The plant‐specific CDKB1‐CYCB1 complex mediates homologous recombination repair in Arabidopsis

• Annika K Weimer ^[1] ; Sascha Biedermann ^[6] ; Hirofumi Harashima ^[7] ; Farshad Roodbarkelari ^[8] ; Naoki Takahashi ^[2] ; Julia Foreman ^[3] ; Yonsheng Guan ^[6] ; Gaëtan Pochon ^[4] ; Maren Heese ^[4] ; Daniël Van Damme ^[9] ; Keiko Sugimoto ^[7] ; Csaba Koncz ^[5] ; Peter Doerner ^[3] ; Masaaki Umeda ^[2] ; Arp Schnittger
  1. [1] Institut de Biologie Moléculaire des Plantes

     Institut de Biologie Moléculaire des Plantes

     Arrondissement de Strasbourg-Ville, Francia

     
  2. [2] Nara Institute of Science and Technology

     Nara Institute of Science and Technology

     Japón

     
  3. [3] University of Edinburgh

     University of Edinburgh

     Reino Unido

     
  4. [4] University of Hamburg

     University of Hamburg

     Hamburg, Freie und Hansestadt, Alemania

     
  5. [5] Max Planck Institute for Plant Breeding Research

     Max Planck Institute for Plant Breeding Research

     Kreisfreie Stadt Köln, Alemania

     
  6. [6] 1 Department of Molecular Mechanisms of Phenotypic Plasticity Institut de Biologie Moléculaire des Plantes du CNRS IBMP‐CNRS UPR2357 Université de Strasbourg Strasbourg Cedex France
  7. [7] 2 RIKEN Center for Sustainable Resource Science Tsurumi, Yokohama Japan
  8. [8] 3 Institut für Biologie III Universität Freiburg Freiburg Germany
  9. [9] 7 Department of Plant Systems Biology VIB Ghent Belgium; 8 Department of Plant Biotechnology and Bioinformatics Ghent University Ghent Belgium

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• Localización: EMBO journal: European Molecular Biology Organization, ISSN 0261-4189, Vol. 35, Nº. 19, 2016, págs. 2068-2086
• Idioma: inglés
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  • Upon DNA damage, cyclin‐dependent kinases (CDKs) are typically inhibited to block cell division. In many organisms, however, it has been found that CDK activity is required for DNA repair, especially for homology‐dependent repair (HR), resulting in the conundrum how mitotic arrest and repair can be reconciled. Here, we show that Arabidopsis thaliana solves this dilemma by a division of labor strategy. We identify the plant‐specific B1‐type CDKs (CDKB1s) and the class of B1‐type cyclins (CYCB1s) as major regulators of HR in plants. We find that RADIATION SENSITIVE 51 (RAD51), a core mediator of HR, is a substrate of CDKB1‐CYCB1 complexes. Conversely, mutants in CDKB1 and CYCB1 fail to recruit RAD51 to damaged DNA. CYCB1;1 is specifically activated after DNA damage and we show that this activation is directly controlled by SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), a transcription factor that acts similarly to p53 in animals. Thus, while the major mitotic cell‐cycle activity is blocked after DNA damage, CDKB1‐CYCB1 complexes are specifically activated to mediate HR.