Eukaryotic mismatch repair: an update.
The discovery that mutations in mismatch repair genes segregate with hereditary nonpolyposis colon cancer has awakened a great deal of interest in the study of the process of postreplicative mismatch repair. The characterisation of the principal players involved in this important metabolic pathway has been greatly facilitated by the amino acid sequence conservation among functional homologues of bacteria, yeast and mammals. The phenotypes of mismatch repair deficient mutants are also similar in many ways. In humans, mismatch repair malfunction demonstrates itself in the form of a mutator phenotype of the affected cells, an instability of microsatellite sequences and increased levels of somatic recombination. Moreover, mismatch repair deficient cells display also varying levels of tolerance to DNA damaging agents and are thought to be involved in the cell killing mediated by these agents. This article discusses some recent developments in this fast-moving field.
Jiricny
J
J
Institute of Medical Radiobiology of the University of Zürich, Switzerland. jiricny@imr.unizh.ch
D000251:Adenosine Triphosphatases; D001426:Bacterial Proteins / Q000235:genetics; D003123:Colorectal Neoplasms, Hereditary Nonpolyposis / Q000235:genetics; D004249:DNA Damage; D004260:DNA Repair; D004261:DNA Replication; D004351:Drug Resistance; D029968:Escherichia coli Proteins; D005057:Eukaryotic Cells; D006801:Humans; D000070956:MutL Proteins; D016296:Mutagenesis / Q000235:genetics
D001426:Bacterial Proteins; D029968:Escherichia coli Proteins; C074770:MutL protein, E coli; D000251:Adenosine Triphosphatases; D000070956:MutL Proteins