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Abstract DNA replication stress promotes cancer development and is associated with DNA synthesis beyond S-phase. Replication stress-induced DNA lesions and under-replicated DNA can persist into G2 and mitosis, where they undergo mitotic DNA synthesis (MiDAS). After cell division, inherited DNA lesions are protected by genome caretaker proteins and show signs of post-mitotic DNA synthesis (post-MiDAS) in G1.
Abstract Under stress conditions, cells reprogram their molecular machineries to mitigate damage and promote survival. Ubiquitin signaling is globally increased during oxidative stress, controlling protein fate and supporting stress defenses at several subcellular compartments. However, the rules driving subcellular ubiquitin localization to promote these concerted response mechanisms remain understudied.
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