Comparisons between human and chimpanzee genomes indicate that a gene that may function as a wild-type or normal gene in one primate may function as a disease-causing gene in another [The Chimpanzee Sequencing and Analysis Consortium (2005). Nature 437:69–87]. For instance, the PPARG locus (regulator of adipocyte differentiation) is a wild-type allele in chimps but is clearly associated with Type 2 diabetes in humans. What factors might cause this apparent contradiction? Would you consider such apparent contradictions to be rare or common? What impact might such findings have on the use of comparative genomics to identify and design therapies for disease-causing genes in humans?
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Verified Solution
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Key Concepts
Genetic Variation
Gene-Environment Interaction
Comparative Genomics
Yeager, M., et al. [(2007) Nature Genetics 39:645–649] and Sladek, R., et al. [(2007) Nature 445:881–885] have used single-nucleotide polymorphisms (SNPs) in genome-wide association studies (GWAS) to identify novel risk loci for prostate cancer and Type 2 diabetes, respectively. Each study suggests that disease-risk genes can be identified that significantly contribute to the disease state. Given your understanding of such complex diseases, what would you determine as reasonable factors to consider when interpreting the results of GWAS?
Dominguez et al. (2004) suggest that by studying genes that determine growth and tissue specification in the eye of Drosophila, much can be learned about human eye development.
What evidence suggests that genetic eye determinants in Drosophila are also found in humans? Include a discussion of orthologous genes in your answer.
Dominguez et al. (2004) suggest that by studying genes that determine growth and tissue specification in the eye of Drosophila, much can be learned about human eye development.
What evidence indicates that the eyeless gene is part of a developmental network?