ArticleMammalian genome : official journal of the International Mammalian Genome Society2008
DA rats from two colonies differ genetically and in their arthritis susceptibility.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Strain-Related Differences in the Immune Response: Relevance to Human Stroke.Translational stroke research · 2016Review
- Article
- Identification of candidate risk gene variations by whole-genome sequence analysis of four rat strains commonly used in inflammation research.BMC genomics · 2014Article
- Rodent preclinical models for developing novel antiarthritic molecules: comparative biology and preferred methods for evaluating efficacy.Journal of biomedicine & biotechnology · 2011Review
- Finemapping of the arthritis QTL Pia7 reveals co-localization with Oia2 and the APLEC locus.Genes and immunity · 2010Article
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2 authors.
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Abstract
The arthritis-susceptible DA rat is one of the most commonly used rat strains for genetic linkage analysis and is instrumental for the identification of many genetic loci. Even though DA rats were kept as inbred lines at different institutes and suppliers, it became obvious that the various breeding stocks differed genetically. To be able to compare the results from different linkage studies it is very import to verify the genetic background of the substrains used in those studies. We performed a genetic and phenotypic analysis of two DA substrains, DA/ZtmRhd and DA/OlaHsd, and found several genetic differences. One of the allelic differences between the DA/ZtmRhd and the DA/OlaHsd strain was located at rat chromosome 3, a 17-Mb large fragment, including the peak marker of a previously identified quantitative trait locus (QTL) for collagen-induced arthritis, Cia11. In addition, the substrains exhibited a significant difference in the susceptibility to pristane-induced arthritis (PIA) and disease severity of collagen-induced arthritis and PIA. However, by generating and testing a congenic line, we could demonstrate that phenotypic differences were not due to the contaminating fragment on chromosome 3. Nevertheless, we conclude that DA substrains show distinct genetic differences and caution should be taken when comparing arthritis data from different DA substrains.
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