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Model for the interplay between ATRX and RECQ5 to regulate distinct subpathways of HR. Repair of two-ended DSBs by ATRX-mediated HR outcompetes RECQ5, possibly through PCNA binding, thereby suppressing SDSA. Upon the completion of DNA repair synthesis, the resulting JM is not subject to dissolution by BLM and is channelled into the resolution pathway by MUS81 and GEN1, leading to equal probability of CO and non-CO products.
