TY - JOUR
T1 - The EGF-CFC protein one-eyed pinhead is essential for nodal signaling
AU - Gritsman, Kira
AU - Zhang, Jiaojiao
AU - Cheng, Simon
AU - Heckscher, Elizabeth
AU - Talbot, William S.
AU - Schier, Alexander F.
N1 - Funding Information:
We thank M. Shen, R. Lehmann, N. Perrimon, and members of the Schier and Talbot labs for discussions; D. Lee for unpublished results; R. Burdine, S. Dougan, and G. Fishell for comments on the manuscript; colleagues in the zebrafish field for probes; R. Harland, A. Hemmati-Brivanlou, M. Rebagliati, R. Toyama, and I. Dawid for expression constructs; and S. McManus and R. Feeney for fish care. This research was supported by NIH grants RO1GM57825 (W. S. T) and RO1GM56211 (A. F. S.).
PY - 1999/4/2
Y1 - 1999/4/2
N2 - The zebrafish EGF-CFC gene one-eyed pinhead (oep) is required zygotically for the formation of the ventral neuroectoderm, endoderm, and prechordal plate. Here we report that embryos lacking both maternal and zygotic Oep activity are defective in germ layer formation, organizer development, and the positioning of the anterior-posterior axis. An identical phenotype is displayed by double mutants for the nodal-related genes squint and cyclops. Mutations in oep eliminate the response to Squint and Cyclops overexpression but are suppressed by expression of Activin and activated forms of the type I receptor ActRIB and Smad2. Expression of the murine EGF- CFC gene cripto rescues oep mutants. These results suggest a conserved role for EGF-CFC proteins as essential extracellular cofactors for Nodal signaling during vertebrate development.
AB - The zebrafish EGF-CFC gene one-eyed pinhead (oep) is required zygotically for the formation of the ventral neuroectoderm, endoderm, and prechordal plate. Here we report that embryos lacking both maternal and zygotic Oep activity are defective in germ layer formation, organizer development, and the positioning of the anterior-posterior axis. An identical phenotype is displayed by double mutants for the nodal-related genes squint and cyclops. Mutations in oep eliminate the response to Squint and Cyclops overexpression but are suppressed by expression of Activin and activated forms of the type I receptor ActRIB and Smad2. Expression of the murine EGF- CFC gene cripto rescues oep mutants. These results suggest a conserved role for EGF-CFC proteins as essential extracellular cofactors for Nodal signaling during vertebrate development.
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U2 - 10.1016/S0092-8674(00)80720-5
DO - 10.1016/S0092-8674(00)80720-5
M3 - Article
C2 - 10199408
AN - SCOPUS:0033515638
SN - 0092-8674
VL - 97
SP - 121
EP - 132
JO - Cell
JF - Cell
IS - 1
ER -