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ORIGINAL RESEARCH ARTICLE

Effects of an S84E Mutation of Bovine Growth Hormone in Transgenic Mice

E. J. H. Schenck^* and C. L. Brooks^*,,1

^* Department of Veterinary Biosciences and Department of Biochemistry, The Ohio State University, Columbus, Ohio 43210

To whom requests for reprints should be addressed at ¹ The Ohio State University, 1925 Coffey Road, Columbus, OH 43210. E-mail: Brooks.8{at}osu.edu

The ability of mutant bovine growth hormones (bGH) to serve as either agonist or antagonist has been demonstrated in transgenic mice. We have prepared two transgenic strains of FVB/N mice, one expressing wild-type bGH and a second with a glutamic acid mutation at serine 84 in helix 2. Comparison of their phenotypes to those of nontransgenic littermates indicates that wild-type bGH induces a previously described phenotype for hyper-somatotrophic mice. In contrast, the replacement of the side chain hydroxyl at serine 84 with acetic acid produced a phenotype that expressed bGH at appreciable concentrations, but failed to elicit the phenotype observed with either an agonist or an antagonist of bGH. These results indicate that serine 84 is crucial for the activity of bGH despite this site being distal to the receptor binding surfaces.

Key Words: somatotrophin • bovine • transgenic mouse • IGF-1