TY - JOUR
T1 - A large gene network in immature Erythroid cells is controlled by the myeloid and B cell transcriptional regulator PU.1
AU - Wontakal, Sandeep N.
AU - Guo, Xingyi
AU - Will, Britta
AU - Shi, Minyi
AU - Raha, Debasish
AU - Mahajan, Milind C.
AU - Weissman, Sherman
AU - Snyder, Michael
AU - Steidl, Ulrich
AU - Zheng, Deyou
AU - Skoultchi, Arthur I.
PY - 2011/6
Y1 - 2011/6
N2 - PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regulates an extensive network of genes that constitute major pathways for controlling growth and survival of immature erythroid cells. By analyzing fetal liver erythroid progenitors from mice with low PU.1 expression, we also show that the earliest erythroid committed cells are dramatically reduced in vivo. Furthermore, we find that PU.1 also regulates many of the same genes and pathways in other blood cells, leading us to propose that PU.1 is a multifaceted factor with overlapping, as well as distinct, functions in several hematopoietic lineages.
AB - PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regulates an extensive network of genes that constitute major pathways for controlling growth and survival of immature erythroid cells. By analyzing fetal liver erythroid progenitors from mice with low PU.1 expression, we also show that the earliest erythroid committed cells are dramatically reduced in vivo. Furthermore, we find that PU.1 also regulates many of the same genes and pathways in other blood cells, leading us to propose that PU.1 is a multifaceted factor with overlapping, as well as distinct, functions in several hematopoietic lineages.
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U2 - 10.1371/journal.pgen.1001392
DO - 10.1371/journal.pgen.1001392
M3 - Article
C2 - 21695229
AN - SCOPUS:79959829827
SN - 1553-7390
VL - 7
JO - PLoS genetics
JF - PLoS genetics
IS - 6
M1 - e1001392
ER -
