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DNA Mismatch Repair: A DNA repair pathway involved in correction of errors introduced during DNA replication when an incorrect base, which cannot form hydrogen bonds with the corresponding base in the parent strand, is incorporated into the daughter strand. Exonucleases recognize the Base pair mismatch and cause a segment of polynucleotide chain to be excised from the daughter strand, thereby removing the mismatched base. (from Oxford Dictionary of Biochemistry and Molecular Biology, 2001)

Mismatch Repair

JoVE 10791

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.

The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic information needs to be replicated. Despite the proofreading ability of the DNA polymerase, a copying error occurs approximately every 1 million base pairs. One type of error is the mismatch of nucleotides, for example, the pairing of A with G or T with C. Such mismatches are detected and repaired by the Mutator protein family. These proteins were first described in the bacteria Escherichia coli (E. coli), but homologs appear throughout prokaryotes and eukaryotes. Mutator S (MutS) initiates the mismatch repair (MMR) by identifying and binding to the mismatch. Subsequently, MutL identifies which strand is the new copy. Only the new strand requires fixing while the template strand needs to remain intact. How can the molecular machinery identify the newly synthesized strand of DNA? In many organisms, cytosine and adenine bases of the new strand receive a methyl group some time after replication. Therefore,

 Core: DNA Structure and Function

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

1Greehey Children's Cancer Research Institute, UT Health Science Center at San Antonio, 2Department of Cellular and Structural Biology, UT Health Science Center at San Antonio, 3Department of Pathology, UT Health Science Center at San Antonio, 4Department of Microbiology, UT Health Science Center at San Antonio, 5Cancer Therapy and Research Center, UT Health Science Center at San Antonio

JoVE 50752

 Immunology and Infection

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

1Department of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, 2Department of General, Gastrointestinal and Transplant Surgery, University of Heidelberg, 3Department of Pathology, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, 4German Cancer Consortium (DKTK), 5German Cancer Research Center (DKFZ)

JoVE 55952

 Cancer Research

Employing Digital Droplet PCR to Detect BRAF V600E Mutations in Formalin-fixed Paraffin-embedded Reference Standard Cell Lines

1Research Institute of Pharmaceutical Science, Department of Pharmacy, College of Pharmacy, Seoul National University, 2The Center for Anti-Cancer CDx, N-Bio, Seoul National University, 3ABION CRO, 4ABION Inc., R&D Center

JoVE 53190

 Biology

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

1Department of Cell Biology and Anatomy, College of Medicine, University of Arizona, Tucson, 2Southern Arizona Veterans Affairs Health Care System, Tucson, AZ, 3Department of Surgery, College of Medicine, University of Arizona, Tucson, 4Biomedical Diagnostics and Research, Tucson, AZ, 5Department of Medicine, College of Medicine, University of Arizona, Tucson

JoVE 1931

 Biology
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