ArticleMolecular biology of the cell1997
Yeast cycloheximide-resistant crl mutants are proteasome mutants defective in protein degradation.
Article in Molecular biology of the cell, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 65 citations in OpenAlex.
- Mechanism of autocatalytic activation during proteasome assembly.Nature structural & molecular biology · 2024Article
- Cycloheximide in the nanomolar range inhibits seed germination ofJournal of pesticide science · 2024Article
- Structure of the preholoproteasome reveals late steps in proteasome core particle biogenesis.Nature structural & molecular biology · 2023Article
- A suite of polymerase chain reaction-based peptide tagging plasmids for epitope-targeted enzymatic functionalization of yeast proteins.Yeast (Chichester, England) · 2020Article
- Versatility of the Mec1Current genetics · 2019Review
- Two alternative mechanisms regulate the onset of chaperone-mediated assembly of the proteasomal ATPases.The Journal of biological chemistry · 2019Article
- Measuring Single-Cell Phenotypic Growth Heterogeneity Using a Microfluidic Cell Volume Sensor.Scientific reports · 2018Article
- Article
- Lean forward: Genetic analysis of temperature-sensitive mutants unfolds the secrets of oligomeric protein complex assembly.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- Assembly and validation of versatile transcription activator-like effector libraries.Scientific reports · 2014Article
- Review
- The Not4 E3 ligase and CCR4 deadenylase play distinct roles in protein quality control.PloS one · 2014Article
- Substrate-induced protein stabilization reveals a predominant contribution from mature proteins to peptides presented on MHC class I.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Synergistic effects of TOR and proteasome pathways on the yeast transcriptome and cell growth.Open biology · 2013Article
- Molecular chaperones and stress-inducible protein-sorting factors coordinate the spatiotemporal distribution of protein aggregates.Molecular biology of the cell · 2012Article
- Functional asymmetries of proteasome translocase pore.The Journal of biological chemistry · 2012Article
- An asymmetric interface between the regulatory and core particles of the proteasome.Nature structural & molecular biology · 2011Article
- The TEA transcription factor Tec1 links TOR and MAPK pathways to coordinate yeast development.Genetics · 2011Article
- Proteasomal degradation of Sfp1 contributes to the repression of ribosome biogenesis during starvation and is mediated by the proteasome activator Blm10.Molecular biology of the cell · 2011Article
- Targeted protein depletion in Saccharomyces cerevisiae by activation of a bidirectional degron.BMC systems biology · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In 1988 McCusker and Haber generated a series of mutants which are resistant to the minimum inhibitory concentration of the protein synthesis inhibitor cycloheximide. These cycloheximide-resistant, temperature-sensitive (crl) mutants, in addition, exhibited other pleiotropic phenotypes, e.g., incorrect response to starvation, hypersensitivity against amino acid analogues, and other protein synthesis inhibitors. Temperature sensitivity of one of these mutants, crl3-2, had been found to be suppressed by a mutation, SCL1-1, which resided in an alpha-type subunit of the 20S proteasome. We cloned the CRL3 gene by complementation and found CRL3 to be identical to the SUG1/CIM3 gene coding for a subunit of the 19S cap complex of the 26S proteasome. Another mutation, crl21, revealed to be allelic with the 20S proteasomal gene PRE3. crl3-2 and crl21 mutant cells show significant defects in proteasome-dependent proteolysis, whereas the SCL1-1 suppressor mutation causes partial restoration of crl3-2-induced proteolytic defects. Notably, cycloheximide resistance was also detected for other proteolytically deficient proteasome mutants (pre1-1, pre2-1, pre3-1, pre4-1). Moreover, proteasomal genes were found within genomic sequences of 9 of 13 chromosomal loci to which crl mutations had been mapped. We therefore assume that most if not all crl mutations reside in the proteasome and that phenotypes found are a result of defective protein degradation.
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