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Expression of Human Beta-amyloid Peptide in Transgenic Caenorhabditis Elegans

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Specialty Science
Date 1995 Sep 26
PMID 7568134
Citations 285
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Abstract

Transgenic Caenorhabditis elegans nematodes have been engineered to express potentially amyloidic human proteins. These animals contain constructs in which the muscle-specific unc-54 promoter/enhancer of C. elegans drives the expression of the appropriate coding regions derived from human cDNA clones. Animals containing constructs expressing the 42-amino acid beta-amyloid peptide (derived from human amyloid precursor protein cDNA) produce muscle-specific deposits immunoreactive with anti-beta-amyloid polyclonal and monoclonal antibodies. A subset of these deposits also bind the amyloid-specific dye thioflavin S, indicating that these deposits have the tinctural characteristics of classic amyloid. Co-expression of beta-peptide and transthyretin, a protein implicated in preventing the formation of insoluble beta-amyloid, leads to a dramatic reduction in the number of dye-reactive deposits. These results suggest that this invertebrate model may be useful for in vivo investigation of factors that modulate amyloid formation.

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References
1.
Glenner G, Wong C . Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun. 1984; 120(3):885-90. DOI: 10.1016/s0006-291x(84)80190-4. View

2.
Durell S, Guy H, Arispe N, Rojas E, Pollard H . Theoretical models of the ion channel structure of amyloid beta-protein. Biophys J. 1994; 67(6):2137-45. PMC: 1225600. DOI: 10.1016/S0006-3495(94)80717-9. View

3.
Ponte P, Schilling J, Miller J, Hsu D, Greenberg B, Davis K . A new A4 amyloid mRNA contains a domain homologous to serine proteinase inhibitors. Nature. 1988; 331(6156):525-7. DOI: 10.1038/331525a0. View

4.
Higuchi R, Krummel B, Saiki R . A general method of in vitro preparation and specific mutagenesis of DNA fragments: study of protein and DNA interactions. Nucleic Acids Res. 1988; 16(15):7351-67. PMC: 338413. DOI: 10.1093/nar/16.15.7351. View

5.
Benson M . Familial amyloidotic polyneuropathy. Trends Neurosci. 1989; 12(3):88-92. DOI: 10.1016/0166-2236(89)90162-8. View