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Genetic control of prion incubation period in mice

G A Carlson1, D Westaway, P A Goodman

  • 1Jackson Laboratory, Bar Harbor, Maine 04609.

Ciba Foundation Symposium
|January 1, 1988
PubMed

Insights

The prion gene complex (Prn) in mice influences scrapie incubation times. Researchers investigated if the prion protein gene (Prn-p) and scrapie incubation time gene (Prn-i) are distinct or the same, impacting prion strain interpretation.

Area of Science:

  • Genetics
  • Neuroscience
  • Molecular Biology

Background:

  • The prion gene complex (Prn) on mouse chromosome 2 contains the prion protein gene (Prn-p) and a scrapie incubation time gene (Prn-i).
  • The Prn-p gene encodes the prion protein (PrP), a key component associated with the infectious scrapie agent.
  • A specific allele of Prn-p (Prn-p^b) is linked to a gene (Prn-i) conferring exceptionally long scrapie incubation periods in certain mouse strains.

Purpose of the Study:

  • To investigate the genetic relationship between the prion protein gene (Prn-p) and the scrapie incubation time gene (Prn-i).
  • To determine if these two genes are distinct loci or a single gene.
  • To explore the implications of Prn-p allelic variations on the interpretation of prion 'strains'.

Main Methods:

  • Analysis of restriction fragment length polymorphisms (RFLPs) to distinguish allelic forms of the Prn-p gene.
  • Phenotypic analysis of scrapie incubation times in different mouse strains.
  • Observation of potential recombinant events between Prn-p genotype and incubation time phenotype.

Main Results:

  • Six allelic forms of the Prn-p gene were identified using RFLPs.
  • A long scrapie incubation time allele (Prn-i) was found exclusively in mouse strains with the Prn-p^b allele.
  • Putative recombinants suggest a possible separation between Prn-p and Prn-i, though other genetic factors could be involved.

Conclusions:

  • The genetic linkage between Prn-p and Prn-i is strong, but their precise relationship (distinct loci vs. single gene) remains uncertain.
  • Differences in host-encoded PrP, stemming from Prn-p allelic variations, could explain prion 'strains' without invoking a nucleic acid-based agent.
  • This finding has significant implications for understanding prion diseases and the nature of the infectious agent.

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