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Mol Cell. 2015 Feb 19;57(4):595-606. doi: 10.1016/j.molcel.2015.01.022.

Top3-Rmi1 dissolve Rad51-mediated D loops by a topoisomerase-based mechanism.

Author information

1
Department of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA.
2
Department of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA; Department of Molecular & Cellular Biology, University of California, Davis, Davis, CA 95616-8665, USA.
3
Department of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA; Department of Molecular & Cellular Biology, University of California, Davis, Davis, CA 95616-8665, USA. Electronic address: wdheyer@ucdavis.edu.

Abstract

The displacement loop (D loop) is a DNA strand invasion product formed during homologous recombination. Disruption of nascent D loops prevents recombination, and during synthesis-dependent strand annealing (SDSA), disruption of D loops extended by DNA polymerase ensures a non-crossover outcome. The proteins implicated in D loop disruption are DNA motor proteins/helicases that act by moving DNA junctions. Here we report that D loops can also be disrupted by DNA topoisomerase 3 (Top3), and this disruption depends on Top3's catalytic activity. Yeast Top3 specifically disrupts D loops mediated by yeast Rad51/Rad54; protein-free D loops or D loop mediated by bacterial RecA protein or human RAD51/RAD54 resist dissolution. Also, the human Topoisomerase IIIa-RMI1-RMI2 complex is capable of dissolving D loops. Consistent with genetic data, we suggest that the extreme growth defect and hyper-recombination phenotype of Top3-deficient yeast cells is partially a result of unprocessed D loops.

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PMID:
25699708
PMCID:
PMC4338411
DOI:
10.1016/j.molcel.2015.01.022
[Indexed for MEDLINE]
Free PMC Article

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