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. 2013 Dec 5;42(4):2380–2390. doi: 10.1093/nar/gkt1263

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© The Author(s) 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Model for the roles of RECQ5 and BLM in suppression of COs during DSBR by HR. RECQ5 promotes SDSA by disrupting aberrant RAD51-filaments formed after unwinding of the extended D-loop. BLM acts as a part of the BTR (BLM-TOPOIIIα-RMI1/2) complex to mediate dissolution of dHJs. RAD51 filaments formed during the post-synaptic phase of SDSA can promote re-invasion of the homologous duplex followed by formation of a dHJ structutre, increasing the risk of COs. RTEL1 promotes SDSA by catalyzing D-loop disruption. SDSA, synthesis-dependent strand annealing; dHJ, double Holliday junction; and DSBR, double-strand break repair.