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

Author

Listed:
  • 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
    CREST)

  • Masaaki Umeda

    (Nara Institute of Science and Technology
    CREST)

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.

Suggested Citation

  • Poyu Chen & Hirotomo Takatsuka & Naoki Takahashi & Rie Kurata & Yoichiro Fukao & Kosuke Kobayashi & Masaki Ito & Masaaki Umeda, 2017. "Arabidopsis R1R2R3-Myb proteins are essential for inhibiting cell division in response to DNA damage," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00676-4
    DOI: 10.1038/s41467-017-00676-4
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