DNA methylation patterning, which indirectly results in dominant transcriptional repression involving a Jumonji-family gene Jmjd8. In the extra-embryonic ectoderm, Tet1 suppresses expression of metabolic genes involved in oxidative phosphorylation. These lineage-specific gene repressive functions, involving distinct modes of regulation by DNA methylation, counteract precocious differentiation of the embryo prior to the onset of gastrulation. Such dysregulation in the absence of Tet1 are surprisingly tolerated in an inbred strain but results in full embryonic lethality in non-inbred mice, thus implicating a complex but essential role of Tet1 in normal gestational development.
Project description:DNA methylation profiling by D-REAM.<br><br>Additional data files (.BED files and heatmap file) are available in the FTP directory for this experiment <A HREF="ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/TABM/E-TABM-551/">FTP directory</A>