Mlh1 is an essential factor of mismatch repair (MMR) and meiotic recombination. It interacts through its C-terminal region with MutL homologs and proteins involved in DNA repair and replication. In this study, we identified the site of yeast Mlh1 critical for the interaction with Exo1, Ntg2, and Sgs1 proteins, designated as site S2 by reference to the Mlh1/Pms1 heterodimerization site S1. We sh...

Genomic stability depends in part on an efficient DNA lesion recognition and correction by the DNA mismatch repair (MMR) system. We investigated mutations arising spontaneously in rice OsMsh6 mutants by specific-locus amplified fragment sequencing. Totally 994 single-nucleotide mutations were identified in three mutants and on average the mutation density is about 1/136.72 Kb per mutant line. T...

Results from the analysis of human tumor cell lines with mutations in DNA mismatch repair genes have contributed to the understanding of the functions of these gene products in DNA mismatch repair, microsatellite instability, cell cycle checkpoint control, transcription-coupled nucleotide excision repair, and resistance to cytotoxic agents. However, complementation of human DNA mismatch repair ...

UvrD is a superfamily I DNA helicase with well documented roles in excision repair and methyldirected mismatch repair (MMR) in addition to poorly understood roles in replication and recombination. The MutL protein is a homodimeric DNAstimulated ATPase that plays a central role in MMR in Escherichia coli. This protein has been characterized as the master regulator of mismatch repair since it int...

The c-Abl nonreceptor tyrosine kinase and the c-Jun NH2-terminal kina.se (JNK/stress.activated protein kinase) are activated during the injury response to the DNA-damaging agent cisplatin. Loss of DNA mis match repair activity results in resistance to cisplatin in human cancer cefts, suggesting that the mismatch repair proteins function as a detector for cisplatinDNA adducts.To Identifysignalin...

Since the discovery of a link between the malfunction of post-replicative mismatch correction and hereditary non-polyposis colon cancer, the study of this complex repair pathway has received a great deal of attention. Our understanding of the mammalian system was facilitated by conservation of the main protagonists of this process from microbes to humans. Thus, biochemical experiments carried o...

The DNA mismatch repair machinery is involved in the correction of a wide variety of mutational intermediates. In bacterial cells, homodimers of the MutS protein bind mismatches and MutL homodimers couple mismatch recognition to downstream processing steps [1]. Eukaryotes possess multiple MutS and MutL homologs that form discrete, heterodimeric complexes with specific mismatch recognition and r...

UNLABELLED Correction of misincorporated nucleotides during DNA replication (mismatch repair) distinguishes histologically similar cancers with distinct biological and clinical behavior. We investigated expression of two mismatch repair genes in testis cancer to determine the expression pattern in histologically distinct subtypes, correlate expression with genetic instability and correlate expr...

The molecular basis for the inviability of dam-3 recA200(Ts) and dam-3 recB270(Ts) cells was studied. The dam-3 recA200(Ts) cells were inviable in yeast extract-nutrient broth or in minimal medium at 42 degrees C. Although the dam-3 recB270(Ts) cells were inviable in yeast extract-nutrient broth at 42 degrees C, they were viable at 42 degrees C in minimal medium, in which the high salt content ...

MSH2 is required for DNA mismatch repair recognition in eukaryotes. Deleterious mutations in human MSH2 account for approximately half of the alleles associated with a common hereditary cancer syndrome. Previously, we characterized clinically identified MSH2 missense mutations, using yeast as a model system, and found that the most common cause of defective DNA mismatch repair was low levels of...