The stabilization of repetitive tracts of DNA by variant repeats requires a functional DNA mismatch repair system
Article Abstract:
Insertion of variant repeats into the poly(GT) tracts of Saccharomyces cerevisiae stabilizes the repetitive GT sequences via a functionally active DNA mismatch repair system. The stabilization is probably due to recognition of the mismatches due to primer-template dissociations during replication. Deletion, addition and changes in the number of repeats in the repetitive tracts usually occur on one side of the variant. This is probably due to the polarity of DNA polymerase slippages. Similar stabilization phenomenon in trinucleotide repeats related to human neurological disorders are discussed.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
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The human mismatch recognition complex hMSH2-hMSH6 functions as a novel molecular switch
Article Abstract:
DNA mismatch repair mechanisms have been modeled on biochemical studies of E.coli DNA adenine methylation-instructed pathway. Initial recognition of the mismatch is undertaken by the MutS protein. It is shown that adenine nucleotide binding and hydrolysis undertaken by hMSH2-hMSH6 complex, acts as a novel molecular switch. The complex is ON in the ADP-bound form and OFF in the ATP-bound form, suggesting a new model for MutS protein functions.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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Recombinational DNA repair: The RecF and RecR proteins limit the extension of RecA filaments beyond single-strand DNA gaps
Article Abstract:
RecA filament extension into adjoining duplex DNA is attenuated in the presence of the RecF and RecR proteins. RecFR cause random binding, mainly to the duplex region of the DNA, and a slow lengthening of RecA filaments, seen in the presence of RecFR, is virtually stopped when RecF is replaced with RecF mutant protein.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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