{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMUS81 is a highly conserved, structure‐specific endonuclease that recognizes and incises a variety of branched DNA substrates—including replication forks, 3′‐flap structures, and Holliday junction–like recombination intermediates—to promote genome stability. By cleaving aberrant DNA structures that arise when replication is disrupted or upon DNA damage, MUS81 facilitates the conversion of otherwise toxic intermediates into substrates accessible to downstream repair processes such as homologous recombination, mitotic DNA synthesis, and fork restart. Its activities have been shown to be critical in preventing chromosomal aberrations under conditions of replication stress and in coordinating the timely resolution of recombination intermediates through associations with accessory factors like EME1/EME2 and the SLX4 scaffold."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMUS81 also functions in concert with key homologous recombination factors and DNA helicases—such as RAD52, BLM, WRN, and Rad54—to regulate the processing of stalled or collapsed replication forks. By promoting controlled double‐strand break formation, MUS81 helps resolve recombination intermediates in a coordinated “nick and counternick” mechanism that is tightly regulated by cell cycle kinases and other post‐translational modifications, ensuring that its nuclease activity is confined to the proper phase of the cell cycle. This strategic interplay minimizes unscheduled DNA cleavage while enabling the appropriate processing of complex DNA structures that arise during repair."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, dysregulation of MUS81 has been implicated in altered responses to DNA‐damaging chemotherapeutics and in the progression of various cancers. 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