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Humanizing mismatch repair in yeast: towards effective identification of hereditary non-polyposis colorectal cancer alleles

By P.M.R Aldred and Rhona H. Borts


The full-text of this item is not available on the LRA. The original published version can be found on the publisher's website at: http://www.biochemsoctrans.org/bst/default.htm\ud doi:10.1042/BST0351525The correction of replication errors is an essential component of genetic stability. This is clearly demonstrated\ud in humans by the observation that mutations in mismatch repair genes lead to HNPCC (hereditary nonpolyposis\ud colorectal cancer). This disease accounts for as many as 2–3% of colon cancers. Of these, most of\ud them are in the two central components of mismatch repair, MLH1 (mutL homologue 1) and MSH2 (mutS\ud homologue 2). MLH1 and MSH2 function as a complex with two other genes PMS2 and MSH6. Mismatch\ud repair genes, and the mechanism that ensures that incorrectly paired bases are removed, are conserved from\ud prokaryotes to human. Thus yeast can serve as a model organism for analysing mutations/polymorphisms\ud found in human mismatch repair genes for their effect on post-replicative repair. To date, this has predominantly\ud been accomplished by making the analogous mutations in yeast genes. However, this approach is only\ud useful for the most highly conserved regions. Here, we discuss some of the benefits and technical difficulties\ud involved in expressing human genes in yeast. Modelling human mismatch repair in yeast will allow the\ud assessment of any functional effect of novel polymorphisms found in patients diagnosed with colon cancers

Publisher: Portland Press
Year: 2007
DOI identifier: 10.1042/BST0351525
OAI identifier: oai:lra.le.ac.uk:2381/8797
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