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Related Concept Videos

In-vitro Mutagenesis01:16

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
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Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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Related Experiment Video

Updated: Jul 27, 2026

Mouse Genome Engineering Using Designer Nucleases
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Published on: April 2, 2014

Molecular mapping of the mouse ob mutation.

J M Friedman1, R L Leibel, D S Siegel

  • 1Howard Hughes Medical Institute, Rockefeller University, New York, New York 10021.

Genomics
|December 1, 1991
PubMed
Summary

Researchers mapped the mouse obesity (ob) gene to chromosome 6. This finding helps understand obesity and diabetes genetics, with potential implications for human gene mapping.

Area of Science:

  • Genetics and Genomics
  • Molecular Biology
  • Mammalian Genetics

Background:

  • The mouse ob mutation is a key genetic factor influencing obesity.
  • Understanding the genetic basis of obesity is crucial for metabolic disease research.
  • Previous mapping efforts for the ob locus were limited.

Purpose of the Study:

  • To precisely map the mouse obesity (ob) gene locus.
  • To identify genetic markers and their order on mouse chromosome 6.
  • To investigate the genetic basis of obesity and associated diabetes in mice.

Main Methods:

  • Utilized three mouse crosses: intraspecific backcross, intraspecific intercross, and interspecific intercross.
  • Employed Restriction Fragment Length Polymorphisms (RFLPs) for genotypic assignment.

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  • Assessed body mass index, plasma glucose, and insulin concentrations.

    • Main Results:

    • Successfully mapped the ob locus on mouse chromosome 6 with the order: centromere-Cola-2-Met-ob-Cpa-Tcrb.
    • Demonstrated that diabetes in ob/ob mice results from unlinked polygenes.
    • Identified that unlinked Mus spretus alleles can reduce obesity in ob/ob mice.

    Conclusions:

    • The mouse ob gene is located on chromosome 6.
    • Homologous regions flanking the ob locus suggest a potential mapping to human chromosome 7q31.
    • Genetic factors beyond the ob gene influence obesity and diabetes development.