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Arabidopsis thaliana FANCD2 Promotes Meiotic Crossover Formation

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Kurzbauer, Marie-Therese and Pradillo Orellana, Mónica and Kerzendorfer, Claudia and Sims, Jason and Ladurner, Rene and Oliver, Cecilia and Janisiw, Michael Peter and Mosiolek, Magdalena and Schweizer, Dieter and Copenhaver, Gregory P. and Schlögelhofer, Peter (2018) Arabidopsis thaliana FANCD2 Promotes Meiotic Crossover Formation. Plant Cell, 30 (2). pp. 415-428. ISSN 1040-4651, ESSN: 1532-298X

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Official URL: http://www.plantcell.org/content/30/2/415



Abstract

Fanconi anemia (FA) is a human autosomal recessive disorder characterized by chromosomal instability, developmental pathologies, predisposition to cancer, and reduced fertility. So far, 19 genes have been implicated in FA, most of them involved in DNA repair. Some are conserved across higher eukaryotes, including plants. The Arabidopsis thaliana genome encodes a homolog of the Fanconi anemia D2 gene (FANCD2) whose function in DNA repair is not yet fully understood. Here, we provide evidence that AtFANCD2 is required for meiotic homologous recombination. Meiosis is a specialized cell division that ensures reduction of genomic content by half and DNA exchange between homologous chromosomes via crossovers (COs) prior to gamete formation. In plants, a mutation in AtFANCD2 results in a 14% reduction of CO numbers. Genetic analysis demonstrated that AtFANCD2 acts in parallel to both MUTS HOMOLOG4 (AtMSH4), known for its role in promoting interfering COs and MMS AND UV SENSITIVE81 (AtMUS81), known for its role in the formation of noninterfering COs. AtFANCD2 promotes noninterfering COs in a MUS81-independent manner and is therefore part of an uncharted meiotic CO-promoting mechanism, in addition to those described previously.


Item Type:Article
Uncontrolled Keywords:Arabidopsis thaliana; Meiosis; Fanconi anemia
Subjects:Medical sciences > Medicine > Hematology
Medical sciences > Biology > Botany
Medical sciences > Biology > Genetics
ID Code:47513
Deposited On:11 May 2018 11:05
Last Modified:10 Dec 2018 15:30

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