Auxin Responses in Mutants of the Arabidopsis CONSTITUTIVE PHOTOMORPHOGENIC9 Signalosome

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2008
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Dohmann, Esther Mirjam Natascha
Levesque, Mitchell Paul
Schmid, Markus
Schwechheimer, Claus
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Plant Physiology. 2008, 147(3), pp. 1369-1379. ISSN 0032-0889. eISSN 1532-2548. Available under: doi: 10.1104/pp.108.121061
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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.

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ISO 690DOHMANN, Esther Mirjam Natascha, Mitchell Paul LEVESQUE, Erika ISONO, Markus SCHMID, Claus SCHWECHHEIMER, 2008. Auxin Responses in Mutants of the Arabidopsis CONSTITUTIVE PHOTOMORPHOGENIC9 Signalosome. In: Plant Physiology. 2008, 147(3), pp. 1369-1379. ISSN 0032-0889. eISSN 1532-2548. Available under: doi: 10.1104/pp.108.121061
BibTex
@article{Dohmann2008-07Auxin-42152,
  year={2008},
  doi={10.1104/pp.108.121061},
  title={Auxin Responses in Mutants of the Arabidopsis CONSTITUTIVE PHOTOMORPHOGENIC9 Signalosome},
  number={3},
  volume={147},
  issn={0032-0889},
  journal={Plant Physiology},
  pages={1369--1379},
  author={Dohmann, Esther Mirjam Natascha and Levesque, Mitchell Paul and Isono, Erika and Schmid, Markus and Schwechheimer, Claus}
}
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    <dcterms:abstract xml:lang="eng">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 SCF&lt;sup&gt;TIR1&lt;/sup&gt;, 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.</dcterms:abstract>
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