Autoregulation in the biosynthesis of ribosomes.
Identifieur interne : 002475 ( PubMed/Curation ); précédent : 002474; suivant : 002476Autoregulation in the biosynthesis of ribosomes.
Auteurs : Yu Zhao [États-Unis] ; Jung-Hoon Sohn ; Jonathan R. WarnerSource :
- Molecular and cellular biology [ 0270-7306 ] ; 2003.
Descripteurs français
- KwdFr :
- ARN (métabolisme), ARN messager (métabolisme), ARN ribosomique (métabolisme), Amorces ADN (métabolisme), Biosynthèse des protéines, Cytoplasme (métabolisme), Délétion de gène, Facteurs temps, Liaison aux protéines, Modèles génétiques, Mutation, Phénotype, Plasmides (métabolisme), Protéines ribosomiques (métabolisme), Ribosomes (métabolisme), Régulation de l'expression des gènes fongiques, Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Technique de Northern, Température, Transcription génétique, Tunicamycine (pharmacologie).
- MESH :
- génétique : Saccharomyces cerevisiae.
- métabolisme : ARN, ARN messager, ARN ribosomique, Amorces ADN, Cytoplasme, Plasmides, Protéines ribosomiques, Ribosomes, Saccharomyces cerevisiae.
- pharmacologie : Tunicamycine.
- Biosynthèse des protéines, Délétion de gène, Facteurs temps, Liaison aux protéines, Modèles génétiques, Mutation, Phénotype, Régulation de l'expression des gènes fongiques, Technique de Northern, Température, Transcription génétique.
English descriptors
- KwdEn :
- Blotting, Northern, Cytoplasm (metabolism), DNA Primers (metabolism), Gene Deletion, Gene Expression Regulation, Fungal, Models, Genetic, Mutation, Phenotype, Plasmids (metabolism), Protein Binding, Protein Biosynthesis, RNA (metabolism), RNA, Messenger (metabolism), RNA, Ribosomal (metabolism), Ribosomal Proteins (metabolism), Ribosomes (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Temperature, Time Factors, Transcription, Genetic, Tunicamycin (pharmacology).
- MESH :
- chemical , metabolism : DNA Primers, RNA, RNA, Messenger, RNA, Ribosomal, Ribosomal Proteins.
- genetics : Saccharomyces cerevisiae.
- metabolism : Cytoplasm, Plasmids, Ribosomes, Saccharomyces cerevisiae.
- chemical , pharmacology : Tunicamycin.
- Blotting, Northern, Gene Deletion, Gene Expression Regulation, Fungal, Models, Genetic, Mutation, Phenotype, Protein Binding, Protein Biosynthesis, Temperature, Time Factors, Transcription, Genetic.
Abstract
The synthesis of ribosomes in Saccharomyces cerevisiae consumes a prodigious amount of the cell's resources and, consequently, is tightly regulated. The rate of ribosome synthesis responds not only to nutritional cues but also to signals dependent on other macromolecular pathways of the cell, e.g., a defect in the secretory pathway leads to severe repression of transcription of both rRNA and ribosomal protein genes. A search for mutants that interrupted this repression revealed, surprisingly, that inactivation of RPL1B, one of a pair of genes encoding the 60S ribosomal protein L1, almost completely blocked the repression of rRNA and ribosomal protein gene transcription that usually follows a defect in the secretory pathway. Further experiments showed that almost any mutation leading to a defect in 60S subunit synthesis had the same effect, whereas mutations affecting 40S subunit synthesis did not. Although one might suspect that this effect would be due to a decrease in the initiation of translation or to the presence of half-mers, i.e., polyribosomes awaiting a 60S subunit, our data show that this is not the case. Rather, a variety of experiments suggest that some aspect of the production of defective 60S particles or, more likely, their breakdown suppresses the signal generated by a defect in the secretory pathway that represses ribosome synthesis.
DOI: 10.1128/mcb.23.2.699-707.2003
PubMed: 12509467
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pubmed:12509467Le document en format XML
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<front><div type="abstract" xml:lang="en">The synthesis of ribosomes in Saccharomyces cerevisiae consumes a prodigious amount of the cell's resources and, consequently, is tightly regulated. The rate of ribosome synthesis responds not only to nutritional cues but also to signals dependent on other macromolecular pathways of the cell, e.g., a defect in the secretory pathway leads to severe repression of transcription of both rRNA and ribosomal protein genes. A search for mutants that interrupted this repression revealed, surprisingly, that inactivation of RPL1B, one of a pair of genes encoding the 60S ribosomal protein L1, almost completely blocked the repression of rRNA and ribosomal protein gene transcription that usually follows a defect in the secretory pathway. Further experiments showed that almost any mutation leading to a defect in 60S subunit synthesis had the same effect, whereas mutations affecting 40S subunit synthesis did not. Although one might suspect that this effect would be due to a decrease in the initiation of translation or to the presence of half-mers, i.e., polyribosomes awaiting a 60S subunit, our data show that this is not the case. Rather, a variety of experiments suggest that some aspect of the production of defective 60S particles or, more likely, their breakdown suppresses the signal generated by a defect in the secretory pathway that represses ribosome synthesis.</div>
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<Abstract><AbstractText>The synthesis of ribosomes in Saccharomyces cerevisiae consumes a prodigious amount of the cell's resources and, consequently, is tightly regulated. The rate of ribosome synthesis responds not only to nutritional cues but also to signals dependent on other macromolecular pathways of the cell, e.g., a defect in the secretory pathway leads to severe repression of transcription of both rRNA and ribosomal protein genes. A search for mutants that interrupted this repression revealed, surprisingly, that inactivation of RPL1B, one of a pair of genes encoding the 60S ribosomal protein L1, almost completely blocked the repression of rRNA and ribosomal protein gene transcription that usually follows a defect in the secretory pathway. Further experiments showed that almost any mutation leading to a defect in 60S subunit synthesis had the same effect, whereas mutations affecting 40S subunit synthesis did not. Although one might suspect that this effect would be due to a decrease in the initiation of translation or to the presence of half-mers, i.e., polyribosomes awaiting a 60S subunit, our data show that this is not the case. Rather, a variety of experiments suggest that some aspect of the production of defective 60S particles or, more likely, their breakdown suppresses the signal generated by a defect in the secretory pathway that represses ribosome synthesis.</AbstractText>
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