The Journal of Experimental Medicine
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Published 21 November 2005. doi:10.1084/jem.20051089
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 10, 1411-1422
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ARTICLE

 PU.1 is not strictly required for B cell development and its absence induces a B-2 to B-1 cell switch

Min Ye, Olga Ermakova, and Thomas Graf

Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461

CORRESPONDENCE Thomas Graf: graf{at}aecom.yu.edu OR Min Ye: ymin{at}aecom.yu.edu

In this paper, we describe the unexpected outgrowth of B lineage cells from PU.1–/– fetal liver cultures. The cells express all early B cell genes tested, including the putative PU.1 target genes IL-7R and EBF but not B220, and can produce immunoglobulin M. However, we observed a delay in the PU.1–/– B cell outgrowth and reduced precursor frequencies, indicating that although PU.1 is not strictly required for B cell commitment, it facilitates B cell development. We also ablated PU.1 in CD19-expressing B lineage cells in vivo, using a Cre-lox approach that allows them to be tracked. PU.1 excision resulted in a shift from B-2 cells to B-1–like cells, which dramatically increased with the age of the mice. Our data indicate that this shift is predominantly caused by a B-2 to B-1 cell reprogramming. Furthermore, we found that B-2 cells express substantially more PU.1 than B-1 cells, which is consistent with the idea that maintenance of the B-2 cell phenotype requires relatively high levels of PU.1, but B-1 cells require little.

Abbreviations used in this paper: BCR, B cell receptor; E, embryonic day; MZB, marginal zone B; SCF, stem cell factor.

O. Ermakova's present address is Mouse Biology Unit, European Molecular Biology Laboratory, I-00016 Monterotondo-Scalo, Rome, Italy.


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