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The epigenome landscape in pluripotent and lineage‐committed human cells
Author(s) -
Ren Bing
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.414.1
Subject(s) - epigenomics , chromatin , epigenome , dna methylation , biology , epigenetics , embryonic stem cell , reprogramming , microbiology and biotechnology , lineage (genetic) , induced pluripotent stem cell , genetics , computational biology , dna , cell , gene , gene expression
Human embryonic stem cells share identical genomic sequences with other lineage‐committed cells yet possess the remarkable properties of self‐renewal and pluripotency. It has been proposed that epigenetic regulatory mechanisms, involving DNA methylation and various chromatin modifications, are at least partly responsible for the distinct cellular properties between different cell types. Using next generation sequencing technologies, we have determined the profiles of a dozen chromatin modification marks and the state of DNA methylation at high resolution throughout the genome in the human embryonic stem cells and primary fetal lung fibroblasts. Analysis of the epigenomic profiles in these cells revealed a new set of relationships between chromatin modifications and DNA methylation. Additionally, we defined two types of chromatin domains: one that forms large blocks and the other that occupies small and punctuated regions. We found that epigenomic landscapes are drastically different between the ES cells and fibroblasts: over a third of the human genome differs in their chromatin structure between the two cell types, and that chromatin dynamics at these sequences are frequently associated with change in DNA methylation. Our results provide new insights into epigenetic regulatory mechanisms underlying properties of pluripotency and cell fate commitment.