PMID- 9640329
OWN - NLM
STAT- MEDLINE
DCOM- 19980721
LR  - 20190721
IS  - 0012-1606 (Print)
IS  - 0012-1606 (Linking)
VI  - 198
IP  - 1
DP  - 1998 Jun 1
TI  - Disregulation of ocular morphogenesis by lens-specific expression of FGF-3/int-2 
      in transgenic mice.
PG  - 13-31
AB  - FGF-3, originally named int-2, was discovered as an oncogene frequently activated 
      in mammary carcinomas resulting from the chromosomal integration of the mouse 
      mammary tumor virus (MMTV). Int-2 was later designated FGF-3 based on sequence 
      homology with other members of the fibroblast growth factor (FGF) family. FGF-1 
      is the prototypical member of the FGF family, and is the only family member which 
      activates all known FGF receptor isoforms. Transgenic mice expressing in the lens 
      a form of FGF-1 engineered to be secreted show premature differentiation of the 
      entire lens epithelium. In contrast, transgenic mice engineered to secrete FGF-2 
      in the lens do not undergo premature differentiation of the lens epithelium (C. 
      M. Stolen et al., 1997, Development 124, 4009-4017). To further assess the roles 
      of FGFs and FGF receptors in lens development, the alpha A-crystallin promoter 
      was used to target expression of FGF-3 to the developing lens of transgenic mice. 
      The expression of FGF-3 in the lens rapidly induced epithelial cells throughout 
      the lens to elongate and to express fiber cell-specific proteins including MIP 
      and beta-crystallins. This premature differentiation of the lens epithelium was 
      followed by the degeneration of the entire lens. Since FGF-1 and FGF-3 can both 
      activate one FGF receptor isoform (FGFR2 IIIb) that is not activated by FGF-2, 
      these results suggest that activation of FGFR2 IIIb is sufficient to induce fiber 
      cell differentiation throughout the lens epithelium in vivo. Furthermore, 
      transgenic lens cells expressing FGF-3 were able to induce the differentiation of 
      neighboring nontransgenic lens epithelial cells in chimeric mice. Expression of 
      FGF-3 in the lens also resulted in developmental alterations of the eyelids, 
      cornea, and retina, and in the most severely affected transgenic lines, the 
      postnatal appearance of intraocular glandular structures.
FAU - Robinson, M L
AU  - Robinson ML
AD  - Children's Hospital Research Foundation, Columbus, Ohio 43205, USA.
FAU - Ohtaka-Maruyama, C
AU  - Ohtaka-Maruyama C
FAU - Chan, C C
AU  - Chan CC
FAU - Jamieson, S
AU  - Jamieson S
FAU - Dickson, C
AU  - Dickson C
FAU - Overbeek, P A
AU  - Overbeek PA
FAU - Chepelinsky, A B
AU  - Chepelinsky AB
LA  - eng
GR  - EY-06511/EY/NEI NIH HHS/United States
GR  - EY-10448/EY/NEI NIH HHS/United States
GR  - EY-10803/EY/NEI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Dev Biol
JT  - Developmental biology
JID - 0372762
RN  - 0 (Aquaporins)
RN  - 0 (Crystallins)
RN  - 0 (Eye Proteins)
RN  - 0 (Fgf3 protein, mouse)
RN  - 0 (Fibroblast Growth Factor 3)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (aquaporin 0)
RN  - 62031-54-3 (Fibroblast Growth Factors)
SB  - IM
MH  - Animals
MH  - Aquaporins
MH  - Cell Differentiation/physiology
MH  - Crystallins/genetics
MH  - Eye/cytology/*embryology
MH  - Eye Proteins/metabolism
MH  - Fibroblast Growth Factor 3
MH  - Fibroblast Growth Factors/*physiology
MH  - Gene Expression Regulation, Developmental/*genetics
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Lens, Crystalline/embryology
MH  - *Membrane Glycoproteins
MH  - Mice
MH  - Mice, Transgenic
MH  - Morphogenesis/*physiology
MH  - Phenotype
MH  - Proto-Oncogene Proteins/*physiology
MH  - RNA, Messenger/analysis
EDAT- 1998/06/26 00:00
MHDA- 1998/06/26 00:01
CRDT- 1998/06/26 00:00
PHST- 1998/06/26 00:00 [pubmed]
PHST- 1998/06/26 00:01 [medline]
PHST- 1998/06/26 00:00 [entrez]
AID - S0012160698988790 [pii]
AID - 10.1006/dbio.1998.8879 [doi]
PST - ppublish
SO  - Dev Biol. 1998 Jun 1;198(1):13-31. doi: 10.1006/dbio.1998.8879.