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Interactions of the COP9 Signalosome with the E3 Ubiquitin Ligase SCF TIR1 in Mediating Auxin Response

Schwechheimer, Claus, Serino, Giovanna, Callis, Judy, Crosby, William L., Lyapina, Svetlana, Deshaies, Raymond J., Gray, William M., Estelle, Mark, Deng, Xing-Wang·2001·Science

Abstract

The COP9 signalosome is an evolutionary conserved multiprotein complex of unknown function that acts as a negative regulator of photomorphogenic seedling development in Arabidopsis . Here, we show that plants with reduced COP9 signalosome levels had decreased auxin response similar to loss-of-function mutants of the E3 ubiquitin ligase SCF TIR1 . Furthermore, we found that the COP9 signalosome and SCF TIR1 interacted in vivo and that the COP9 signalosome was required for efficient degradation of PSIAA6, a candidate substrate of SCF TIR1 . Thus, the COP9 signalosome may play an important role in mediating E3 ubiquitin ligase–mediated responses.

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Metadata

Authors
Schwechheimer, C., Serino, G., Callis, J., Crosby, W. L., Lyapina, S., Deshaies, R. J., Gray, W. M., Estelle, M., & Deng, X.-W.
Venue
Science
Published
2001-05-18
Volume
292
Issue
5520
Pages
1379-1382
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2053763318
Cited by
474
References
0
FWCI
72.84
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Interactions of the COP9 Signalosome with the E3 Ubiquitin Ligase SCF TIR1 in Mediating Auxin Response. https://app.cochat.ai/papers/10.1126/science.1059776
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Schwechheimer, C., Serino, G., Callis, J., Crosby, W. L., Lyapina, S., Deshaies, R. J., Gray, W. M., Estelle, M., & Deng, X.-W. (2001). Interactions of the COP9 Signalosome with the E3 Ubiquitin Ligase SCF TIR1 in Mediating Auxin Response. Science. https://doi.org/10.1126/science.1059776

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.