RT Journal Article SR Electronic T1 A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis JF bioRxiv FD Cold Spring Harbor Laboratory SP 495200 DO 10.1101/495200 A1 Takahashi, Naoki A1 Ogita, Nobuo A1 Takahashi, Tomonobu A1 Taniguchi, Shoji A1 Tanaka, Maho A1 Seki, Motoaki A1 Umeda, Masaaki YR 2018 UL http://biorxiv.org/content/early/2018/12/13/495200.abstract AB 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.