@article{370b709a09034dbfac2d24805df13fec,
title = "Transcription factor EBF restricts alternative lineage options and promotes B cell fate commitment independently of Pax5",
abstract = "Alternative lineage restriction and B cell fate commitment require the transcription factor Pax5, but the function of early B cell factor (EBF) in these processes remains mostly unexplored. Here we show that in the absence of EBF, 'expandable' and clonal lymphoid progenitor cells retained considerable myeloid potential. Conversely, ectopic expression of EBF in multipotential progenitor cells directed B cell generation at the expense of myeloid cell fates. EBF induced Pax5 and antagonized expression of genes encoding the transcription factors C/EBPα, PU.1 and Id2. Notably, sustained expression of EBF in Pax5-/- hematopoietic progenitor cells was sufficient to block their myeloid and T lineage potential in vivo. Furthermore, in Pax5-/- pro-B cells, higher EBF expression repressed alternative lineage genes. Thus, EBF can restrict alternative lineage 'choice' and promote commitment to the B cell fate independently of Pax5.",
author = "Pongubala, {Jagan M.R.} and Northrup, {Daniel L.} and Lancki, {David W.} and Medina, {Kay L.} and Thomas Treiber and Eric Bertolino and Matthew Thomas and Rudolf Grosschedl and David Allman and Harinder Singh",
note = "Funding Information: constructs; J. Hagman (National Jewish Medical and Research Center) for the epitope-tagged EBF construct; S. Firner (Max Planck Institute of Immunobiology) for doing {\textquoteleft}ChIP-on-ChIP{\textquoteright} chromatin immunnoprecipitation with EBF; the Immunology Applications Core Facility and the Functional Genomics Facility of the University of Chicago for advice on cell sorting and microarray analysis, respectively; and members of the Singh lab for suggestions and critical comments. Supported by the Irvington Institute (K.L.M.), the Leukemia Lymphoma Society (M.T. and D.A.), the Howard Hughes Medical Institute (H.S.), the National Institute of Allergy and Infectious Diseases and National Institute on Aging of the National Institutes of Health (D.A.) and the German Research Foundation (Deutsche Forschungsgemeinschaft; R.G.).",
year = "2008",
month = feb,
doi = "10.1038/ni1555",
language = "English (US)",
volume = "9",
pages = "203--215",
journal = "Nature Immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "2",
}