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A dose-dependent role for EBF1 in repressing non-B-cell-specific genes
National Jewish Health.
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2011 (Engelska)Ingår i: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 41, nr 6, s. 1787-1793Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

In the absence of early B-cell factor 1 (EBF1), B-cell development is arrested at an uncommitted progenitor stage that exhibits increased lineage potentials. Previously, we investigated the roles of EBF1 and its DNA-binding partner Runx1 by evaluating B lymphopoiesis in single (EBF1(het) and Runx1(het)) and compound haploinsufficent (Ebf1(+/-) Runx1(+/-), ER(het)) mice. Here, we demonstrate that decreased Ebf1 gene dosage results in the inappropriate expression of NK-cell lineage-specific genes in B-cell progenitors. Moreover, prolonged expression of Ly6a/Sca-1 suggested the maintenance of a relatively undifferentiated phenotype. These effects were exacerbated by reduced expression of Runx1 and occurred despite expression of Pax5. Repression of inappropriately expressed genes was restored in most pre-B and all immature B cells of ER(het) mice. Enforced EBF1 expression repressed promiscuous transcription in pro-B cells of ER(het) mice and in Ebf1(-/-) Pax5(-/-) fetal liver cells. Together, our studies suggest that normal levels of EBF1 are critical for maintaining B-cell identity by directing repression of non-B-cell-specific genes.

Ort, förlag, år, upplaga, sidor
John Wiley and Sons, Ltd , 2011. Vol. 41, nr 6, s. 1787-1793
Nyckelord [en]
B-cell development; Gene regulation; NK cells; Transcription factors
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:liu:diva-69899DOI: 10.1002/eji.201041137ISI: 000291559700028OAI: oai:DiVA.org:liu-69899DiVA, id: diva2:433290
Tillgänglig från: 2011-08-09 Skapad: 2011-08-08 Senast uppdaterad: 2017-12-08

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Zandi, SasanSigvardsson, Mikael

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Zandi, SasanSigvardsson, Mikael
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Experimentell hematologiHälsouniversitetet
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