Regulation of DSB Repair by Cell Cycle Signaling and the DNA Damage Response
Of the many types of DNA lesions, DNA double-strand breaks (DSBs) are considered the most harmful, because one unrepaired DSB is sufficient to trigger permanent growth arrest and cell death. In addition, DSBs are potent inducers of gross chromosomal rearrangements such as deletions, translocations, and amplifications. DSB signaling and repair through different pathways is crucial to preserve genomic integrity and maintain cellular homeostasis. Therefore, it is no wonder if the cell finely regulates DSB repair pathways in the different cell cycle phases and following activation of the DNA damage checkpoint. In this short entry we will illustrate some known aspects of the regulation of DSB repair in the mitotic cell cycle. In particular we will focus on the balance of the two main DSB repair pathways – NHEJ, nonhomologous end joining, and H(D)R, homologous (directed) recombination – as well as on the regulation of the resolution of joint molecules that arise during H(D)R.
KeywordsRecombination Serine Ligase Exo1
- Aparicio T, Baer R, Gautier J (2014) DNA double-strand break repair pathway choice and cancer. DNA Repair (Amst) 19:169–175Google Scholar
- Donnianni RA, Ferrari M, Lazzaro F, Clerici M, Tamilselvan Nachimuthu B, Plevani P, Muzi-Falconi M, Pellicioli A (2010) Elevated levels of the polo kinase Cdc5 override the Mec1/ATR checkpoint in budding yeast by acting at different steps of the signaling pathway. PLoS Genet 6:e1000763PubMedCentralPubMedCrossRefGoogle Scholar
- Herzberg K, Bashkirov VI, Rolfsmeier M, Haghnazari E, McDonald WH, Anderson S, Bashkirova EV, Yates JR 3rd, Heyer WD (2006) Phosphorylation of Rad55 on serines 2, 8, and 14 is required for efficient homologous recombination in the recovery of stalled replication forks. Mol Cell Biol 26:8396–8409PubMedCentralPubMedCrossRefGoogle Scholar