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Fanconi anaemia and the repair of Watson and Crick DNA crosslinks

Author

Listed:
  • Molly C. Kottemann

    (Laboratory of Genome Maintenance, The Rockefeller University)

  • Agata Smogorzewska

    (Laboratory of Genome Maintenance, The Rockefeller University)

Abstract

The function of Fanconi anaemia proteins is to maintain genomic stability. Their main role is in the repair of DNA interstrand crosslinks, which, by covalently binding the Watson and the Crick strands of DNA, impede replication and transcription. Inappropriate repair of interstrand crosslinks causes genomic instability, leading to cancer; conversely, the toxicity of crosslinking agents makes them a powerful chemotherapeutic. Fanconi anaemia proteins can promote stem-cell function, prevent tumorigenesis, stabilize replication forks and inhibit inaccurate repair. Recent advances have identified endogenous aldehydes as possible culprits of DNA damage that may induce the phenotypes seen in patients with Fanconi anaemia.

Suggested Citation

  • Molly C. Kottemann & Agata Smogorzewska, 2013. "Fanconi anaemia and the repair of Watson and Crick DNA crosslinks," Nature, Nature, vol. 493(7432), pages 356-363, January.
    • Handle: RePEc:nat:nature:v:493:y:2013:i:7432:d:10.1038_nature11863
    DOI: 10.1038/nature11863
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    Cited by:

    1. Aron Ferenczi & Yen Peng Chew & Erika Kroll & Charlotte Koppenfels & Andrew Hudson & Attila Molnar, 2021. "Mechanistic and genetic basis of single-strand templated repair at Cas12a-induced DNA breaks in Chlamydomonas reinhardtii," Nature Communications, Nature, vol. 12(1), pages 1-12, December.
    2. Sebastian M. Siegner & Laura Ugalde & Alexandra Clemens & Laura Garcia-Garcia & Juan A. Bueren & Paula Rio & Mehmet E. Karasu & Jacob E. Corn, 2022. "Adenine base editing efficiently restores the function of Fanconi anemia hematopoietic stem and progenitor cells," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    3. Wei Liu & Hongchao Cao & Jing Wang & Areeg Elmusrati & Bing Han & Wei Chen & Ping Zhou & Xiyao Li & Stephen Keysar & Antonio Jimeno & Cun-Yu Wang, 2024. "Histone-methyltransferase KMT2D deficiency impairs the Fanconi anemia/BRCA pathway upon glycolytic inhibition in squamous cell carcinoma," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    4. Jessica D. Tischler & Hiroshi Tsuchida & Rosevalentine Bosire & Tommy T. Oda & Ana Park & Richard O. Adeyemi, 2024. "FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    5. Karl-Heinz Tomaszowski & Sunetra Roy & Carolina Guerrero & Poojan Shukla & Caezaan Keshvani & Yue Chen & Martina Ott & Xiaogang Wu & Jianhua Zhang & Courtney D. DiNardo & Detlev Schindler & Katharina , 2023. "Hypomorphic Brca2 and Rad51c double mutant mice display Fanconi anemia, cancer and polygenic replication stress," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    6. Carla Umansky & Agustín E. Morellato & Matthias Rieckher & Marco A. Scheidegger & Manuela R. Martinefski & Gabriela A. Fernández & Oleg Pak & Ksenia Kolesnikova & Hernán Reingruber & Mariela Bollini &, 2022. "Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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