Abstract
Saccharomyces cerevisiae mating-type switching is initiated by a double-strand break (DSB) at MATa, leaving one cut end perfectly homologous to the HMLα donor, while the second end must be processed to remove a non-homologous tail before completing repair by gene conversion (GC). When homology at the matched end is ≤150 bp, efficient repair depends on the recombination enhancer, which tethers HMLα near the DSB. Thus, homology shorter than an apparent minimum efficient processing segment can be rescued by tethering the donor near the break. When homology at the second end is ≤150 bp, second-end capture becomes inefficient and repair shifts from GC to break-induced replication (BIR). But when pol32 or pif1 mutants block BIR, GC increases 3-fold, indicating that the steps blocked by these mutations are reversible. With short second-end homology, absence of the RecQ helicase Sgs1 promotes gene conversion, whereas deletion of the FANCM-related Mph1 helicase promotes BIR.
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•Tethering an inefficient donor near a DSB rescues repair efficiency•Capture of the second DSB end is inefficient when homology at the second end is ≤150 bp•Reduced homology at the second end shifts repair from gene conversion to BIR•Sgs1 and Mph1 helicases promote opposing repair pathways in these strains
Mehta et al. demonstrate how the extent of homology at the two ends of a double-strand break influences repair efficiency and repair pathway choice between gene conversion and break-induced replication.