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Chicken α‐globin switching depends on autonomous silencing of the embryonic π globin gene by epigenetics mechanisms
Author(s) -
RincónArano Héctor,
Guerrero Georgina,
ValdesQuezada Christian,
RecillasTarga Félix
Publication year - 2009
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22304
Subject(s) - gene silencing , biology , epigenetics , chromatin , gene expression , gene , regulation of gene expression , enhancer , pair rule gene , histone , globin , embryonic stem cell , genetics , locus control region , microbiology and biotechnology , regulator gene
Switching in hemoglobin gene expression is an informative paradigm for studying transcriptional regulation. Here we determined the patterns of chicken α‐globin gene expression during development and erythroid differentiation. Previously published data suggested that the promoter regions of α‐globin genes contain the complete information for proper developmental regulation. However, our data show a preferential trans ‐activation of the embryonic α‐globin gene independent of the developmental or differentiation stage. We also found that DNA methylation and histone deacetylation play key roles in silencing the expression of the embryonic π gene in definitive erythrocytes. However, drug‐mediated reactivation of the embryonic gene during definitive erythropoiesis dramatically impaired the expression of the adult genes, suggesting gene competition or interference for enhancer elements. Our results also support a model in which the lack of open chromatin marks and localized recruitment of chicken MeCP2 contribute to autonomous gene silencing of the embryonic α‐globin gene in a developmentally specific manner. We propose that epigenetic mechanisms are necessary for in vivo chicken α‐globin gene switching through differential gene silencing of the embryonic α‐globin gene in order to allow proper activation of adult α‐globin genes. J. Cell. Biochem. 108: 675–687, 2009. © 2009 Wiley‐Liss, Inc.