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Transcription factor EBF restricts alternative lineage options and promotes B cell fate commitment independent of Pax5
Area: Immunology
In the absence of early B cell factor (EBF), 'expandable' and clonal lymphoid progenitor cells seem to retain considerable myeloid potential. EBF is assumed to play a part in the lineage restriction and B cell fate commitment that also require transcription factor Pax5. EBF induces Pax5 and inhibits the expression of genes encoding for the transcription factors C/EBPalpha, PU.1 and ID2.
Ectopic expression of EBF in multipotent progenitor cells directs B cell generation against the myeloid cell fates. Continuing expression of EBF in Pax5-/- hematopoietic progenitor cells blocks the myeloid and T lineage potential of those cells in vivo. In Pax5-/- pro-B cells increased EBF expression also blocks the alternative lineage genes.
EBF can therefore act independent of Pax5 in limiting alternative lineage 'choice' and initiating commitment to the B cell fate.
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