| Literature DB >> 23880533 |
Christian Valdes-Quezada1, Cristian Arriaga-Canon, Yael Fonseca-Guzmán, Georgina Guerrero, Félix Recillas-Targa.
Abstract
Genomic loci composed of more than one gene are frequently subjected to differential gene expression, with the chicken α-globin domain being a clear example. In the present study we aim to understand the globin switching mechanisms responsible for the epigenetic silencing of the embryonic π gene and the transcriptional activation of the adult α(D) and α(A) genes at the genomic domain level. In early stages, we describe a physical contact between the embryonic π gene and the distal 3' enhancer that is lost later during development. We show that such a level of regulation is achieved through the establishment of a DNA hypermethylation sub-domain that includes the embryonic gene and the adjacent genomic sequences. The multifunctional CCCTCC-binding factor (CTCF), which is located upstream of the α(D) gene promoter, delimits this sub-domain and creates a transition between the inactive sub-domain and the active sub-domain, which includes the adult α(D) gene. In avian-transformed erythroblast HD3 cells that are induced to differentiate, we found active DNA demethylation of the adult α(D) promoter, coincident with the incorporation of 5-hydroxymethylcytosine (5hmC) and concomitant with adult gene transcriptional activation. These results suggest that autonomous silencing of the embryonic π gene is needed to facilitate an optimal topological conformation of the domain. This model proposes that CTCF is contributing to a specific chromatin configuration that is necessary for differential α-globin gene expression during development.Entities:
Keywords: 5-hydroxymethylcytosine; CTCF; DNA methylation; chromosome conformation capture; enhancer-promoter interaction; epigenetic silencing
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Year: 2013 PMID: 23880533 PMCID: PMC3883786 DOI: 10.4161/epi.25472
Source DB: PubMed Journal: Epigenetics ISSN: 1559-2294 Impact factor: 4.528