Arabidopsis R1R2R3-Myb proteins are essential for inhibiting cell division in response to DNA damage

Poyu Chen, Hirotomo Takatsuka, Naoki Takahashi, Rie Kurata, Yoichiro Fukao, Kosuke Kobayashi, Masaki Ito and Masaaki Umeda ()
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Poyu Chen: Nara Institute of Science and Technology
Hirotomo Takatsuka: Nara Institute of Science and Technology
Naoki Takahashi: Nara Institute of Science and Technology
Rie Kurata: Nara Institute of Science and Technology
Yoichiro Fukao: Ritsumeikan University
Kosuke Kobayashi: Nagoya University
Masaki Ito: Nagoya University
Masaaki Umeda: Nara Institute of Science and Technology

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract Inhibition of cell division is an active response to DNA damage that enables cells to maintain genome integrity. However, how DNA damage arrests the plant cell cycle is largely unknown. Here, we show that the repressor-type R1R2R3-Myb transcription factors (Rep-MYBs), which suppress G2/M-specific genes, are required to inhibit cell division in response to DNA damage. Knockout mutants are resistant to agents that cause DNA double-strand breaks and replication stress. Cyclin-dependent kinases (CDKs) can phosphorylate Rep-MYBs in vitro and are involved in their proteasomal degradation. DNA damage reduces CDK activities and causes accumulation of Rep-MYBs and cytological changes consistent with cell cycle arrest. Our results suggest that CDK suppressors such as CDK inhibitors are not sufficient to arrest the cell cycle in response to DNA damage but that Rep-MYB-dependent repression of G2/M-specific genes is crucial, indicating an essential function for Rep-MYBs in the DNA damage response.

Date: 2017
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DOI: 10.1038/s41467-017-00676-4

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