Major histocompatibility complex
non-obese diabetic mouse
non-obese non-diabetic mouse
restriction fragment length polymorphisms
Springer Online Journal Archives 1860-2000
Summary It has been suggested that one of the recessive genes controlling diabetes in non-obese diabetic mice is linked to the major histocompatibility complex. We, therefore, performed restriction fragment length polymorphism studies of major histocompatibility complex genes (class I, II, and III) in non-obese diabetic mice in comparison with those of their non-diabetic sister strains, non-obese non-diabetic, cataract, and ILI mice which were derived from the same Jcl-ICR mice as the non-obese diabetic mouse was. When class II and III probes and a minimum of four restriction enzymes were used, class II and III genes of non-obese diabetic mice were indistinguishable from those of cataract and ILI mice but totally different from those of non-obese non-diabetic mice. The studies also indicated that Aβ, Eβ, and C4-Slp genes of non-obese diabetic, cataract, and ILI mice, and Aα, Aβ, Eβ and C4-Slp genes of non-obese non-diabetic mice are different from those of BALB/c and C57BL/6 mice, respectively. While non-obese non-diabetic mice expressed the Eα gene, non-obese diabetic, cataract, and ILI mice appeared to carry a deletion in the 5′ end of the Eα gene resulting in failure to transcribe the Eα gene. When class I probe was used, cataract mice showed very different band patterns from those of the other ICR-derived mice. It is suggested that non-obese diabetic, non-obese non-diabetic, and ILI mice contain only a single class I D region gene. Taken together, these results indicate that, although class I loci of non-obese diabetic and ILI mice were serologically typed as Kd and Db, and those of non-obese non-diabetic mice were typed as Kb and Db, no H-2g type recombination between K and D loci of non-obese diabetic, cataract, and ILI mice was evident. Since cataract and ILI mice are suggested to share the same class II and III regions with non-obese diabetic mice, they should be feasible strains for further studies to characterise the major histocompatibility complex-linked diabetogenic gene(s) of the non-obese diabetic mouse strain.
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