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Vol. 16, No. 21, pp. 2749-2754, November 1, 2002
1 Department of Physiology and Functional Genomics,
University of Florida College of Medicine, Gainesville, Florida 32610, USA; 2 Department of Cell Biology, Harvard Medical School,
Boston, Massachusetts 02115, USA; 3 Department of
Developmental Biology, Max-Planck-Institut für Immunbiologie,
Freiburg, Germany; 4 Cutaneous Biology Research
Center and Cardiovascular Research Center, Harvard Medical School,
Massachusetts General Hospital-East,
Charlestown, Massachusetts 02129, USA
Vertebral bodies are segmented along the anteroposterior (AP) body
axis, and the segmental identity of the vertebrae is determined by the
unique expression pattern of multiple Hox genes. Recent studies have
demonstrated that a transforming growth factor 
(TGF-) family
protein, Gdf11 (growth and differentiation
factor 11), and the activin type II receptor,
ActRIIB, are involved in controlling the spatiotemporal expression of
multiple Hox genes along the AP axis, and that the disruption of each
of these genes causes anterior transformation of the vertebrae.
Skeletal defects are more severe in Gdf11-null mice than in
ActRIIB-null mice, however, leaving it uncertain whether Gdf11 signals
via ActRIIB. Here we demonstrate using genetic and biochemical studies
that ActRIIB and its subfamily receptor, ActRIIA, cooperatively mediate the Gdf11 signal in patterning the axial vertebrae, and that Gdf11 binds to both ActRIIA and ActRIIB, and induces phosphorylation of
Smad2. In addition, we also show that these two receptors can functionally compensate for one another to mediate signaling of another
TGF- ligand, nodal, during left-right patterning and the
development of anterior head structure.
[Key Words: Activin receptor; nodal; Gdf11; vertebrae; left-right asymmetry]
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