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Significance Homologous recombination (HR) repairs DNA double-strand breaks by using a homologous template to retrieve sequence information lost at the break site. The broken DNA molecule first engages with the homologous donor molecule and is then separated from it to complete the process. Depending on the HR subpathways used, the separation step can lead to crossovers (COs) between the participating molecules. Such events can cause genomic alterations and eventually cancer if a donor molecule other than the identical sister chromatid is used. Here, we characterize two subpathways of HR with different propensities to form COs. We show the unexpected dominance of the CO-forming subpathway and characterize the processes involved in CO formation and subpathway choice in cancer and normal, untransformed cells.

ATRX and RECQ5 define distinct homologous recombination subpathways