Journal
EMBO JOURNAL
Volume 35, Issue 19, Pages 2068-2086Publisher
WILEY
DOI: 10.15252/embj.201593083
Keywords
CDK; cell cycle; cyclin; DNA damage; homologous recombination
Categories
Funding
- postdoctoral fellowship of the German Research Foundation (DFG)
- German Academic Exchange Program (DAAD)
- German Research Foundation (DFG) [SCHN 736/2-2]
- European Research Council
- Grants-in-Aid for Scientific Research [26840096, 26291061, 26291064, 26113515, 16H01243] Funding Source: KAKEN
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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.
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