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Vol. 15, No. 16, pp. 2094-2110, August 15, 2001
1 Laboratory of Molecular Biology, NINDS, National
Institutes of Health, Bethesda, Maryland 20892-4092, USA;
2 Laboratory of Stem Cell and Tumor Biology, Neurosurgery and
Cellular Biochemistry and Biophysics, Memorial Sloan Kettering Cancer
Center; New York, New York 10021, USA
Bone morphogenetic proteins (BMPs) have diverse and sometimes
paradoxical effects during embryonic development. To determine the
mechanisms underlying BMP actions, we analyzed the expression and
function of two BMP receptors, BMPR-IA and BMPR-IB, in neural precursor
cells in vitro and in vivo. Neural precursor cells always express
Bmpr-1a, but Bmpr-1b is not expressed until embryonic day 9 and is restricted to the dorsal neural tube surrounding the
source of BMP ligands. BMPR-IA activation induces (and Sonic hedgehog
prevents) expression of Bmpr-1b along with dorsal identity genes in precursor cells and promotes their proliferation. When BMPR-IB
is activated, it limits precursor cell numbers by causing mitotic
arrest. This results in apoptosis in early gestation embryos and
terminal differentiation in mid-gestation embryos. Thus, BMP actions
are first inducing (through BMPR-IA) and then terminating (through
BMPR-IB), based on the accumulation of BMPR-IB relative to BMPR-IA. We
describe a feed-forward mechanism to explain how the sequential actions
of these receptors control the production and fate of dorsal precursor
cells from neural stem cells.
[Key Words: Bone morphogenetic protein; receptor; neural; development; precursor cell]
Baltimore County, Baltimore, MD
21201, USA;
5NeuralStem Biopharmaceuticals, Bethesda, MD 20817, USA.
6
Corresponding author.
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