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Molecular cloning of a mink prion protein gene
H A Kretzschmar1, M Neumann, G Riethmüller
1Institute of Neuropathology, University of Munich, Germany.
Abstract:
Transmissible mink encephalopathy (TME) is a rare disease which is presumably transmitted to ranch-raised mink from scrapie-infected sheep offal or bovine spongiform encephalopathy-infected cattle products. Although the infectious agent of TME has not been isolated, there is circumstantial evidence that TME is caused by prions. The experimental host range of TME includes sheep, cattle, monkeys and hamsters. However, TME has never been transmitted to mice. Since experiments in transgenic animals have shown that the prion protein (PrP) gene modulates the susceptibility, incubation time and neuropathology of prion-induced disease, we have started to analyse the mink PrP gene. PrP, as deduced from a genomic DNA sequence, consists of 257 amino acids and overall shows similarity of 84 to 90% with the sequences of the PrPs of other mammalian species. It remains to be determined whether these differences in the primary structure of PrP will explain the peculiar host range of TME.
Insights
Transmissible mink encephalopathy (TME) is a prion disease. Researchers analyzed the mink prion protein (PrP) gene, finding it similar to other mammals, but its role in TME
Area of Science:
- Veterinary Neurology
- Prion Diseases
- Molecular Biology
Background:
- Transmissible mink encephalopathy (TME) is a rare prion disease.
- TME is suspected to originate from scrapie-infected sheep or bovine spongiform encephalopathy-infected cattle products.
- The TME infectious agent has not been isolated, but prions are the suspected cause.
Purpose of the Study:
- To analyze the prion protein (PrP) gene in mink.
- To investigate potential genetic factors influencing TME susceptibility and host range.
Main Methods:
- Genomic DNA sequencing of the mink PrP gene.
- Deduction of the PrP amino acid sequence.
- Comparison of mink PrP sequence with PrPs from other mammalian species.
Main Results:
- The mink PrP gene encodes a 257-amino acid protein.
- Mink PrP exhibits 84-90% sequence similarity to PrPs of other mammals.
- TME has a peculiar experimental host range, not including mice.
Conclusions:
- The primary structure of mink PrP shows significant similarity to other mammals.
- Differences in PrP structure may explain TME's unique host range.
- Further research is needed to fully understand the role of PrP in TME pathogenesis.