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Related Experiment Videos

GFAP: functional implications gleaned from studies of genetically engineered mice.

Albee Messing1, Michael Brenner2,3

  • 1Department of Pathobiological Sciences, Waisman Center and School of Veterinary Medicine; University of Wisconsin, Madison, Wisconsin.

Glia
|May 23, 2003
PubMed
Summary

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Glial fibrillary acidic protein (GFAP) absence has subtle effects, but over-expression reveals its critical role in astrocyte function and Alexander disease. GFAP mouse models illuminate astrocyte biology and disease mechanisms.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Glial fibrillary acidic protein (GFAP) is a major intermediate filament protein in mature astrocytes.
  • Its specific expression suggests a crucial function in astrocyte biology.
  • Understanding GFAP's role is key to comprehending astrocyte function and related neurological disorders.

Purpose of the Study:

  • To investigate the function of the GFAP gene using genetically modified mouse models.
  • To explore the consequences of GFAP absence, alteration, and over-expression.
  • To elucidate the link between GFAP mutations and Alexander disease.

Main Methods:

  • Generation of mice with null, modified, or added wild-type GFAP alleles.
  • Analysis of GFAP-deficient, altered, and over-expressing mouse phenotypes.

Related Experiment Videos

  • Correlation of GFAP gene modifications with astrocyte function and disease pathology.

    • Main Results:

    • Absence of GFAP resulted in surprisingly subtle developmental effects.
    • GFAP over-expression was often lethal.
    • GFAP coding mutations were identified as the cause of most Alexander disease cases.

    Conclusions:

    • GFAP plays a critical, non-redundant role in astrocyte function, particularly under conditions of stress or over-expression.
    • GFAP mouse models are invaluable tools for studying astrocyte biology.
    • These models have significantly advanced our understanding of Alexander disease pathogenesis.