Genome-wide mapping of in vivo SCL/DNA interactions in erythroid cells
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ABSTRACT: We have previously proposed two distinct molecular mechanisms by which SCL binds its targets in hematopoiesis; either by direct contact with specific DNA sequences or by indirect recruitment through interaction with other proteins. We have established that direct DNA binding is the major non-redundant mechanism SCL exerts in red cells. A DNA-binding mutant form of SCL (SCLRER) had detrimental effect on erythropoiesis in vivo. To extend these data to a molecular and mechanistic level, we have set out to identify the genomic sequences bound by SCL in vivo in erythroid precursors; we performed anti-SCL ChIP assays on immature, Ter119- erythroid cell populations isolated from day E12.5 wild-type (SCLWT/WT) fetal livers followed by ultra-throughput sequencing (ChIP-SEQ). To compare SCL’s direct versus indirect DNA-binding activities and, thus, gain insight into its mechanisms of action, we also analysed material isolated from SCLRER/RER fetal livers.
ORGANISM(S): Mus musculus
PROVIDER: GSE18720 | GEO | 2010/05/18
SECONDARY ACCESSION(S): PRJNA121675
REPOSITORIES: GEO
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