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Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes

Cody M Rogers1, Robert H Simmons Iii1, Gabriella E Fluhler Thornburg1

  • 1Molecular and Cellular Biochemistry Department, Indiana University, 212 S. Hawthorne Dr., Simon Hall MSB1 room 405B, Bloomington, IN, 47405, USA.

Progress in Biophysics and Molecular Biology
|September 3, 2020
PubMed

Insights

DNA inter-strand crosslinks (ICLs) are dangerous DNA lesions. This review explores Fanconi anemia-independent repair pathways, offering insights into ICL repair mechanisms and chemotherapeutic applications.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA inter-strand crosslinks (ICLs) pose significant threats to DNA replication and transcription.
  • The Fanconi anemia (FA) pathway is the primary known mechanism for ICL repair.
  • Cells can distinguish between different ICL types, activating specific repair pathways.

Purpose of the Study:

  • To review current research on Fanconi anemia-independent ICL repair pathways.
  • To highlight key unanswered questions in the field of ICL repair.
  • To explore the therapeutic potential of understanding ICL repair mechanisms.

Main Methods:

  • Literature review of ICL repair mechanisms.
  • Analysis of FA-independent pathways including transcription-coupled, base excision, acetaldehyde-induced, and SNM1A/RecQ4 pathways.
  • Identification of knowledge gaps in ICL repair.

Main Results:

  • Multiple FA-independent ICL repair pathways exist.
  • These pathways are activated based on the specific type of ICL.
  • Specific pathways reviewed include transcription-coupled, base excision, acetaldehyde-induced, and SNM1A/RecQ4.

Conclusions:

  • Understanding diverse ICL repair pathways is crucial for cellular survival.
  • Further research into these pathways will elucidate ICL repair mechanisms.
  • This knowledge can enhance the efficacy of ICL-inducing chemotherapeutics.
Keywords:
DNA helicaseDNA inter-Strand crosslink repairFanconi anemiaHrq1NucleasePso2

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