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Blood, 15 August 2000, Vol. 96, No. 4, pp. 1358-1365
HEMATOPOIESIS
Myeloid differentiation of FdCP1 cells is dependent on
Stat5 processing
Flavia Piazza,
Jason Valens,
Eric Lagasse, and
Christian Schindler
From the Departments of Microbiology and Medicine,
Columbia University, New York, NY, and StemCells Inc, Sunnyvale, CA.
The IL-3 family of cytokines transduces signals through Stat5 and
regulates myeloid development. Previous studies have determined that a
carboxy terminally truncated isoform of Stat5 is activated in immature
myeloid cells. This isoform, which lacks a transcriptional activation
domain, is generated by a protein-processing event. To determine
whether Stat5 cleavage plays an important role in the growth and
maturation of myeloid progenitors, the FdCP1 model of myeloid
maturation was evaluated. FdCP1 cells are IL-3-dependent myeloid
progenitors that differentiate into monocytes when cultured in
granulocyte macrophage-colony-stimulating factor (GM-CSF). Consistent
with their immature phenotype, when FdCP1 cells are cultured in IL-3
they exhibit robust protease activity and signal through truncated
Stat5 isoforms. In contrast, maturation leads to a loss of protease
activity and a switch to the expression to full-length Stat5 isoforms.
Introduction of a noncleavable, full-length Stat5 mutant into
undifferentiated FdCP1 cells leads to a partially differentiated
phenotype and prevents further differentiation in response to GM-CSF.
These results support our hypothesis that Stat5 processing is important
for myeloid maturation.
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