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Studying DNA Double-Strand Break Repair: An Ever-Growing Toolbox

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmolb.2020.00024

关键词

DNA repair; homologous recombination (HR); non-homologous DNA end joining; chromatin; DNA damage

资金

  1. Fundacao para a Ciencia e a Tecnologia (FCT), Portugal [PTDC/BIM-ONC/0016/2014, PTDC/BIA-MOL/30438/2017]
  2. FEDER through POR Lisboa, Portugal 2020-Programa Operacional Regional de Lisboa
  3. FCT
  4. IMM-Laco Fund
  5. European Research Council [ERC-2014-CoG 647344]
  6. Agence Nationale pour la Recherche [ANR-18-CE12-0015-02]
  7. Institut National contre le Cancer (INCA)
  8. Ligue Nationale contre le Cancer (LNCC)
  9. [LISBOA-01-0145-FEDER-007391]
  10. Fundação para a Ciência e a Tecnologia [PTDC/BIM-ONC/0016/2014, PTDC/BIA-MOL/30438/2017] Funding Source: FCT
  11. Agence Nationale de la Recherche (ANR) [ANR-18-CE12-0015] Funding Source: Agence Nationale de la Recherche (ANR)

向作者/读者索取更多资源

To ward off against the catastrophic consequences of persistent DNA double-strand breaks (DSBs), eukaryotic cells have developed a set of complex signaling networks that detect these DNA lesions, orchestrate cell cycle checkpoints and ultimately lead to their repair. Collectively, these signaling networks comprise the DNA damage response (DDR). The current knowledge of the molecular determinants and mechanistic details of the DDR owes greatly to the continuous development of ground-breaking experimental tools that couple the controlled induction of DSBs at distinct genomic positions with assays and reporters to investigate DNA repair pathways, their impact on other DNA-templated processes and the specific contribution of the chromatin environment. In this review, we present these tools, discuss their pros and cons and illustrate their contribution to our current understanding of the DDR.

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