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A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis

Naoki Takahashi, Nobuo Ogita, Tomonobu Takahashi, Shoji Taniguchi, Maho Tanaka, Motoaki Seki, View ORCID ProfileMasaaki Umeda
doi: https://doi.org/10.1101/495200
Naoki Takahashi
1Graduate School of Science and Technology, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0192, Japan
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Nobuo Ogita
1Graduate School of Science and Technology, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0192, Japan
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Tomonobu Takahashi
1Graduate School of Science and Technology, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0192, Japan
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Shoji Taniguchi
1Graduate School of Science and Technology, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0192, Japan
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Maho Tanaka
2RIKEN Center for Sustainable Resource Science, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan
3RIKEN Cluster for Pioneering Research, Wako, Saitama 351-0198, Japan
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Motoaki Seki
2RIKEN Center for Sustainable Resource Science, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan
3RIKEN Cluster for Pioneering Research, Wako, Saitama 351-0198, Japan
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Masaaki Umeda
1Graduate School of Science and Technology, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara 630-0192, Japan
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  • ORCID record for Masaaki Umeda
  • For correspondence: mumeda@bs.naist.jp
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Abstract

Cell cycle arrest is an active response to stresses that enables organisms to survive under fluctuating environmental conditions. While signalling pathways that inhibit cell cycle progression have been elucidated, the putative core module orchestrating cell cycle arrest in response to various stresses is still elusive. Here we report that in Arabidopsis thaliana, the NAC-type transcription factors ANAC044 and ANAC085 are required for DNA damage-induced G2 arrest. Under genotoxic stress conditions, ANAC044 and ANAC085 enhance protein accumulation of the R1R2R3-type Myb transcription factor (Rep-MYB), which represses G2/M-specific genes. ANAC044/ANAC085-dependent accumulation of Rep-MYB and cell cycle arrest are also observed in the response to heat stress that causes G2 arrest, but not to osmotic stress that retards G1 progression. These results suggest that plants deploy the ANAC044/ANAC085-mediated signalling module as a hub which perceives distinct stress signals and leads to G2 arrest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted December 13, 2018.
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A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis
Naoki Takahashi, Nobuo Ogita, Tomonobu Takahashi, Shoji Taniguchi, Maho Tanaka, Motoaki Seki, Masaaki Umeda
bioRxiv 495200; doi: https://doi.org/10.1101/495200
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A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis
Naoki Takahashi, Nobuo Ogita, Tomonobu Takahashi, Shoji Taniguchi, Maho Tanaka, Motoaki Seki, Masaaki Umeda
bioRxiv 495200; doi: https://doi.org/10.1101/495200

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