Regulation of ribosomal DNA amplification by the TOR pathway.
Identifieur interne : 000C20 ( Main/Corpus ); précédent : 000C19; suivant : 000C21Regulation of ribosomal DNA amplification by the TOR pathway.
Auteurs : Carmen V. Jack ; Cristina Cruz ; Ryan M. Hull ; Markus A. Keller ; Markus Ralser ; Jonathan HouseleySource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2015.
English descriptors
- KwdEn :
- Acetylation (drug effects), DNA, Ribosomal (genetics), Environment (MeSH), Gene Amplification (drug effects), Histone Deacetylases (metabolism), Histones (metabolism), Homologous Recombination (drug effects), Homologous Recombination (genetics), Lysine (metabolism), Models, Biological (MeSH), NAD (metabolism), Protein-Serine-Threonine Kinases (metabolism), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (enzymology), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects), Sirolimus (pharmacology).
- MESH :
- chemical , genetics : DNA, Ribosomal.
- drug effects : Acetylation, Gene Amplification, Homologous Recombination, Saccharomyces cerevisiae, Signal Transduction.
- enzymology : Saccharomyces cerevisiae.
- genetics : Homologous Recombination, Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- chemical , metabolism : Histone Deacetylases, Histones, Lysine, NAD, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins.
- chemical , pharmacology : Sirolimus.
- Environment, Models, Biological.
Abstract
Repeated regions are widespread in eukaryotic genomes, and key functional elements such as the ribosomal DNA tend to be formed of high copy repeated sequences organized in tandem arrays. In general, high copy repeats are remarkably stable, but a number of organisms display rapid ribosomal DNA amplification at specific times or under specific conditions. Here we demonstrate that target of rapamycin (TOR) signaling stimulates ribosomal DNA amplification in budding yeast, linking external nutrient availability to ribosomal DNA copy number. We show that ribosomal DNA amplification is regulated by three histone deacetylases: Sir2, Hst3, and Hst4. These enzymes control homologous recombination-dependent and nonhomologous recombination-dependent amplification pathways that act in concert to mediate rapid, directional ribosomal DNA copy number change. Amplification is completely repressed by rapamycin, an inhibitor of the nutrient-responsive TOR pathway; this effect is separable from growth rate and is mediated directly through Sir2, Hst3, and Hst4. Caloric restriction is known to up-regulate expression of nicotinamidase Pnc1, an enzyme that enhances Sir2, Hst3, and Hst4 activity. In contrast, normal glucose concentrations stretch the ribosome synthesis capacity of cells with low ribosomal DNA copy number, and we find that these cells show a previously unrecognized transcriptional response to caloric excess by reducing PNC1 expression. PNC1 down-regulation forms a key element in the control of ribosomal DNA amplification as overexpression of PNC1 substantially reduces ribosomal DNA amplification rate. Our results reveal how a signaling pathway can orchestrate specific genome changes and demonstrate that the copy number of repetitive DNA can be altered to suit environmental conditions.
DOI: 10.1073/pnas.1505015112
PubMed: 26195783
PubMed Central: PMC4534215
Links to Exploration step
pubmed:26195783Le document en format XML
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Hull</name><affiliation><nlm:affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</nlm:affiliation></affiliation></author><author><name sortKey="Keller, Markus A" sort="Keller, Markus A" uniqKey="Keller M" first="Markus A" last="Keller">Markus A. 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Jack</name><affiliation><nlm:affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</nlm:affiliation></affiliation></author><author><name sortKey="Cruz, Cristina" sort="Cruz, Cristina" uniqKey="Cruz C" first="Cristina" last="Cruz">Cristina Cruz</name><affiliation><nlm:affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</nlm:affiliation></affiliation></author><author><name sortKey="Hull, Ryan M" sort="Hull, Ryan M" uniqKey="Hull R" first="Ryan M" last="Hull">Ryan M. Hull</name><affiliation><nlm:affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</nlm:affiliation></affiliation></author><author><name sortKey="Keller, Markus A" sort="Keller, Markus A" uniqKey="Keller M" first="Markus A" last="Keller">Markus A. Keller</name><affiliation><nlm:affiliation>Cambridge Systems Biology Centre and Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom;</nlm:affiliation></affiliation></author><author><name sortKey="Ralser, Markus" sort="Ralser, Markus" uniqKey="Ralser M" first="Markus" last="Ralser">Markus Ralser</name><affiliation><nlm:affiliation>Cambridge Systems Biology Centre and Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom; Division of Physiology and Metabolism, Medical Research Council National Institute for Medical Research, London NW7 1AA, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Houseley, Jonathan" sort="Houseley, Jonathan" uniqKey="Houseley J" first="Jonathan" last="Houseley">Jonathan Houseley</name><affiliation><nlm:affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom; jon.houseley@babraham.ac.uk.