COP9 signalosome-mediated deneddylation of CULLIN1 is necessary for SCF EBF1 assembly in Arabidopsis thaliana.
| Autor: | Dong J; Institute of Crop Science, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou 310058, China., Li Y; Institute of Crop Science, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou 310058, China., Cheng S; Institute of Crop Science, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou 310058, China., Li X; National Key Laboratory of Wheat Improvement, Peking University Institute of Advanced Agricultural Sciences, Shandong Laboratory of Advanced Agriculture Sciences at Weifang, Weifang 261325, China., Wei N; School of Life Sciences, Southwest University, Chongqing 400715, China. Electronic address: weining@swu.edu.cn. |
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| Jazyk: | angličtina |
| Zdroj: | Cell reports [Cell Rep] 2024 Jan 23; Vol. 43 (1), pp. 113638. Date of Electronic Publication: 2024 Jan 06. |
| DOI: | 10.1016/j.celrep.2023.113638 |
| Abstrakt: | Functions of the SKP1-CUL1-F box (SCF) ubiquitin E3 ligases are essential in plants. The F box proteins (FBPs) are substrate receptors that recruit substrates and assemble an active SCF complex, but the regulatory mechanism underlying the FBPs binding to CUL1 to activate the SCF cycle is not fully understood. We show that Arabidopsis csn1-10 is defective in SCF EBF1 -mediated PIF3 degradation during de-etiolation, due to impaired association of EBF1 with CUL1 in csn1-10. EBF1 preferentially associates with un-neddylated CUL1 that is deficient in csn1-10 and the EBF1-CUL1 binding is rescued by the neddylation inhibitor MLN4924. Furthermore, we identify a subset of FBPs with impaired binding to CUL1 in csn1-10, indicating their assembly to form SCF complexes may depend on COP9 signalosome (CSN)-mediated deneddylation of CUL1. This study reports that a key role of CSN-mediated CULLIN deneddylation is to gate the binding of the FBP-substrate module to CUL1, thus initiating the SCF cycle of substrate ubiquitination. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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