Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 561271
Title The Arabidopsis SIAMESE-RELATED cyclin-dependent Kinase Inhibitors SMR5 and SMR7 Regulate the DNA damage checkpoint in response to reactive oxygen species
Author(s) Yi, Dalong; Kamei, Claire Lessa Alvim; Cools, Toon; Vanderauwera, Sandy; Takahashi, Naoki; Okushima, Yoko; Eekhout, Thomas; Yoshiyama, Kaoru Okamoto; Larkin, John; Daele, Hilde Van den; Conklin, Phillip; Britt, Anne; Umeda, Masaaki; Veylder, Lieven De
Source The Plant Cell 26 (2014)1. - ISSN 1040-4651 - p. 296 - 309.
DOI https://doi.org/10.1105/tpc.113.118943
Department(s) Plant Breeding
Publication type Refereed Article in a scientific journal
Publication year 2014
Abstract

Whereas our knowledge about the diverse pathways aiding DNA repair upon genome damage is steadily increasing, little is known about the molecular players that adjust the plant cell cycle in response to DNA stress. By a meta-analysis of DNA stress microarray data sets, three family members of the SIAMESE/SIAMESE-RELATED (SIM/SMR) class of cyclin-dependent kinase inhibitors were discovered that react strongly to genotoxicity. Transcriptional reporter constructs corroborated specific and strong activation of the three SIM/SMR genes in the meristems upon DNA stress, whereas overexpression analysis confirmed their cell cycle inhibitory potential. In agreement with being checkpoint regulators, SMR5 and SMR7 knockout plants displayed an impaired checkpoint in leaf cells upon treatment with the replication inhibitory drug hydroxyurea (HU). Surprisingly, HU-induced SMR5/SMR7 expression depends on ATAXIA TELANGIECTASIA MUTATED (ATM) and SUPPRESSOR OF GAMMA RESPONSE1, rather than on the anticipated replication stress-activated ATM AND RAD3-RELATED kinase. This apparent discrepancy was explained by demonstrating that, in addition to its effect on replication, HU triggers the formation of reactive oxygen species (ROS). ROS-dependent transcriptional activation of the SMR genes was confirmed by different ROS-inducing conditions, including high-light treatment. We conclude that the identified SMR genes are part of a signaling cascade that induces a cell cycle checkpoint in response to ROS-induced DNA damage.

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