@article {625804,
	title = {Asymmetric Processing of DNA Ends at a Double-Strand Break Leads to Unconstrained Dynamics and Ectopic Translocation},
	journal = {Cell Rep},
	volume = {24},
	number = {10},
	year = {2018},
	month = {2018 Sep 04},
	pages = {2614-2628.e4},
	abstract = {Multiple pathways regulate the repair of double-strand breaks (DSBs) to suppress potentially dangerous ectopic recombination. Both sequence and chromatin context are thought to influence pathway choice between non-homologous end-joining (NHEJ) and homology-driven recombination. To test the effect of repetitive sequences on break processing, we have inserted TG-rich repeats on one side of an inducible DSB at the budding yeast MAT locus on chromosome III. Five clustered Rap1 sites within a break-proximal TG repeat are sufficient to block Mre11-Rad50-Xrs2 recruitment, impair resection, and favor elongation by telomerase. The two sides of the break lose end-to-end tethering and show enhanced, uncoordinated movement. Only the TG-free side is resected and shifts to the nuclear periphery. In contrast to persistent DSBs without TG repeats that are repaired by imprecise NHEJ, nearly all survivors of repeat-proximal DSBs repair the break by a homology-driven, non-reciprocal translocation from ChrIII-R to ChrVII-L. This suppression of imprecise NHEJ at TG-repeat-flanked DSBs requires the Uls1 translocase activity.},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2018.07.102},
	author = {Marcomini, Isabella and Shimada, Kenji and Delgoshaie, Neda and Yamamoto, Io and Seeber, Andrew and Cheblal, Anais and Horigome, Chihiro and Naumann, Ulrike and Gasser, Susan M}
}
