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

J C Manson, A R Clarke, M L Hooper, L Aitchison, I McConnell, J Hope

Research output: Contribution to journalArticlepeer-review

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 with neo/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.

Original languageEnglish
Pages (from-to)121-7
Number of pages7
JournalMolecular Neurobiology
Volume8
Issue number2-3
DOIs
Publication statusPublished - 1 Apr 1994

Keywords

  • Aging
  • Animals
  • Blotting, Northern
  • Brain
  • Chimera
  • Embryo, Mammalian
  • Gene Expression
  • Genetic Vectors
  • Heterozygote
  • Homozygote
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Mutant Strains
  • Mutation
  • Prions
  • RNA, Messenger
  • Reference Values
  • Scrapie

Fingerprint

Dive into the research topics of '129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal'. Together they form a unique fingerprint.

Cite this