International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

Table of Contents * Genes, Physical Mapping and Sequencing * Gene Identification * Bioinformatics * Common Resources * RIKEN Session * Functional Genomics * Complex Traits * Mutagenesis * Developmental Genetics and Differentiation * Verne Chapman Memorial Lecture I and II

G14. Functional Variation of QTL for Non-Insulin Dependent Diabetes Mellitus in Mice

Sei Komatsu^{1, 2, 4}, Atsushi Yoshiki^{2, 3}, Yasushi Okazaki^{1, 2}, Yasuhiro Tomaru¹, Sachihiko Watanabe¹, Masami Muramatsu¹, Moriaki Kusakabe^{2, 3}, and Yoshihide Hayashizaki^1,2,4
1Laboratory for Genome Exploration Research Group, RIKEN Genomic Sciences Center (GSC) and Genome Science Laboratory, RIKEN Tsukuba Institute;
²Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST); ³Experimental Animal Research Division, Biogenic Resources Center, RIKEN Tsukuba Institute,
⁴Institute of Basic Medical Sciences, University of Tsukuba, 3-1-1 Koyadai, Tsukuba 305-0074, JAPAN

Non-insulin dependent diabetes mellitus (NIDDM) accounts for serious secondary sequelae with the high mortality. Diabetic KKAy strain and either non-diabetic PWK or C3H strain were mated and two sets of the resultant F2 progeny ((KKAyPWK) F2; n=229 and (KKAyC3H) F2; n=284) were analyzed in the following three phenotypes: hyperglycemia (HG), glucose intolerance (GI), and obesity (OB). Nine QTLs (Nidd1k through Nidd8k, and Bwt1k) including four novels (Nidd1k, Nidd4k, Nidd5k, and Nidd7k) were detected. Two QTLs (Nidd1k and Nidd2k) were commonly identified for both progeny set. The five QTLs (Nidd4k, Nidd5k, Nidd6k and Nidd7k) were unique to (KKAyPWK) F2 and one QTL (Nidd8k) was found specifically only (KKAyC3H) F2. Interestingly, Nidd1k affected GI as well as HG in (KKAyPWK) F2, whereas only HG was affected in (KKAyC3H) F2. This might suggest that Nidd1k affected differently on phenotypic expression on F2 progeny set. Nidd2k including agouti gene had linkage to GI and OB in both progeny. Thus, Nidd1k for NIDDM generates functional variation depending upon genetic background of mating partner for affected mice.