A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis
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 stress...
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doaj-3cadbe661e0c43b8a15af4c9aedf11c72021-05-05T17:30:58ZengeLife Sciences Publications LtdeLife2050-084X2019-04-01810.7554/eLife.43944A regulatory module controlling stress-induced cell cycle arrest in ArabidopsisNaoki Takahashi0https://orcid.org/0000-0002-9526-277XNobuo Ogita1Tomonobu Takahashi2Shoji Taniguchi3Maho Tanaka4Motoaki Seki5Masaaki Umeda6https://orcid.org/0000-0003-3934-7936Graduate School of Science and Technology, Nara Institute of Science and Technology, Nara, JapanGraduate School of Science and Technology, Nara Institute of Science and Technology, Nara, JapanGraduate School of Science and Technology, Nara Institute of Science and Technology, Nara, JapanGraduate School of Science and Technology, Nara Institute of Science and Technology, Nara, JapanRIKEN Center for Sustainable Resource Science, Yokohama, Japan; RIKEN Cluster for Pioneering Research, Wako, JapanRIKEN Center for Sustainable Resource Science, Yokohama, Japan; RIKEN Cluster for Pioneering Research, Wako, JapanGraduate School of Science and Technology, Nara Institute of Science and Technology, Nara, JapanCell 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.https://elifesciences.org/articles/43944cell cycle arrestDNA damageheat stresstranscription factorsprotein stabilitygene expression |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Naoki Takahashi Nobuo Ogita Tomonobu Takahashi Shoji Taniguchi Maho Tanaka Motoaki Seki Masaaki Umeda |
spellingShingle |
Naoki Takahashi Nobuo Ogita Tomonobu Takahashi Shoji Taniguchi Maho Tanaka Motoaki Seki Masaaki Umeda A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis eLife cell cycle arrest DNA damage heat stress transcription factors protein stability gene expression |
author_facet |
Naoki Takahashi Nobuo Ogita Tomonobu Takahashi Shoji Taniguchi Maho Tanaka Motoaki Seki Masaaki Umeda |
author_sort |
Naoki Takahashi |
title |
A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis |
title_short |
A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis |
title_full |
A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis |
title_fullStr |
A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis |
title_full_unstemmed |
A regulatory module controlling stress-induced cell cycle arrest in Arabidopsis |
title_sort |
regulatory module controlling stress-induced cell cycle arrest in arabidopsis |
publisher |
eLife Sciences Publications Ltd |
series |
eLife |
issn |
2050-084X |
publishDate |
2019-04-01 |
description |
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. |
topic |
cell cycle arrest DNA damage heat stress transcription factors protein stability gene expression |
url |
https://elifesciences.org/articles/43944 |
work_keys_str_mv |
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