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For example, the mouse counterpart of atm, the gene that causes the human disease ataxia telangiectasia, was identified. In humans the symptoms of this disease include movement problems, abnormal blood vessels, immune defects, and a predisposition to cancer. The mouse atm gene was specifically disrupted by gene targeting, and mice lacking this gene exhibit a range of problems similar to those exhibited by the human patients. This mouse model is useful not only for studying and understanding the function of the gene in humans and its role in the disease process, but also for testing potential therapies.

Now that the sequencing of the human and mouse genes is completed, there is a large gap between the number of genes that have been identified and our understanding of how those genes function. The next challenge is to start to determine how those genes function in normal development and how these genes are disrupted in various disease conditions. Arguably, mouse models will become even more important during this phase of the analysis of the genome, as mice are amenable to a systematic genome-wide mutation of genes, which will allow the function of large numbers of genes to be determined. see also Gene Targeting; Model Organisms; Recombinant DNA; Transgenic Animals.

Seth G. N. Grant and Douglas J. C. Strathdee


Jackson, Ian J., and Catherine M. Abbot, eds. Mouse Genetics and Transgenics: A Practical Approach. New York: Oxford University Press, 2000.

Lyon, Mary F., Sohaila Rastan, and S. D. M. Brown. Genetic Variants and Strains of the Laboratory Mouse, 3rd ed. New York: Oxford University Press, 1996.

Rossant, Janet, and Patrick P. L. Tam, eds. Mouse Development: Patterning, Morphogenesis, and Organogenesis. San Diego: Academic Press, 2001.

Roundworm: Caenorhabditis elegans nematode worm of the Caenorhabditis elegans is a nonparasitic nematode that normally lives in the soil. Nematoda pbiyluin, Although studied since the 1800s, the modern use of C. elegans as a model sys-

rnany ° wic are para tem dates to the mid-1960s. By the start of that decade, scientists thought that the "classical" problems in molecular biology were about to be solved. They began to search for a model system that would support the new challenges presented by research on multicellular organisms, particularly in developmental biology and neurology. In 1965 Sydney Brenner proposed what he thought was the ideal model organism, one that provided the best compromise between biological complexity and ease of manipulation: C. elegans.

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