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Brca2 is involved in meiosis in Arabidopsis thaliana as suggested by its interaction with Dmc1

Nicolas Siaud, Eloïse Dray, Isabelle Gy, Emmanuelle Gérard, Najat Takvorian, Marie‐Pascale Doutriaux

Author Affiliations

  1. Nicolas Siaud,
  2. Eloïse Dray,
  3. Isabelle Gy,
  4. Emmanuelle Gérard,
  5. Najat Takvorian§ and
  6. Marie‐Pascale Doutriaux*,1
  1. 1 Institut de Biotechnologie des Plantes, CNRS UMR8618, Université Paris XI, Orsay, France
  1. *Corresponding author. Institut de Biotechnologie des Plantes, CNRS UMR 8618, Université Paris XI, F‐91405 Orsay Cedex, France. Tel.: +33 1 69 15 33 40/46; Fax: +33 1 69 15 34 23; E-mail: doutriau{at}ibp.u-psud.fr
  • Present address: Laboratoire de Biologie Cellulaire, INRA, 78026 Versailles Cedex, France

  • Present address: Unité d'Ecologie, Systématique et Evolution, CNRS UMR 8079, Université Paris XI, 91405 Orsay Cedex, France

  • § Present address: UFR 927, Laboratoire d'Endocrinologie Moléculaire et Evolution, Université Paris VI, 75251 Paris, France

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Abstract

Two BRCA2‐like sequences are present in the Arabidopsis genome. Both genes are expressed in flower buds and encode nearly identical proteins, which contain four BRC motifs. In a yeast two‐hybrid assay, the Arabidopsis Brca2 proteins interact with Rad51 and Dmc1. RNAi constructs aimed at silencing the BRCA2 genes at meiosis triggered a reproducible sterility phenotype, which was associated with dramatic meiosis alterations. We obtained the same phenotype upon introduction of RNAi constructs aimed at silencing the RAD51 gene at meiosis in dmc1 mutant plants. The meiotic figures we observed strongly suggest that homologous recombination is highly disturbed in these meiotic cells, leaving aberrant recombination events to repair the meiotic double‐strand breaks. The ‘brca2’ meiotic phenotype was eliminated in spo11 mutant plants. Our experiments point to an essential role of Brca2 at meiosis in Arabidopsis. We also propose a role for Rad51 in the dmc1 context.

  • Received September 1, 2003.
  • Accepted February 10, 2004.
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