| First Author | Dahl R | Year | 2002 |
| Journal | EMBO J | Volume | 21 |
| Issue | 9 | Pages | 2220-30 |
| PubMed ID | 11980719 | Mgi Jnum | J:76489 |
| Mgi Id | MGI:2179579 | Doi | 10.1093/emboj/21.9.2220 |
| Citation | Dahl R, et al. (2002) Spi-B can functionally replace PU.1 in myeloid but not lymphoid development. EMBO J 21(9):2220-30 |
| abstractText | Mature macrophages, neutrophils and lymphoid cells do not develop in PU.1(-/-) mice. In contrast, mice lacking the highly related protein Spi-B generate all hematopoietic lineages but display a B-cell receptor signaling defect. These distinct phenotypes could result from functional differences between PU.1 and Spi-B or their unique temporal and tissue-specific expression (PU.1: myeloid and B cells; Spi-B: B cells only). To address this question, we introduced the Spi-B cDNA into the murine PU.1 locus by homologous recombination. In the absence of PU.1, Spi-B rescued macrophage and granulocyte development when assayed by in vitro differentiation of embryonic stem cells. Adherent, CD11b(+)/F4/80(+) cells capable of phagocytosis were detected in PU.1(Spi-B/Spi-B) embryoid bodies, and myeloid colonies were present in hematopoietic progenitor assays. Despite its ability to rescue myeloid differentiation, Spi-B did not rescue lymphoid development in a RAG-2(-/-) complementation assay. These results demonstrate an important difference between PU.1 and Spi-B. Careful comparison of these Ets factors will delineate important functional domains of PU.1 involved in lymphocyte lineage commitment and/or maturation. |
