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First published online May 8, 2008; 10.1104/pp.108.121061

Plant Physiology 147:1369-1379 (2008)
© 2008 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

Auxin Responses in Mutants of the Arabidopsis CONSTITUTIVE PHOTOMORPHOGENIC9 Signalosome1,[C],[W],[OA]

Esther Mirjam Natascha Dohmann, Mitchell Paul Levesque, Erika Isono, Markus Schmid and Claus Schwechheimer*

Department of Developmental Genetics, Center for Plant Molecular Biology, Tübingen University, 72076 Tuebingen, Germany (E.M.N.D., E.I., C.S.); and Department of Genetics (M.P.L.) and Department of Molecular Biology (M.S.), Max Planck Institute for Developmental Biology, 72076 Tuebingen, Germany

The CONSTITUTIVE PHOTOMORPHOGENIC9 (COP9) signalosome (CSN) is an evolutionarily conserved multiprotein complex that interacts with cullin-RING type E3 ubiquitin ligases (CRLs). CSN subunit 5 (CSN5), which, when incorporated into CSN, can deconjugate the NEDD8 modification from the cullin subunit of CRLs, is essential for CSN's role in controlling CRL activity. Whether the CSN5 monomer, which is maintained in csn mutants such as csn3 or csn4, has a functional role, remains to be established. We performed a comparative gene expression-profiling experiment with Arabidopsis (Arabidopsis thaliana) csn3, csn4, and csn5 mutants, and we show here that these mutants cannot be distinguished at the transcriptional level. Furthermore, we show that csn3 csn5 mutants are morphologically indistinguishable from csn3 or csn5 mutants. Taken together, these data suggest that the CSN5 monomer does not have a function that leads to transcriptional or morphological changes in the csn mutants. We further examined auxin responses in csn mutants. Whereas CSN had previously been shown to be required for the auxin response-regulatory E3 complexes, specifically SCFTIR1, the csn mutant phenotype suggests that CSN is not essential for auxin responses. We present physiological and genetic data that indicate that auxin responses are indeed only partially impaired in csn mutants and that this is not the result of maternally contributed CSN. Finally, we discuss these findings in the context of the current understanding of the role of neddylation and CSN-mediated deneddylation for CRL activity.


1 This work was supported by the Deutsche Forschungsgemeinschaft and the Sonderforschungsbereich 446 (C.S. and E.M.N.D.), the Landesgraduiertenförderung Baden-Württemberg (E.M.N.D.), the National Science Foundation (M.P.L.), and the Japanese Society for the Promotion of Sciences (E.I.).

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Claus Schwechheimer (claus.schwechheimer{at}zmbp.uni-tuebingen.de).

[C] Some figures in this article are displayed in color online but in black and white in the print edition.

[W] The online version of this article contains Web-only data.

[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.108.121061

* Corresponding author; e-mail claus.schwechheimer{at}zmbp.uni-tuebingen.de.

Received April 11, 2008; accepted April 4, 2008; published May 8, 2008.







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