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A DNA damage checkpoint is a pause in the cell cycle that is induced in response to DNA damage to ensure that the damage is repaired before cell division resumes. Proteins that accumulate at the damage site typically activate the checkpoint and halt cell growth at the G1/S or G2/M boundaries.
Transcription-replication conflicts (TRCs) promote tumor aggressiveness by affecting genome stability. Here, the authors identify ANP32E as driver of TRCs in breast cancer, causing R-loop accumulation and genomic instability, which elicit vulnerability to ATR inhibition.
The DNA damage checkpoint needs to be turned off to allow cellular recovery from genotoxic exposure. Here, the authors report that the scaffold proteins Rtt107 and Mms22 and their associated ubiquitin ligase enable this downregulation and reduces the level of a key checkpoint mediator Rad9.
The TRAIP E3 ubiquitin ligase is essential for genome integrity, mutations lead to primordial dwarfism in patients. Here, the authors show that TRAIP degradation in S-phase, results in cell arrest due to DNA damage caused by replication-transcription conflicts.
The expression of two DNA repair factors improves the recombination of single-stranded oligodeoxynucleotides with Cas9-induced double-strand breaks, facilitating precise and efficient gene editing.
DNA damage-induced histone degradation results in decreased nucleosome occupancy, which promotes homologous recombination by enhancing the dynamicity of chromatin.
