Standard Article

Mouse models

Part 2. Genomics

2.4. Model Organisms: Functional and Comparative Genomics

Specialist Review

  1. Michelle E. Goldsworthy,
  2. Roger D. Cox

Published Online: 15 APR 2005

DOI: 10.1002/047001153X.g204202

Encyclopedia of Genetics, Genomics, Proteomics and Bioinformatics

Encyclopedia of Genetics, Genomics, Proteomics and Bioinformatics

How to Cite

Goldsworthy, M. E. and Cox, R. D. 2005. Mouse models. Encyclopedia of Genetics, Genomics, Proteomics and Bioinformatics. 2:2.4:38.

Author Information

  1. Medical Research Council Harwell, Harwell, UK

Publication History

  1. Published Online: 15 APR 2005

Abstract

The mouse has a proven track record as a model organism that has made a significant contribution to the understanding of disease and biology relevant to the human. It is not the only model organism by any means but for the study of human disease it is perhaps one of the most widely used. We have tried to illustrate in this review the multiple approaches that have been utilized using as examples the study of type 2 diabetes and obesity in the mouse. Spontaneous mutations and knockouts have given insight into the relative contributions of differing genes in the regulation of glucose homeostasis, insulin resistance, β-cell function, and adiposity. Tissue-specific knockouts have gone some way in dissecting the relative contributions of multiple tissues and organs to disease progression. Combinations of different mutants, which individually would not produce disease, have provided polygenic models of type 2 diabetes. Sensitized ENU mutagenesis screens may yield additional novel diabetes genes. The mouse has only been one of the approaches available to us to investigate human disease but together with studies in human populations, other model organisms, and in vitro systems, it has opened unprecedented opportunities in this new century to tackle the problem of common human disease.

Keywords:

  • mouse models;
  • polygenic models of human disease;
  • type 2 diabetes;
  • glucose homeostasis;
  • obesity;
  • mutations;
  • knockouts;
  • QTLs;
  • gene-driven screen