Abstract-Huntington's disease is a hereditary neurodegenerative disease in which a few cell types in the sub-cortical brains undergo selective degeneration leading to neurological and cognitive decline and death. The disease is caused by expanded CAG repeat within the first exon of the Huntington gene (HTT). However, the mechanisms of molecular pathogenesis of this disease are not well understood. There is currently no therapy or a cure. We used a model of the disease in the simple organism Saccharomyces cerevisiae that previous workers in the field had successfully utilized to determine putative molecular mechanisms related to the disease. Using this model, we identified 41 novel genes that appear to suppress the toxic effects of the mutant genes. We generated a network of physical and genetic interactions among the human homologs of these novel suppressor genes, and analysis of this network allowed us to propose for the first time that mRNA degradation mechanisms might be affected in the diseased cells.Index Terms-huntington's disease, systems biology, disease model, genetic modifier, suppressor network, disease gene network
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