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First published online 23 April 2008
doi: 10.1242/dev.020743

Development 135, 2013-2022 (2008)
Published by The Company of Biologists 2008
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The Arabidopsis COP9 signalosome is essential for G2 phase progression and genomic stability

Esther M. N. Dohmann1, Mitchell P. Levesque2, Lieven De Veylder3,4, Ilka Reichardt1, Gerd Jürgens1, Markus Schmid5 and Claus Schwechheimer1,*

1 Tübingen University, Center for Plant Molecular Biology, Department of Developmental Genetics, Auf der Morgenstelle 3-5, 72076 Tübingen, Germany.
2 Max Planck Institute for Developmental Biology, Department of Genetics, Spemannstrasse 32, 72076 Tübingen, Germany.
3 Department of Plant Systems Biology, Flanders Institute for Biotechnology, Ghent University, Technologiepark 927, 9052 Gent, Belgium.
4 Department of Molecular Genetics, Ghent University, Technologiepark 927, 9052 Gent, Belgium.
5 Max-Planck Institute for Developmental Biology, Department of Molecular Biology, Spemannstrasse 32, 72076 Tübingen, Germany.

* Author for correspondence (e-mail: claus.schwechheimer{at}zmbp.uni-tuebingen.de)

Accepted 1 April 2008

The COP9 signalosome (CSN) is required for the full activity of cullin-RING E3 ubiquitin ligases (CRLs) in eukaryotes. CSN exerts its function on CRLs by removing the ubiquitin-related NEDD8 conjugate from the cullin subunit of CRLs. CSN seems, thereby, to control CRL disassembly or CRL subunit stability. In Arabidopsis thaliana, loss of CSN function leads to constitutive photomorphogenic (cop) seedling development and a post-germination growth arrest. The underlying molecular cause of this growth arrest is currently unknown. Here, we show that Arabidopsis csn mutants are delayed in G2 phase progression. This cell cycle arrest correlates with the induction of the DNA damage response pathway and is suggestive of the activation of a DNA damage checkpoint. In support of this hypothesis, we detected gene conversion events in csn mutants that are indicative of DNA double-strand breaks. DNA damage is also apparent in mutants of the NEDD8 conjugation pathway and in mutants of the E3 ligase subunits CULLIN4, COP1 and DET1, which share phenotypes with csn mutants. In summary, our data suggest that Arabidopsis csn mutants undergo DNA damage, which might be the cause of the delay in G2 cell cycle progression.

Key words: COP9 signalosome, Cell cycle, DNA damage






© The Company of Biologists Ltd 2008