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The inability to construct animal models of human diseases caused by mutated mitochondrial DNA (mtDNA) has been a major obstacle to investigating pathogenetic mechanisms associated with specific mtDNA mutations. Mice carrying a large-scale deletion in mtDNA have now been produced. They display some of the key features of the human disorder, but there are surprising differences.
Positional cloning of common disease genes is a central but elusive goal of human geneticists. Progress is now reported by Bell and colleagues in their study of NIDDM1, a locus implicated in type 2 diabetes. The complex nature of the reported association illustrates the challenge of implicating a specific gene and mutation in the causation of polygenic disease.