PMID- 10191046
OWN - NLM
STAT- MEDLINE
DCOM- 19990511
LR  - 20120605
IS  - 0012-1606 (Print)
IS  - 0012-1606 (Linking)
VI  - 208
IP  - 2
DP  - 1999 Apr 15
TI  - Murine fibroblast growth factor receptor 1alpha isoforms mediate node regression 
      and are essential for posterior mesoderm development.
PG  - 293-306
AB  - Alternative splicing in the fibroblast growth factor receptor 1 (Fgfr1) locus
      generates a variety of splicing isoforms, including FGFR1alpha isoforms, which
      contain three immunoglobulin-like loops in the extracellular domain of the
      receptor. It has been previously shown that embryos carrying targeted disruptions
      of all major isoforms die during gastrulation, displaying severe growth
      retardation and defective mesodermal structures. Here we selectively disrupted
      the FGFR1alpha isoforms and found that they play an essential role in posterior
      mesoderm formation during gastrulation. We show that the mutant embryos lack
      caudal somites, develop spina bifida, and die at 9.5-12.5 days of embryonic
      development because they are unable to establish embryonic circulation. The
      primary defect is a failure of axial mesoderm cell migration toward the posterior
      portions of the embryos during gastrulation, as revealed by regional marker
      analysis and DiI labeling. In contrast, the anterior migration of the notochord
      is unaffected and the embryonic structures rostral to the forelimb are relatively
      normal. These data demonstrate that FGF/FGFR1alpha signals are posteriorizing
      factors that control node regression and posterior embryonic development.
CI  - Copyright 1999 Academic Press.
FAU - Xu, X
AU  - Xu X
AD  - National Institute of Diabetes, Digestive and Kidney Diseases, National
      Institutes of Health, Bethesda, Maryland, 20892, USA.
FAU - Li, C
AU  - Li C
FAU - Takahashi, K
AU  - Takahashi K
FAU - Slavkin, H C
AU  - Slavkin HC
FAU - Shum, L
AU  - Shum L
FAU - Deng, C X
AU  - Deng CX
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Dev Biol
JT  - Developmental biology
JID - 0372762
RN  - 0 (Protein Isoforms)
RN  - 0 (Receptors, Fibroblast Growth Factor)
RN  - EC 2.7.10.1 (Fgfr1 protein, mouse)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
SB  - IM
MH  - Abnormalities, Multiple
MH  - Animals
MH  - Brain/abnormalities
MH  - Cell Communication
MH  - *Cell Movement
MH  - Crosses, Genetic
MH  - Embryo, Mammalian/pathology
MH  - Gastrula
MH  - Genes, Lethal
MH  - Genotype
MH  - Mesoderm/*cytology
MH  - Mice
MH  - Mice, Mutant Strains/*embryology
MH  - Mutagenesis, Site-Directed
MH  - Mutation
MH  - Protein Isoforms/deficiency/genetics/metabolism
MH  - Receptor Protein-Tyrosine Kinases/deficiency/*genetics/metabolism
MH  - Receptor, Fibroblast Growth Factor, Type 1
MH  - Receptors, Fibroblast Growth Factor/deficiency/*genetics/metabolism
MH  - Somites
MH  - Spinal Dysraphism/etiology/genetics
EDAT- 1999/04/07 00:00
MHDA- 1999/04/07 00:01
CRDT- 1999/04/07 00:00
PHST- 1999/04/07 00:00 [pubmed]
PHST- 1999/04/07 00:01 [medline]
PHST- 1999/04/07 00:00 [entrez]
AID - S0012-1606(99)99227-8 [pii]
AID - 10.1006/dbio.1999.9227 [doi]
PST - ppublish
SO  - Dev Biol. 1999 Apr 15;208(2):293-306. doi: 10.1006/dbio.1999.9227.