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

Annika Weimer (UGent) , Sascha Biedermann, Hirofumi Harashima, Farshad Roodbarkelari, Naoki Takahashi, Julia Foreman, Yonsheng Guan, Gaëtan Pochon, Maren Heese, Daniël Van Damme (UGent) , et al.
(2016) EMBO JOURNAL. 35(19). p.2068-2086
Author
Organization
Abstract
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.
Keywords
GENOTOXIC STRESS, RAD51 PARALOGS, END RESECTION, DEPENDENT-KINASES, IONIZING-RADIATION, CELL-CYCLE CONTROL, DNA-DAMAGE RESPONSE, DOUBLE-STRAND BREAKS, homologous recombination, DNA damage, cyclin, cell cycle, CDK, MESSENGER-RNA, GAMMA-RAYS

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MLA
Weimer, Annika, et al. “The Plant-Specific CDKB1-CYCB1 Complex Mediates Homologous Recombination Repair in Arabidopsis.” EMBO JOURNAL, vol. 35, no. 19, 2016, pp. 2068–86, doi:10.15252/embj.201593083.
APA
Weimer, A., Biedermann, S., Harashima, H., Roodbarkelari, F., Takahashi, N., Foreman, J., … Schnittger, A. (2016). The plant-specific CDKB1-CYCB1 complex mediates homologous recombination repair in Arabidopsis. EMBO JOURNAL, 35(19), 2068–2086. https://doi.org/10.15252/embj.201593083
Chicago author-date
Weimer, Annika, Sascha Biedermann, Hirofumi Harashima, Farshad Roodbarkelari, Naoki Takahashi, Julia Foreman, Yonsheng Guan, et al. 2016. “The Plant-Specific CDKB1-CYCB1 Complex Mediates Homologous Recombination Repair in Arabidopsis.” EMBO JOURNAL 35 (19): 2068–86. https://doi.org/10.15252/embj.201593083.
Chicago author-date (all authors)
Weimer, Annika, Sascha Biedermann, Hirofumi Harashima, Farshad Roodbarkelari, Naoki Takahashi, Julia Foreman, Yonsheng Guan, Gaëtan Pochon, Maren Heese, Daniël Van Damme, Keiko Sugimoto, Csaba Koncz, Peter Doerner, Masaaki Umeda, and Arp Schnittger. 2016. “The Plant-Specific CDKB1-CYCB1 Complex Mediates Homologous Recombination Repair in Arabidopsis.” EMBO JOURNAL 35 (19): 2068–2086. doi:10.15252/embj.201593083.
Vancouver
1.
Weimer A, Biedermann S, Harashima H, Roodbarkelari F, Takahashi N, Foreman J, et al. The plant-specific CDKB1-CYCB1 complex mediates homologous recombination repair in Arabidopsis. EMBO JOURNAL. 2016;35(19):2068–86.
IEEE
[1]
A. Weimer et al., “The plant-specific CDKB1-CYCB1 complex mediates homologous recombination repair in Arabidopsis,” EMBO JOURNAL, vol. 35, no. 19, pp. 2068–2086, 2016.
@article{8174727,
  abstract     = {{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.}},
  author       = {{Weimer, Annika and Biedermann, Sascha and Harashima, Hirofumi and Roodbarkelari, Farshad and Takahashi, Naoki and Foreman, Julia and Guan, Yonsheng and Pochon, Gaëtan and Heese, Maren and Van Damme, Daniël and Sugimoto, Keiko and Koncz, Csaba and Doerner, Peter and Umeda, Masaaki and Schnittger, Arp}},
  issn         = {{0261-4189}},
  journal      = {{EMBO JOURNAL}},
  keywords     = {{GENOTOXIC STRESS,RAD51 PARALOGS,END RESECTION,DEPENDENT-KINASES,IONIZING-RADIATION,CELL-CYCLE CONTROL,DNA-DAMAGE RESPONSE,DOUBLE-STRAND BREAKS,homologous recombination,DNA damage,cyclin,cell cycle,CDK,MESSENGER-RNA,GAMMA-RAYS}},
  language     = {{eng}},
  number       = {{19}},
  pages        = {{2068--2086}},
  title        = {{The plant-specific CDKB1-CYCB1 complex mediates homologous recombination repair in Arabidopsis}},
  url          = {{http://doi.org/10.15252/embj.201593083}},
  volume       = {{35}},
  year         = {{2016}},
}
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