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Elife. 2019 Apr 9;8. pii: e43944. doi: 10.7554/eLife.43944.

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

Author information

1
Graduate School of Science and Technology, Nara Institute of Science and Technology, Nara, Japan.
2
RIKEN Center for Sustainable Resource Science, Yokohama, Japan.
3
RIKEN Cluster for Pioneering Research, Wako, Japan.

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, 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.

KEYWORDS:

A. thaliana; DNA damage; cell cycle arrest; gene expression; heat stress; plant biology; protein stability; transcription factors

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