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Dynamics of GATA1 binding and expression response in a GATA1-induced erythroid differentiation system.


ABSTRACT: During the maturation phase of mammalian erythroid differentiation, highly proliferative cells committed to the erythroid lineage undergo dramatic changes in morphology and function to produce circulating, enucleated erythrocytes. These changes are caused by equally dramatic alterations in gene expression, which in turn are driven by changes in the abundance and binding patterns of transcription factors such as GATA1. We have studied the dynamics of GATA1 binding by ChIP-seq and the global expression responses by RNA-seq in a GATA1-dependent mouse cell line model for erythroid maturation, in both cases examining seven progressive stages during differentiation. Analyses of these data should provide insights both into mechanisms of regulation (early versus late targets) and the consequences in cell physiology (e.g. distinctive categories of genes regulated at progressive stages of differentiation). The data are deposited in the Gene Expression Omnibus, series GSE36029, GSE40522, GSE49847, and GSE51338.

SUBMITTER: Jain D 

PROVIDER: S-EPMC4338950 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature

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Dynamics of GATA1 binding and expression response in a GATA1-induced erythroid differentiation system.

Jain Deepti D   Mishra Tejaswini T   Giardine Belinda M BM   Keller Cheryl A CA   Morrissey Christapher S CS   Magargee Susan S   Dorman Christine M CM   Long Maria M   Weiss Mitchell J MJ   Hardison Ross C RC  

Genomics data 20150601


During the maturation phase of mammalian erythroid differentiation, highly proliferative cells committed to the erythroid lineage undergo dramatic changes in morphology and function to produce circulating, enucleated erythrocytes. These changes are caused by equally dramatic alterations in gene expression, which in turn are driven by changes in the abundance and binding patterns of transcription factors such as GATA1. We have studied the dynamics of GATA1 binding by ChIP-seq and the global expre  ...[more]

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