International Mammalian Genome Society


The 13th International Mouse Genome Conference
October 31-November 3, 1999

Table of Contents * Structure * Bioinformatics * Sequence * Mapping * New Tools * Gene Discovery * Developmental * Mutagenesis * Functional Genomics

E45 Genome Wide Scan for Modifiers of BSE Susceptibility

K. Manolakou1, M. Bruce2, I. Jackson1. 1MRC Human Genetics Unit, Edinburgh, 2Neuropathogenesis Unit, University of Edinburgh

Susceptibility to transmissible spongiform encephalopathies in mice is mainly determined by variants of the PrP gene, located on distal chromosome 2. However there is not a one-to-one relationship between genotype and phenotype suggesting that prion susceptibility might be a complex trait. When RIII and C57BL6 strains of mice are challenged with BSE inoculum, the latency of the disease differs between these strains although they are apparently identical for the PrP gene, suggesting the existence of modifiers responsible for prion susceptibility.

In order to identify and map those modifiers we have set up backcrosses between the two strains and a total of 1200 N1 backcross animals have been challenged intra-cerebrally with BSE inoculum. Currently phenotypic data for approximately of these animals, corresponding to the left tail of the distribution of the incubation period of the disease (days till death), are available. Microsatellite genotype data have been collected for the first 376 animals challenged, with 80 markers spread through out the genome. Among the genotyped animals has already succumbed to the disease and preliminary analysis pinpoints few autosomes. However, judging from the number of animals on which the preliminary analysis is based and the fact that these animals correspond only to one of the extremities of the distribution, it is likely that among the autosomes detected there might be false positives.

Genotypic data for all the chromosomes are currently collected for the rest of the N1 backcross animals corresponding to the short incubation extremity of the phenotypic distribution, while shortly we expect to reach the other extremity of the distribution and genotype those animals as well. We will present our latest results localising potential modifiers of BSE incubation period.

 


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