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Blood, Vol. 92 No. 5 (September 1), 1998:
pp. 1491-1496
RAPID COMMUNICATION
The Prolactin Receptor Rescues EpoR / Erythroid
Progenitors and Replaces EpoR in a Synergistic Interaction With
c-kit
Merav Socolovsky,
Amy E.J. Fallon, and
Harvey F. Lodish
From the Whitehead Institute for Biomedical Research, Cambridge, MA;
and the Department of Biology, Massachusetts Institute of Technology,
Cambridge.
We recently showed that a retrovirally transduced prolactin receptor
(PrlR) efficiently supports the differentiation of wild-type burst-forming unit erythroid (BFU-e) and colony-forming unit erythroid (CFU-e) progenitors in response to prolactin and in the absence of
erythropoietin (Epo). To examine directly whether the Epo receptor (EpoR) expressed by wild-type erythroid progenitors was essential for
their terminal differentiation, we infected EpoR /
progenitors with retroviral constructs encoding either the PrlR or a
chimeric receptor containing the extracellular domain of the PrlR and
intracellular domain of EpoR. In response to prolactin, both receptors
were equally efficient in supporting full differentiation of the
EpoR/ progenitors into erythroid colonies in vitro.
Therefore, there is no requirement for an EpoR-unique signal in
erythroid differentiation; EpoR signaling has no instructive role in
red blood cell differentiation. A synergistic interaction between EpoR
and c-kit is essential for the production of normal numbers of
red blood cells, as demonstrated by the severe anemia of mice mutant
for either c-kit or its ligand, stem cell factor. We show that
the addition of stem cell factor potentiates the ability of the PrlR to
support differentiation of both EpoR/ and wild-type
CFU-e progenitors. This synergism is quantitatively equivalent to that
observed between c-kit and EpoR. Therefore, there is no
requirement for an EpoR-unique signal in the synergistic interaction
between c-kit and EpoR.
© 1998 by The American Society of Hematology.
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