Molecular Neurobiology

, Volume 8, Issue 2, pp 121–127

129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal

Authors

  • J. C. Manson
    • Institute for Animal HealthAFRC and MRC Neuropathogenesis Unit
  • A. R. Clarke
    • CRC Laboratories, Department of PathologyUniversity of Edinburgh
  • M. L. Hooper
    • CRC Laboratories, Department of PathologyUniversity of Edinburgh
  • L. Aitchison
    • Institute for Animal HealthAFRC and MRC Neuropathogenesis Unit
  • I. McConnell
    • Institute for Animal HealthAFRC and MRC Neuropathogenesis Unit
  • J. Hope
    • Institute for Animal HealthAFRC and MRC Neuropathogenesis Unit
Neurodegenerative Diseases Part II: Transmissible Neurodegenerative Disorders (Proceedings of the symposium “Transmissible and Nontransmissible Neurodegenerative Disorders” held in Ocho Rios, Jamaica, February 28–March 5, 1993)

DOI: 10.1007/BF02780662

Cite this article as:
Manson, J.C., Clarke, A.R., Hooper, M.L. et al. Mol Neurobiol (1994) 8: 121. doi:10.1007/BF02780662

Abstract

The neural membrane glycoprotein PrP is implicated in the pathogenesis of the transmissible spongiform encephalopathies; however, the normal function of PrP and its precise role in disease are not understood. Recently, gene targeting has been used to produce mice withneo/PrP fusion transcripts, but no detectable PrP protein in the brain (1). Here we report the use of a different targeting strategy, to produce inbred mice with a complete absence of both PrP protein and mRNA sequences. At 7 mo of age, these mice show no overt phenotypic abnormalities despite the normal high levels of expression of PrP during mouse development. The mice are being used in experiments designed to address the role of PrP in the pathogenesis of scrapie and the replication of infectivity.

Index Entries

Gene targetingPrP genenull mutation

Copyright information

© Humana Press Inc 1994