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PLoS Genet. 2013;9(2):e1003275. doi: 10.1371/journal.pgen.1003275. Epub 2013 Feb 7.

Control of multicellular development by the physically interacting deneddylases DEN1/DenA and COP9 signalosome.

Author information

1
Department of Molecular Microbiology and Genetics, Institute of Microbiology and Genetics, Georg-August-Universität Göttingen, Göttingen, Germany.

Abstract

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.

PMID:
23408908
PMCID:
PMC3567183
DOI:
10.1371/journal.pgen.1003275
[Indexed for MEDLINE]
Free PMC Article

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