Abstract
During genetic recombination and the recombinational repair of chromosome breaks, DNA molecules become linked at points of strand exchange. Branch migration and resolution of these crossovers, or Holliday junctions (HJs), complete the recombination process. Here, we show that extracts from cells carrying mutations in the recombination/repair genes RAD51C or XRCC3 have reduced levels of HJ resolvase activity. Moreover, depletion of RAD51C from fractionated human extracts caused a loss of branch migration and resolution activity, but these functions were restored by complementation with a variety of RAD51 paralog complexes containing RAD51C. We conclude that the RAD51 paralogs are involved in HJ processing in human cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Substitution
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Animals
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CHO Cells
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Cell Line
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Cricetinae
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DNA Repair
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DNA, Cruciform / chemistry
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DNA, Cruciform / metabolism*
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DNA-Binding Proteins / chemistry
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / isolation & purification
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DNA-Binding Proteins / metabolism*
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Electrophoresis, Polyacrylamide Gel
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Female
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HeLa Cells
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Holliday Junction Resolvases / metabolism*
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Humans
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Mutation
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Protein Structure, Tertiary
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Recombinant Proteins / metabolism
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Recombination, Genetic
Substances
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DNA, Cruciform
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DNA-Binding Proteins
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RAD51B protein, human
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RAD51C protein, human
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RAD51D protein, human
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Recombinant Proteins
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X-ray repair cross complementing protein 3
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XRCC2 protein, human
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Holliday Junction Resolvases