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The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats
The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats
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The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats
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The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats
The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats

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The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats
The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats
Journal Article

The Rad1-Rad10 nuclease promotes chromosome translocations between dispersed repeats

2012
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Overview
The structure-specific endonucleases Mus81-Mms4 and Yen1 are involved in the resolution of Holliday junctions and in crossover formation in the budding yeast. Now genetic work implicates the nucleotide excision repair nuclease complex Rad1-Rad10 in the processing of recombination intermediates formed between substrates with limited homology. Holliday junctions can be formed during homology-dependent repair of DNA double-strand breaks, and their resolution is essential for chromosome segregation and generation of crossover products. The Mus81-Mms4 and Yen1 nucleases are required for mitotic crossovers between chromosome homologs in Saccharomyces cerevisiae ; however, crossovers between dispersed repeats are still detected in their absence. Here we show that the Rad1-Rad10 nuclease promotes formation of crossover and noncrossover recombinants between ectopic sequences. Crossover products were not recovered from the mus81Δ rad1Δ yen1Δ triple mutant, indicating that all three nucleases participate in processing recombination intermediates that form between dispersed repeats. We suggest a new mechanism for crossovers that involves Rad1-Rad10 clipping and resolution of a single Holliday junction–containing intermediate by Mus81-Mms4 or Yen1 cleavage or by replication. Consistent with the model, we show accumulation of Rad1-dependent joint molecules in the mus81Δ yen1Δ mutant.