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Next Article 
Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3621-3632
BSAP/Pax5A Expression Blocks Survival and Expansion of Early Myeloid
Cells Implicating Its Involvement in Maintaining Commitment to the
B-Lymphocyte Lineage
Mark Y. Chiang and
John G. Monroe
From the Department of Pathology and Laboratory Medicine, University
of Pennsylvania School of Medicine, Philadelphia, PA.
Early B lymphopoiesis is marked by plasticity between the myeloid
and B lineages. An attractive model for B-lineage development is that
commitment to this lineage is partly determined by the ordered
expression of genes that prohibit switching to the myeloid lineage. In
this regard, whereas the role of the B-cell-specific transcription
factor BSAP/Pax5A in regulating B-lymphoid-restricted gene expression
has been well-established, its role in maintaining B-lineage commitment
is unclear. Thus, BSAP/Pax5A was constitutively expressed in the
multipotent EML cell line, which can be directed toward the myeloid
lineage by culture with interleukin-3 (IL-3) and retinoic acid. EML
cells expressing BSAP/Pax5A successfully acquired the myeloid lineage
markers CD11b and F4/80 in response to IL-3 and retinoic acid,
indicating differentiation to the myeloid lineage. However, these early
myeloid cells failed to expand in culture with granulocyte-macrophage
colony-stimulating factor and were directed instead toward an apoptotic
pathway. In parallel, primary bone marrow stem cells transduced with
retrovirus constitutively expressing BSAP/Pax5A began myeloid cell
differentiation, but like the transformed EML model failed to expand in
response to myeloid growth factors. These studies identify a role for
BSAP/Pax5A in suppressing the response to myeloid growth factors, which
may be a component of the regulatory processes that limit plasticity of
early B-lymphoid progenitors.
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