1. Exp Anim. 2001 Apr;50(2):115-23.
Identification of epistatic interactions involved in non-insulin-dependent
diabetes mellitus in the Otsuka Long-Evans Tokushima Fatty rat.
Yamada T(1), Miyake T, Sugiura K, Narita A, Wei K, Wei S, Moralejo DH, Ogino T,
Gaillard C, Sasaki Y, Matsumoto K.
Author information:
(1)Laboratory of Animal Breeding and Genetics, Graduate School of Agriculture,
Kyoto University, Kyoto, Kyoto 606-8502.
The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for
obese-type non-insulin-dependent diabetes mellitus (NIDDM) in humans. Our present
investigation was designed to identify epistatic interactions influencing NIDDM
by performing least squares analysis of variance of all pairs of informative
markers in 160 F2 progenies bred from an intercross of OLETF and Fischer-344
rats. We identified four interactions between Nidd15/of (chromosome 7) and
Nidd16/of (chromosome 14), Nidd15/of and Nidd17/of (chromosome 15), Nidd16/of and
Nidd18/of (chromosome 15), and Nidd16/of and Nidd19/of (chromosome 17), which
account for a total of approximately 40% of the genetic variation of entire
glucose levels after glucose challenge in the F2. The Nidd16/of locus, which is
involved in three of four digenic interactions, and the Nidd19/of are likely to
correspond to Nidd2/of and Nidd14/of, NIDDM loci previously identified in the F2
by single-QTL model and multiple-QTL model, respectively, while Nidd15/of,
Nidd17/of and Nidd18/of loci reflect novel NIDDM loci. An aberrant increase of
the entire glucose level due to synergism occurs in the double OLETF homozygote
genotype of Nidd15/of and Nidd16/of, and of Nidd16/of and Nidd19/of, as well as
in the OLETF homozygote genotypes of Nidd15/of and Nidd16/of, respectively,
combined with the heterozygote genotypes of Nidd17/of and Nidd18/of. These
findings demonstrate that inter-allelic interactions are likely to be an
important component of NIDDM susceptibility.
PMID: 11381614 [PubMed - indexed for MEDLINE]
PUBMED: 11381614
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