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Title: Programmed induction of endoreduplication by DNA double-strand breaks in Arabidopsis
Authors: Adachi, Sumiko
Minamisawa, Kazunori
Okushima, Yoko
Inagaki, Soichi
Yoshiyama, Kaoru
Kondou, Youichi
Kaminuma, Eli
Kawashima, Mika
Toyoda, Tetsuro
Matsui, Minami
Kurihara, Daisuke
Matsunaga, Sachihiro
Umeda, Masaaki
Issue Date: 14-Jun-2011
Publisher: National Academy of Science
Volume: 108
Issue: 24
Start page: 10004
End page: 10009
Abstract: Genome integrity is continuously threatened by external stresses and by endogenous hazards such as DNA replication errors and reactive oxygen species. The DNA damage checkpoint in metazoans ensures genome integrity, by delaying cell cycle progression to repair damaged DNA or by inducing apoptosis. ATM and ATR (ataxia-telangiectasia-mutated and -Rad3-related) are sensor kinases that relay the damage signal to transducer kinases Chk1 and Chk2, and to downstream cell cycle regulators. Plants also possess ATM and ATR orthologues, but lack obvious counterparts of downstream regulators. Instead, the plant-specific transcription factor SOG1 (suppressor of gamma response 1) plays a central role in the transmission of signals from both ATM and ATR kinases. Here we show that, in Arabidopsis, endoreduplication is induced by DNA double-strand breaks (DSBs), but not directly by DNA replication stress. When root or sepal cells, or undifferentiated suspension cells, were treated with DSB inducers, they displayed increased cell size and DNA ploidy. We found that the ATM–SOG1 and ATR–SOG1 pathways both transmit DSB-derived signals, and that either one suffices for endocycle induction. These signaling pathways govern the expression of distinct sets of cell cycle regulators, such as cyclin-dependent kinases (CDKs) and their suppressors. Our results demonstrate that Arabidopsis undergoes a programmed endoreduplicative response to DSBs, suggesting that plants have evolved a distinct strategy to sustain growth under genotoxic stress.
ISSN: 0027-8424
Rights: Copyright (c) 2011 by the National Academy of Sciences
Text Version: author
Publisher DOI: 10.1073/pnas.1103584108
Appears in Collections:バイオサイエンス研究科 / Graduate School of Biological Sciences

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