TY - JOUR
T1 - FGF10 acts as a major ligand for FGF receptor 2 IIIb in mouse multi-organ development
AU - Ohuchi, Hideyo
AU - Hori, Yukiko
AU - Yamasaki, Masahiro
AU - Harada, Hidemitsu
AU - Sekine, Keisuke
AU - Kato, Shigeaki
AU - Itoh, Nobuyuki
N1 - Funding Information:
We thank Dr. Sabine Werner for suggestions on the skin analysis and Dr. Sumihare Noji for critical reading of the manuscript. This work was partly funded by grants from the Japanese Ministry of Education, Science, Sports, and Culture to H.O., and from the Human Frontier Science Program to N.I.
PY - 2000/11/2
Y1 - 2000/11/2
N2 - FGF receptor 2 isoform IIIb (FGFR2b), originally discovered as a receptor for FGF7, is known to be an important receptor in vertebrate morphogenesis, because FGFR2b null mice exhibit agenesis or dysgenesis of various organs, which undergo budding and branching morphogenesis. Since FGF7 null mice do not exhibit marked defects in organogenesis, it has been considered that other FGF(s) than FGF7 might function as a major ligand for FGFR2b during organogenesis. One of the candidate ligands is FGF10, because FGF10 binds to FGFR2b with high affinity and the formation of the limb and lung is arrested in FGF10 null mice as found in FGFR2b-deficient mice. Previous analyses of FGF10 null mice revealed that FGF10 is required for limb and lung development. To elucidate the role of FGF10 in wide-range organogenesis, we further analyzed the phenotypes of the FGF10 knockout mice. We found diverse phenotypes closely related to those for FGFR2b-deficient mice, which includes the absence of thyroid, pituitary, and salivary glands, while minor defects were observed in the formarion of teeth, kidneys, hair follicles, and digestive organs. These results suggest that FGF10 acts as a major ligand for FGFR2b in mouse multi-organ development. (C) 2000 Academic Press.
AB - FGF receptor 2 isoform IIIb (FGFR2b), originally discovered as a receptor for FGF7, is known to be an important receptor in vertebrate morphogenesis, because FGFR2b null mice exhibit agenesis or dysgenesis of various organs, which undergo budding and branching morphogenesis. Since FGF7 null mice do not exhibit marked defects in organogenesis, it has been considered that other FGF(s) than FGF7 might function as a major ligand for FGFR2b during organogenesis. One of the candidate ligands is FGF10, because FGF10 binds to FGFR2b with high affinity and the formation of the limb and lung is arrested in FGF10 null mice as found in FGFR2b-deficient mice. Previous analyses of FGF10 null mice revealed that FGF10 is required for limb and lung development. To elucidate the role of FGF10 in wide-range organogenesis, we further analyzed the phenotypes of the FGF10 knockout mice. We found diverse phenotypes closely related to those for FGFR2b-deficient mice, which includes the absence of thyroid, pituitary, and salivary glands, while minor defects were observed in the formarion of teeth, kidneys, hair follicles, and digestive organs. These results suggest that FGF10 acts as a major ligand for FGFR2b in mouse multi-organ development. (C) 2000 Academic Press.
KW - Budding morphogenesis
KW - Epithelial-mesenchymal interactions
KW - FGF10
KW - FGFR2b
KW - Fibroblast growth factor 10
KW - Knockout mouse
KW - Organogenesis
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U2 - 10.1006/bbrc.2000.3721
DO - 10.1006/bbrc.2000.3721
M3 - Article
C2 - 11062007
AN - SCOPUS:0034597752
SN - 0006-291X
VL - 277
SP - 643
EP - 649
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -