Search Organism: All OrganismsArabidopsis thalianaBacillus subtilis 168Bos taurusCaenorhabditis elegansCanis familiarisDanio rerioDrosophila melanogasterEquus caballusEscherichia coli K12Gallus gallusHomo sapiensMacaca mulattaMus musculusNematostella vectensisOryza sativaPan troglodytesRattus norvegicusSaccharomyces cerevisiaeSchizosaccharomyces pombeStrongylocentrotus purpuratusTakifugu rubripesXenopus laevis home help / support contribute downloads mirrors about us Eukaryotic Cell Apr (2006); 5(4):712-22 Endoplasmic reticulum-associated degradation is required for cold adaptation and regulation of sterol biosynthesis in the yeast Saccharomyces cerevisiae- Loertscher J, Larson LL, Matson CK, Parrish ML, Felthauser A, Sturm A, Tachibana C, Bard M, Wright R Department of Chemistry, Seattle University, Seattle, WI 98122, USA- Abstract: Endoplasmic reticulum-associated degradation -ERAD- mediates the turnover of short-lived and misfolded proteins in the ER membrane or lumen- In spite of its important role, only subtle growth phenotypes have been associated with defects in ERAD- We have discovered that the ERAD proteins Ubc7 -Qri8-, Cue1, and Doa10 -Ssm4- are required for growth of yeast that express high levels of the sterol biosynthetic enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase -HMGR-- Interestingly, the observed growth defect was exacerbated at low temperatures, producing an HMGR-dependent cold sensitivity- Yeast strains lacking UBC7, CUE1, or DOA10 also assembled aberrant karmellae -ordered arrays of membranes surrounding the nucleus that assemble when HMGR is expressed at high levels-- However, rather than reflecting the accumulation of abnormal karmellae, the cold sensitivity of these ERAD mutants was due to increased HMGR catalytic activity- Mutations that compromise proteasomal function also resulted in cold-sensitive growth of yeast with elevated HMGR, suggesting that improper degradation of ERAD targets might be responsible for the observed cold-sensitive phenotype- However, the essential ERAD targets were not the yeast HMGR enzymes themselves- The sterol metabolite profile of ubc7Delta cells was altered relative to that of wild-type cells- Since sterol levels are known to regulate membrane fluidity, the viability of ERAD mutants expressing normal levels of HMGR was examined at low temperatures- Cells lacking UBC7, CUE1, or DOA10 were cold sensitive, suggesting that these ERAD proteins have a role in cold adaptation, perhaps through effects on sterol biosynthesis- [PUBMED: 16607018] Copyright © 2009, Tyers Lab, The Samuel Lunenfeld Research Institute, Mount Sinai Hospital, All Rights Reserved. terms and conditions - privacy policy - Osprey Network Visualization System BioGRID: A General Repository for Interaction Datasets. Chris Stark, Bobby-Joe Breitkreutz, Teresa Reguly, Lorrie Boucher, Ashton Breitkreutz, Mike Tyers. Nucleic Acids Res. Jan 1;34:D535-9.