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211 results on '"Dickson, Clive"'

14. Disregulation of ocular morphogenesis by lens-specific expression of FGF-3/Int-2 in transgenic mice

Author

Robinson, Michael L., Ohtaka-Maruyama, Chiaki, Chan, Chi-Chao, Jamieson, Susan, Dickson, Clive, Overbeek, Paul A., and Chepelinsky, Ana B.

Subjects
Genetically modified mice -- Research, Fibroblast growth factors -- Research, Eye -- Genetic aspects, Morphogenesis -- Research, Biological sciences
Abstract

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.

Published
1998

20. Subcellular fate of the int-2 oncoprotein is determined by choice of initiation codon

Author

Acland, Piers, Dixon, Mark, Peters, Gordon, and Dickson, Clive

Subjects
Cells -- Genetic aspects, Proteins -- Genetic aspects, Fibroblast growth factors -- Physiological aspects, Mice as laboratory animals -- Genetic aspects, Carcinogenesis -- Genetic aspects, Oncogenes -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Published
1990

25. Fibroblast Growth Factor Receptor 2-IIIb Acts Upstream of Shh and Fgf4 and Is Required for Limb Bud Maintenance but Not for the Induction of Fgf8, Fgf10, Msx1, or Bmp4

Author

Revest, Jean-Michel, Spencer-Dene, Bradley, Kerr, Karen, De Moerlooze, Laurence, Rosewell, Ian, and Dickson, Clive

Subjects
Developmental biology -- Research, Mice as laboratory animals -- Usage, Fibroblast growth factors -- Analysis, Extremities (Anatomy) -- Genetic aspects, Biological sciences
Abstract

Mice deficient for FgfR2-IIIb were generated by placing translational stop codons and an IRES-LacZ cassette into exon IIIb of FgfR2. Expression of the alternatively spliced receptor isoform, FgfR2-IIIc, was not affected in mice deficient for the IIIb isoform. FgfR2-[IIIb.sup.-/- lacZ] mice survive to term but show dysgenesis of the kidneys, salivary glands, adrenal glands, thymus, pancreas, skin, otic vesicles, glandular stomach, and hair follicles, and agenesis of the lungs, anterior pituitary, thyroid, teeth, and limbs. Detailed analysis of limb development revealed an essential role for FgfR2-IIIb in maintaining the AER. Its absence did not prevent expression of Fgf8, Fgf10, Bmp4, and Msx1, but did prevent induction of Shh and Fgf4, indicating that they are downstream targets of FgfR2-IIIb activation. In the absence of FgfR2-IIIb, extensive apoptosis of the limb bud ectoderm and mesenchyme occurs between E10 and E10.5, providing evidence that Fgfs act primarily as survival factors. We propose that FgfR2-IIIb is not required for limb bud initiation, but is essential for its maintenance and growth. [C] 2001 Academic Press Key Words: fibroblast growth factor receptor-2; IIIb isoform; Fgfs; limb development; mesenchymal-epithelial interactions.

Published
2001

32. Fibroblast growth factor 9 secretion is mediated by a non-cleaved amino- terminal signal sequence

Author

Revest, Jean-Michel, De Moerlooze, Laurence, Dickson, Clive, Revest, Jean-Michel, De Moerlooze, Laurence, and Dickson, Clive

Abstract

Fibroblast growth factors are a family of intercellular signaling molecules with multiple and varied roles in animal development. Most are exported from cells by means of a classical amino-terminal signal sequence that is cleaved from the mature protein during its passage through the secretory pathway. Fibroblast growth factor-9 (Fgf-9) does not contain a recognizable signal sequence, although it is efficiently secreted. In this study, we show that Fgf-9 enters the endoplasmic reticulum and traverses the Golgi complex in a similar manner to other constitutively secreted proteins. Deletion and point mutation analysis has revealed an atypical non-cleaved signal sequence within the amino-terminal region of Fgf-9. Moreover, the first 28 amino acids of Fgf-9 can function as an efficient non-cleaved signal peptide when appended to the amino terminus of green fluorescent protein., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2000

33. An important role for the IIIb isoform of fibroblast growth factor receptor 2 (FGFR2) in mesenchymal-epithelial signalling during mouse organogenesis

Author

De Moerlooze, Laurence, Spencer-Dene, Bradley, Revest, Jean-Michel, Hajihosseini, Mohammad, Rosewell, Ian, Dickson, Clive, De Moerlooze, Laurence, Spencer-Dene, Bradley, Revest, Jean-Michel, Hajihosseini, Mohammad, Rosewell, Ian, and Dickson, Clive

Abstract

The fibroblast growth factor receptor 2 gene is differentially spliced to encode two transmembrane tyrosine kinase receptor proteins that have different ligand-binding specificities and exclusive tissue distributions. We have used Cre-mediated excision to generate mice lacking the IIIb form of fibroblast growth factor receptor 2 whilst retaining expression of the IIIc form. Fibroblast growth factor receptor 2(IIIb) null mice are viable until birth, but have severe defects of the limbs, lung and anterior pituitary gland. The development of these structures appears to initiate, but then fails with the tissues undergoing extensive apoptosis. There are also developmental abnormalities of the salivary glands, inner ear, teeth and skin, as well as minor defects in skull formation. Our findings point to a key role for fibroblast growth factor receptor 2(IIIb) in mesenchymal-epithelial signalling during early organogenesis., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2000

43. Growth factors in development, repair and disease

Author

Braun, Susanne, primary, auf dem Keller, Ulrich, additional, Beer, Hans-Dietmar, additional, Krampert, Monika, additional, Müller, Mischa, additional, Werner, Silke, additional, Dickson, Clive, additional, and Werner, Sabine, additional

Published
2002
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