ArticleNucleic acids research2009
The Walker B motif in avian FANCM is required to limit sister chromatid exchanges but is dispensable for DNA crosslink repair.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 80 citations in OpenAlex.
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Shared genetics between nonobstructive azoospermia and primary ovarian insufficiency.F&S reviews · 2021Article
- FANCM regulates repair pathway choice at stalled replication forks.Molecular cell · 2021Article
- The Bloom syndrome complex senses RPA-coated single-stranded DNA to restart stalled replication forks.Nature communications · 2021Article
- Canonical and Noncanonical Roles of Fanconi Anemia Proteins: Implications in Cancer Predisposition.Cancers · 2020Review
- Review
- Function and Interactions of ERCC1-XPF in DNA Damage Response.Molecules (Basel, Switzerland) · 2018Review
- Bi-allelic Recessive Loss-of-Function Variants in FANCM Cause Non-obstructive Azoospermia.American journal of human genetics · 2018Article
- Biallelic truncating FANCM mutations cause early-onset cancer but not Fanconi anemia.Genetics in medicine : official journal of the American College of Medical Genetics · 2018Article
- DNA replication stress: from molecular mechanisms to human disease.Chromosoma · 2017Review
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
- FANCM interacts with PCNA to promote replication traverse of DNA interstrand crosslinks.Nucleic acids research · 2016Article
- Differential regulation of the anti-crossover and replication fork regression activities of Mph1 by Mte1.Genes & development · 2016Article
- Bloom syndrome complex promotes FANCM recruitment to stalled replication forks and facilitates both repair and traverse of DNA interstrand crosslinks.Cell discovery · 2016Article
- The Fanconi Anemia Pathway Maintains Genome Stability by Coordinating Replication and Transcription.Molecular cell · 2015Article
- Functions and regulation of the multitasking FANCM family of DNA motor proteins.Genes & development · 2015Review
- Review
- The genetic and biochemical basis of FANCD2 monoubiquitination.Molecular cell · 2014Article
- The histone-fold complex MHF is remodeled by FANCM to recognize branched DNA and protect genome stability.Cell research · 2014Article
- Damage-dependent regulation of MUS81-EME1 by Fanconi anemia complementation group A protein.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
FANCM, the most highly conserved component of the Fanconi Anaemia (FA) pathway can resolve recombination intermediates and remodel synthetic replication forks. However, it is not known if these activities are relevant to how this conserved protein activates the FA pathway and promotes DNA crosslink repair. Here we use chicken DT40 cells to systematically dissect the function of the helicase and nuclease domains of FANCM. Our studies reveal that these domains contribute distinct roles in the tolerance of crosslinker, UV light and camptothecin-induced DNA damage. Although the complete helicase domain is critical for crosslink repair, a predicted inactivating mutation of the Walker B box domain has no impact on FA pathway associated functions. However, this mutation does result in elevated sister chromatid exchanges (SCE). Furthermore, our genetic dissection indicates that FANCM functions with the Blm helicase to suppress spontaneous SCE events. Overall our results lead us to reappraise the role of helicase domain associated activities of FANCM with respect to the activation of the FA pathway, crosslink repair and in the resolution of recombination intermediates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.