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Related Experiment Videos

Androgen receptor functions from reverse genetic models.

Takahiro Matsumoto1, Ken-ichi Takeyama, Takashi Sato

  • 1Laboratory of Nuclear Signaling, Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.

The Journal of Steroid Biochemistry and Molecular Biology
|August 29, 2003
PubMed
Summary

Researchers created androgen receptor knockout (ARKO) mice and a Drosophila model to study AR dysfunction. ARKO mice showed testicular feminization and obesity, while fruit flies with mutant human AR developed neurodegeneration when exposed to androgens.

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Area of Science:

  • Endocrinology
  • Neuroscience
  • Genetics

Background:

  • The androgen receptor (AR) regulates physiological processes, and its dysfunction is linked to conditions like prostate cancer and Kennedy's disease.
  • Lack of genetic models has hindered understanding the molecular basis of AR-related disorders.

Purpose of the Study:

  • To generate and characterize androgen receptor knockout (ARKO) mice.
  • To investigate the role of polyglutamine (polyQ)-expanded human AR mutants in neurodegeneration using a Drosophila model.

Main Methods:

  • Conditional targeting using the Cre-loxP system to generate ARKO mice.
  • Ectopic expression of wild-type and polyQ-expanded human AR in Drosophila.

Main Results:

Related Experiment Videos

  • ARKO male mice displayed testicular feminization abnormalities and late-onset obesity with white adipose tissue accumulation.
  • While adult fly neurons expressing mutant hAR showed no overt phenotype, androgen ingestion induced significant neurodegeneration.

    • Conclusions:

    • ARKO mice serve as a valuable model for studying AR-related disorders, including Tfm syndrome and obesity.
    • The Drosophila model demonstrates that polyQ-expanded human AR can lead to neurodegeneration in response to androgens, suggesting a mechanism for certain neurodegenerative diseases.