The glucocorticoid receptor (GR) coordinates a multitude of physiological r
esponses in vivo. In vitro, glucocorticoids are required for sustained prol
iferation of erythroid progenitors (ebls). Here, we analyze the impact of t
he GR on erythropoiesis in vive, using GR-deficient mice or mice expressing
a GR defective for transactivation. In vitro, sustained proliferation of p
rimary ebls requires an intact GR. In vive, the GR is required for rapid ex
pansion of ebls under stress situations like erythrolysis or hypoxia. A par
ticular, GR-sensitive progenitor could be identified as being responsible f
or the stress response. Thus, GR-mediated regulation of ebl proliferation i
s essential for stress erythropoiesis in vivo.