2004
DOI: 10.1016/j.molcel.2004.08.009
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The Fanconi Anaemia Gene FANCC Promotes Homologous Recombination and Error-Prone DNA Repair

Abstract: The Fanconi anemia (FA) protein FANCC is essential for chromosome stability in vertebrate cells, a feature underscored by the extreme sensitivity of FANCC-deficient cells to agents that crosslink DNA. However, it is not known how this FA protein facilitates the repair of both endogenously acquired and mutagen-induced DNA damage. Here, we use the model vertebrate cell line DT40 to address this question. We discover that apart from functioning in homologous recombination, FANCC also promotes the mutational repai… Show more

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Cited by 280 publications
(332 citation statements)
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“…The stabilization and repair of the collapsed fork is currently thought to require the Fanconi anemia and other homologous recombination proteins [35]. Cells deficient in the translesion bypass polymerase REV3 are also highly sensitive to ICL inducing agents suggesting that this enzyme also has a role in the recombination-dependent pathway of ICL repair [16][17][18].…”
Section: Discussionmentioning
confidence: 99%
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“…The stabilization and repair of the collapsed fork is currently thought to require the Fanconi anemia and other homologous recombination proteins [35]. Cells deficient in the translesion bypass polymerase REV3 are also highly sensitive to ICL inducing agents suggesting that this enzyme also has a role in the recombination-dependent pathway of ICL repair [16][17][18].…”
Section: Discussionmentioning
confidence: 99%
“…Rev3 cells have also been shown to be highly sensitive to ICL-inducing agents [16][17][18]. We therefore examined MEF cells that contain a homozygous disruption of Rev3 in our assay.…”
Section: Role Of Hr and Ner/translesion Bypass In Icl-mediated Stimulmentioning
confidence: 99%
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“…The activated FANCore complex monoubiquitinates the FANCD2-FANCI heterodimer (ID complex) [36,37] and the activated ID complex relocates to the damaged DNA in an ATR and BRCA1-dependent manner [36][37][38]. The ID complex promotes nucleolytic cleavage of the 3´ and 5´ sites of DNA to unhook the ICL and successively induces trans-lesion polymerases Rev1 and pol [39][40][41][42]. These reactions extend the leading DNA strand above and past the unhooked ICL to produce a substrate that is processed by successive HRR reactions [34].…”
Section: Fa Genes (Fanca B C D1 D2 E F G I J L N P Q) Fmentioning
confidence: 99%
“…Multiple translesion DNA synthesis TLS polymerases are implicated in the lesion bypass of DNA intra-strand cross-links, including those generated by DDP. Replicative bypass of DDP adducts requires the cooperative actions of at least three TLS Pol isoforms : Pol , REV1, and Pol [7][8][9][10][11][12][13][14][15][16] . A reduction in Pol or REV1 function renders cells more sensitive to the cytotoxic effects of DDP, and also markedly decreases its mutagenicity in vitro 11 14 .…”
Section: Cis-diamminedichloroplatinummentioning
confidence: 99%