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylation (drug effects)</term><term>DNA, Ribosomal (genetics)</term><term>Environment (MeSH)</term><term>Gene Amplification (drug effects)</term><term>Histone Deacetylases (metabolism)</term><term>Histones (metabolism)</term><term>Homologous Recombination (drug effects)</term><term>Homologous Recombination (genetics)</term><term>Lysine (metabolism)</term><term>Models, Biological (MeSH)</term><term>NAD (metabolism)</term><term>Protein-Serine-Threonine Kinases (metabolism)</term><term>Saccharomyces cerevisiae (drug effects)</term><term>Saccharomyces cerevisiae (enzymology)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (growth & development)</term><term>Saccharomyces cerevisiae Proteins (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Sirolimus (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Ribosomal</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Acetylation</term><term>Gene Amplification</term><term>Homologous Recombination</term><term>Saccharomyces cerevisiae</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Homologous Recombination</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Histone Deacetylases</term><term>Histones</term><term>Lysine</term><term>NAD</term><term>Protein-Serine-Threonine Kinases</term><term>Saccharomyces cerevisiae Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Environment</term><term>Models, Biological</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Repeated regions are widespread in eukaryotic genomes, and key functional elements such as the ribosomal DNA tend to be formed of high copy repeated sequences organized in tandem arrays. In general, high copy repeats are remarkably stable, but a number of organisms display rapid ribosomal DNA amplification at specific times or under specific conditions. Here we demonstrate that target of rapamycin (TOR) signaling stimulates ribosomal DNA amplification in budding yeast, linking external nutrient availability to ribosomal DNA copy number. We show that ribosomal DNA amplification is regulated by three histone deacetylases: Sir2, Hst3, and Hst4. These enzymes control homologous recombination-dependent and nonhomologous recombination-dependent amplification pathways that act in concert to mediate rapid, directional ribosomal DNA copy number change. Amplification is completely repressed by rapamycin, an inhibitor of the nutrient-responsive TOR pathway; this effect is separable from growth rate and is mediated directly through Sir2, Hst3, and Hst4. Caloric restriction is known to up-regulate expression of nicotinamidase Pnc1, an enzyme that enhances Sir2, Hst3, and Hst4 activity. In contrast, normal glucose concentrations stretch the ribosome synthesis capacity of cells with low ribosomal DNA copy number, and we find that these cells show a previously unrecognized transcriptional response to caloric excess by reducing PNC1 expression. PNC1 down-regulation forms a key element in the control of ribosomal DNA amplification as overexpression of PNC1 substantially reduces ribosomal DNA amplification rate. Our results reveal how a signaling pathway can orchestrate specific genome changes and demonstrate that the copy number of repetitive DNA can be altered to suit environmental conditions. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26195783</PMID><DateCompleted><Year>2015</Year><Month>11</Month><Day>17</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>112</Volume><Issue>31</Issue><PubDate><Year>2015</Year><Month>Aug</Month><Day>04</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc Natl Acad Sci U S A</ISOAbbreviation></Journal><ArticleTitle>Regulation of ribosomal DNA amplification by the TOR pathway.</ArticleTitle><Pagination><MedlinePgn>9674-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1505015112</ELocationID><Abstract><AbstractText>Repeated regions are widespread in eukaryotic genomes, and key functional elements such as the ribosomal DNA tend to be formed of high copy repeated sequences organized in tandem arrays. In general, high copy repeats are remarkably stable, but a number of organisms display rapid ribosomal DNA amplification at specific times or under specific conditions. Here we demonstrate that target of rapamycin (TOR) signaling stimulates ribosomal DNA amplification in budding yeast, linking external nutrient availability to ribosomal DNA copy number. We show that ribosomal DNA amplification is regulated by three histone deacetylases: Sir2, Hst3, and Hst4. These enzymes control homologous recombination-dependent and nonhomologous recombination-dependent amplification pathways that act in concert to mediate rapid, directional ribosomal DNA copy number change. Amplification is completely repressed by rapamycin, an inhibitor of the nutrient-responsive TOR pathway; this effect is separable from growth rate and is mediated directly through Sir2, Hst3, and Hst4. Caloric restriction is known to up-regulate expression of nicotinamidase Pnc1, an enzyme that enhances Sir2, Hst3, and Hst4 activity. In contrast, normal glucose concentrations stretch the ribosome synthesis capacity of cells with low ribosomal DNA copy number, and we find that these cells show a previously unrecognized transcriptional response to caloric excess by reducing PNC1 expression. PNC1 down-regulation forms a key element in the control of ribosomal DNA amplification as overexpression of PNC1 substantially reduces ribosomal DNA amplification rate. Our results reveal how a signaling pathway can orchestrate specific genome changes and demonstrate that the copy number of repetitive DNA can be altered to suit environmental conditions. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jack</LastName><ForeName>Carmen V</ForeName><Initials>CV</Initials><AffiliationInfo><Affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cruz</LastName><ForeName>Cristina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hull</LastName><ForeName>Ryan M</ForeName><Initials>RM</Initials><AffiliationInfo><Affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United Kingdom;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Keller</LastName><ForeName>Markus A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Cambridge Systems Biology Centre and Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ralser</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cambridge Systems Biology Centre and Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom; Division of Physiology and Metabolism, Medical Research Council National Institute for Medical Research, London NW7 1AA, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Houseley</LastName><ForeName>Jonathan</ForeName><Initials>J</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-8509-1500</Identifier><AffiliationInfo><Affiliation>Epigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, United 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