ArticleNucleic acids research2007
Disparate contributions of the Fanconi anemia pathway and homologous recombination in preventing spontaneous mutagenesis.
Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- The homologous recombination protein RAD51D protects the genome from large deletions.Nucleic acids research · 2017Article
- Regulation of the Rev1-pol ζ complex during bypass of a DNA interstrand cross-link.The EMBO journal · 2015Article
- Damage-dependent regulation of MUS81-EME1 by Fanconi anemia complementation group A protein.Nucleic acids research · 2014Article
- Imprinting control region (ICR) of the Peg3 domain.Human molecular genetics · 2012Article
- Genomic instability in mice is greater in Fanconi anemia caused by deficiency of Fancd2 than Fancg.Cancer research · 2010Article
- Cellular and molecular consequences of defective Fanconi anemia proteins in replication-coupled DNA repair: mechanistic insights.Mutation research · 2009Review
- RAD51D- and FANCG-dependent base substitution mutagenesis at the ATP1A1 locus in mammalian cells.Mutation research · 2009Article
- How the fanconi anemia pathway guards the genome.Annual review of genetics · 2009Review
- Impaired removal of DNA interstrand cross-link in Nijmegen breakage syndrome and Fanconi anemia, but not in BRCA-defective group.Cancer science · 2008Article
- Remodeling of DNA replication structures by the branch point translocase FANCM.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- FANCG promotes formation of a newly identified protein complex containing BRCA2, FANCD2 and XRCC3.Oncogene · 2008Article
- MEN1 and FANCD2 mediate distinct mechanisms of DNA crosslink repair.DNA repair · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a chromosomal instability disorder in which DNA-damage processing defects are reported for translesion synthesis (TLS), non-homologous end joining (NHEJ) and homologous recombination (HR; both increased and decreased). To reconcile these diverse findings, we compared spontaneous mutagenesis in FA and HR mutants of hamster CHO cells. In the fancg mutant we find a reduced mutation rate accompanied by an increased proportion of deletions within the hprt gene. Moreover, in fancg cells gene amplification at the CAD and dhfr loci is elevated, another manifestation of inappropriate processing of damage during DNA replication. In contrast, the rad51d HR mutant has a greatly elevated rate of hprt mutations, >85% of which are deletions. Our analysis supports the concept that HR faithfully restores broken replication forks, whereas the FA pathway acts more globally to ensure chromosome stability by promoting efficient end joining of replication-derived breaks, as well as TLS and HR.
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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.