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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [ChIP-seq]

ABSTRACT: A large fraction of the mammalian genome is organized into inactive chromosomal domains associated with the nuclear lamina. Using genomic repositioning assays we show that Lamina associated domains (LADs), spanning the developmentally regulated IgH and Cyp3a loci, contain transportable DNA regions that associate chromatin with the nuclear lamina and repress gene activity in fibroblasts. We characterized DNA regions within LADs that are functionally capable of positioning chromatin domains at the inner nuclear membrane (INM) lamina. We mapped and characterized the IgH and other LADs in murine fibroblasts. We show that these murine LADs have a unique chromatin structure with discrete boundaries. We demonstrate DNA regions within LADs that are capable of directing the association of chromatin domains with the INM-lamina as well as the silencing of a co-integrated reporter gene.

ORGANISM(S): Mus musculus

SUBMITTER: Joseph Zullo

PROVIDER: E-GEOD-36048 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina

Project description:This SuperSeries is composed of the following subset Series: GSE35777: A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [Tiling Array] GSE36048: A molecular mechanism for compartmentalization and silencing of chromatin domains at the nuclear lamina [ChIP-seq] Refer to individual Series

2012-02-24 | E-GEOD-36049 | biostudies-arrayexpress

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2010-11-23 | E-GEOD-25197 | biostudies-arrayexpress

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2014-06-04 | E-GEOD-57406 | biostudies-arrayexpress

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2011-12-23 | E-GEOD-32509 | biostudies-arrayexpress

Epigenomic profiling of Non-small-cell Lung Cancer (NSCLC) cells with or without Eed

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2016-01-15 | E-GEOD-61190 | biostudies-arrayexpress

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Epigenomic comparison of distinct pluripotent stem cell states reveals a new class of enhancers with roles throughout mammalian development (ChIP-seq)

Project description:NaM-CM-/ve mouse embryonic stem cells (mESCs) and primed epiblast stem cells (mEpiSCs) represent successive snapshots of pluripotency during embryogenesis. Using transcriptomic and epigenomic mapping, we show that a small fraction of transcripts are differentially expressed between mESCs and mEpiSCs and these genes show expected changes in chromatin at their promoters and enhancers. Unexpectedly, the cis-regulatory circuitry of genes that are expressed at identical levels between these cell states also differs dramatically. In mESCs, these genes are associated with dominant proximal enhancers and dormant distal enhancers, which we term seed enhancers. In mEpiSCs, the naM-CM-/ve-dominant enhancers are lost, and the seed enhancers take up primary transcriptional control. Seed enhancers have increased sequence conservation and show preferential usage in downstream somatic tissues, often expanding into super enhancers. We propose that seed enhancers ensure proper enhancer utilization and transcriptional fidelity as mammalian cells transition from naM-CM-/ve pluripotency to a somatic regulatory program. ChIP sequencing of histone modifications in mouse epiblast stem cells

2014-06-04 | E-GEOD-57407 | biostudies-arrayexpress

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2014-10-01 | E-GEOD-53327 | biostudies-arrayexpress

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2015-05-18 | E-GEOD-60606 | biostudies-arrayexpress

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