Control of Multicellular Development by the Physically Interacting Deneddylases DEN1/DenA and COP9 Signalosome

Christmann, Martin and Schmaler, Tilo and Gordon, Colin and Huang, Xiachua and Bayram, Ozgur and Schinke, Josua and Stumpf, Sina (2013) Control of Multicellular Development by the Physically Interacting Deneddylases DEN1/DenA and COP9 Signalosome. PLoS Genetics, 9 (2). e1003275. ISSN 1553-7390

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Deneddylases remove the ubiquitin-like protein Nedd8 from modified proteins. An increased deneddylase activity has been associated with various human cancers. In contrast, we show here that a mutant strain of the model fungus Aspergillus nidulans deficient in two deneddylases is viable but can only grow as a filament and is highly impaired for multicellular development. The DEN1/DenA and the COP9 signalosome (CSN) deneddylases physically interact in A. nidulans as well as in human cells, and CSN targets DEN1/DenA for protein degradation. Fungal development responds to light and requires both deneddylases for an appropriate light reaction. In contrast to CSN, which is necessary for sexual development, DEN1/DenA is required for asexual development. The CSN-DEN1/DenA interaction that affects DEN1/DenA protein levels presumably balances cellular deneddylase activity. A deneddylase disequilibrium impairs multicellular development and suggests that control of deneddylase activity is important for multicellular development.

Item Type: Article
Additional Information: © 2013 Christmann et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Keywords: Multicellular Development; Physically Interacting; Deneddylases; DEN1/DenA; COP9; Signalosome;
Academic Unit: Faculty of Science and Engineering > Biology
Item ID: 6245
Identification Number: 10.1371/journal.pgen.1003275
Depositing User: Ozgur Bayram
Date Deposited: 13 Jul 2015 15:19
Journal or Publication Title: PLoS Genetics
Publisher: Public Library of Science
Refereed: Yes

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