The COP9 signalosome counteracts the accumulation of cullin SCF ubiquitin E3 RING ligases during fungal development

Molecular Microbiology
Marcia Regina von Zeska KressGerhard H Braus

Abstract

Defects in the COP9 signalosome (CSN) impair multicellular development, including embryonic plant or animal death or a block in sexual development of the fungus Aspergillus nidulans. CSN deneddylates cullin-RING ligases (CRLs), which are activated by covalent linkage to ubiquitin-like NEDD8. Deneddylation allows CRL disassembly for subsequent reassembly. An attractive hypothesis is a consecutive order of CRLs for development, which demands repeated cycles of neddylation and deneddylation for reassembling CRLs. Interruption of these cycles could explain developmental blocks caused by csn mutations. This predicts an accumulation of neddylated CRLs exhibiting developmental functions when CSN is dysfunctional. We tested this hypothesis in A. nidulans, which tolerates reduced levels of neddylation for growth. We show that only genes for CRL subunits or neddylation are essential, whereas CSN is primarily required for development. We used functional tagged NEDD8, recruiting all three fungal cullins. Cullins are associated with the CSN1/CsnA subunit when deneddylation is defective. Two CRLs were identified which are specifically involved in differentiation and accumulate during the developmental block. This suggests that an active CSN ...Continue Reading

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Citations

Aug 22, 2014·Applied Microbiology and Biotechnology·Jennifer Gerke, Gerhard H Braus
Nov 28, 2013·Molecular Microbiology·Rebekka HartingGerhard H Braus
May 7, 2013·Fungal Genetics and Biology : FG & B·Satoshi SuzukiGerhard H Braus
Jun 22, 2014·Eukaryotic Cell·Saturnino HerreroReinhard Fischer
Apr 13, 2018·Microbiology and Molecular Biology Reviews : MMBR·Meritxell RiquelmeReinhard Fischer
Feb 6, 2018·PLoS Genetics·Miriam Kolog GulkoGerhard H Braus

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