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Submitted on August 27, 2003
Accepted on January 9, 2004
Ingenium Pharmaceuticals AG, Fraunhoferstrasse 13, D-82152 Martinsried, Germany; GSF National Research Center for Environment and Health, Institute of Experimental Genetics, Ingolstaedter Landstrasse 1, D-85764 Oberschleissheim, Germany; Dept. of Psychiatry, Obesity Research Center, University of Cincinnati - Genome Research Institute, Ohio 45267-0559, USA
* To whom correspondence should be addressed. E-mail: meyerc{at}staff.uni-marburg.de.
The SMA1-mouse is a novel ENU (ethyl-nitroso-urea) induced mouse mutant that carries an a
g missense mutation in exon 5 of the growth hormone (GH) gene, which translates to a D167G amino acid exchange in the mature protein. Mice carrying the mutation are characterized by dwarfism, predominantly due to the reduction (sma1/+) or absence (sma1/sma1) of the GH mediated peripubertal growth spurt, with sma1/+ mice displaying a less pronounced phenotype. All genotypes are viable and fertile, and the mode of inheritance is in accordance with a semidominant Mendelian trait. Adult SMA1 mice accumulate excessive amounts of subcutaneous and visceral fat in the presence of elevated plasma ghrelin levels, possibly reflecting altered energy partitioning. Our results suggest impaired storage and/or secretion of pituitary GH in mutants, resulting in reduced pituitary GH and reduced GH stimulated IGF-1 (insulin-like growth factor 1) expression. Generation and identification of the SMA1 mouse exemplifies the power of the combination of random mouse mutagenesis with a highly detailed phenotype-analysis as a successful strategy for the detection and analysis of novel gene-function relationships.
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