Translesion synthesis

  • Article
    | Open Access

    The human DNA primase and DNA polymerase PrimPol replicates through the major oxidative DNA damage lesion 7,8-dihydro-8-oxoguanine (oxoG) via translesion synthesis in a mostly error-free manner thus suppressing oxoG-induced mutagenesis in mitochondria and the nucleus. Here, the authors present crystal structures of PrimPol in complex with an oxoG lesion in different contexts that provide mechanistic insights into how PrimPol performs predominantly accurate synthesis on oxidative-damaged DNAs in human cells.

    • Olga Rechkoblit
    • , Robert E. Johnson
    •  & Aneel K. Aggarwal
  • Article
    | Open Access

    REV7 has emerged as a critical regulator of DNA double-strand breaks repair. Here, the authors show that REV7 is crucial for both antibody class switch recombination and somatic hypermutation in activated B cells, in addition to their survival upon AID-deamination.

    • Dingpeng Yang
    • , Ying Sun
    •  & Fei-Long Meng
  • Article
    | Open Access

    Recent research has shown that mutational signatures reflective of the history of a cancer can be detected in a cancer genome. Here, using whole genome sequencing of DNA repair deficient and proficient nematodes exposed to genotoxins, the authors show that these mutational signatures reflect both the initial DNA damage that was inflicted and the repair processes that ensue.

    • Nadezda V. Volkova
    • , Bettina Meier
    •  & Moritz Gerstung
  • Article
    | Open Access

    Polη is a key player in translesion DNA synthesis. Here, the authors uncover that, in response to DNA damage, Polη undergoes O-GlcNAcylation at threonine 457 by O-GlcNAc transferase to facilitate the timely disassembly of Polη after DNA lesion bypass.

    • Xiaolu Ma
    • , Hongmei Liu
    •  & Caixia Guo
  • Article
    | Open Access

    Translesion synthesis polymerase eta has a well characterized role in replicating past UV-induced DNA lesions and has recently been shown to act at difficult to replicate sequences. Here the authors show that its SUMOylation is required to recruit pol eta at the replication fork and to prevent under-replicated DNA.

    • Emmanuelle Despras
    • , Méghane Sittewelle
    •  & Patricia L Kannouche