RapamycinFungusV1, Main, Exploration, bibRecord, 000087

Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect.

Identifieur interne : 000087 ( Main/Exploration ); précédent : 000086; suivant : 000088

Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect.

Auteurs : Robin Green [États-Unis] ; Sonal [États-Unis] ; Lin Wang [États-Unis] ; Samuel F M. Hart [États-Unis] ; Wenyun Lu [États-Unis] ; David Skelding [États-Unis] ; Justin C. Burton [États-Unis] ; Hanbing Mi [États-Unis] ; Aric Capel [États-Unis] ; Hung Alex Chen [États-Unis] ; Aaron Lin [États-Unis] ; Arvind R. Subramaniam [États-Unis] ; Joshua D. Rabinowitz [États-Unis] ; Wenying Shou [États-Unis]

Source :

PLoS biology [ 1545-7885 ] ; 2020.

RBID : pubmed:32833957

Descripteurs français

KwdFr :
- Adaptation physiologique (génétique), Autophagie (effets des médicaments et des substances chimiques), Autophagie (génétique), Azote (métabolisme), Azote (pharmacologie), Glucose (métabolisme), Glucose (pharmacologie), Lysine (déficit), Lysine (pharmacologie), Nutriments (métabolisme), Nutriments (pharmacologie), Ribosomes (effets des médicaments et des substances chimiques), Ribosomes (métabolisme), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Stress physiologique (MeSH), Voies et réseaux métaboliques (effets des médicaments et des substances chimiques), Voies et réseaux métaboliques (génétique), Évolution biologique (MeSH).
MESH :
- croissance et développement : Saccharomyces cerevisiae.
- déficit : Lysine.
- effets des médicaments et des substances chimiques : Autophagie, Ribosomes, Saccharomyces cerevisiae, Voies et réseaux métaboliques.
- génétique : Adaptation physiologique, Autophagie, Saccharomyces cerevisiae, Voies et réseaux métaboliques.
- métabolisme : Azote, Glucose, Nutriments, Ribosomes, Saccharomyces cerevisiae.
- pharmacologie : Azote, Glucose, Lysine, Nutriments, Sirolimus.
- Stress physiologique, Évolution biologique.

English descriptors

KwdEn :
- Adaptation, Physiological (genetics), Autophagy (drug effects), Autophagy (genetics), Biological Evolution (MeSH), Glucose (metabolism), Glucose (pharmacology), Lysine (deficiency), Lysine (pharmacology), Metabolic Networks and Pathways (drug effects), Metabolic Networks and Pathways (genetics), Nitrogen (metabolism), Nitrogen (pharmacology), Nutrients (metabolism), Nutrients (pharmacology), Ribosomes (drug effects), Ribosomes (metabolism), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Sirolimus (pharmacology), Stress, Physiological (MeSH).
MESH :
- chemical , deficiency : Lysine.
- chemical , metabolism : Glucose, Nitrogen.
- drug effects : Autophagy, Metabolic Networks and Pathways, Ribosomes, Saccharomyces cerevisiae.
- genetics : Adaptation, Physiological, Autophagy, Metabolic Networks and Pathways, Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Nutrients, Ribosomes, Saccharomyces cerevisiae.
- chemical , pharmacology : Glucose, Lysine, Nitrogen, Nutrients, Sirolimus.
- Biological Evolution, Stress, Physiological.

Abstract

In eukaryotes, conserved mechanisms ensure that cell growth is coordinated with nutrient availability. Overactive growth during nutrient limitation ("nutrient-growth dysregulation") can lead to rapid cell death. Here, we demonstrate that cells can adapt to nutrient-growth dysregulation by evolving major metabolic defects. Specifically, when yeast lysine-auxotrophic mutant lys- encountered lysine limitation, an evolutionarily novel stress, cells suffered nutrient-growth dysregulation. A subpopulation repeatedly evolved to lose the ability to synthesize organosulfurs (lys-orgS-). Organosulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by lys- cells during lysine limitation when growth was dysregulated, but not during glucose limitation when growth was regulated. Limiting organosulfurs conferred a frequency-dependent fitness advantage to lys-orgS- by eliciting a proper slow growth program, including autophagy. Thus, nutrient-growth dysregulation is associated with rapid organosulfur release, which enables the selection of organosulfur auxotrophy to better tune cell growth to the metabolic environment. We speculate that evolutionarily novel stresses can trigger atypical release of certain metabolites, setting the stage for the evolution of new ecological interactions.

DOI: 10.1371/journal.pbio.3000757
PubMed: 32833957
PubMed Central: PMC7470746

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000028
to stream Main, to step Curation: 000028

Le document en format XML

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<author><name sortKey="Capel, Aric" sort="Capel, Aric" uniqKey="Capel A" first="Aric" last="Capel">Aric Capel</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation, Physiological (genetics)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy (genetics)</term>
<term>Biological Evolution (MeSH)</term>
<term>Glucose (metabolism)</term>
<term>Glucose (pharmacology)</term>
<term>Lysine (deficiency)</term>
<term>Lysine (pharmacology)</term>
<term>Metabolic Networks and Pathways (drug effects)</term>
<term>Metabolic Networks and Pathways (genetics)</term>
<term>Nitrogen (metabolism)</term>
<term>Nitrogen (pharmacology)</term>
<term>Nutrients (metabolism)</term>
<term>Nutrients (pharmacology)</term>
<term>Ribosomes (drug effects)</term>
<term>Ribosomes (metabolism)</term>
<term>Saccharomyces cerevisiae (drug effects)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (growth & development)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Sirolimus (pharmacology)</term>
<term>Stress, Physiological (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adaptation physiologique (génétique)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (génétique)</term>
<term>Azote (métabolisme)</term>
<term>Azote (pharmacologie)</term>
<term>Glucose (métabolisme)</term>
<term>Glucose (pharmacologie)</term>
<term>Lysine (déficit)</term>
<term>Lysine (pharmacologie)</term>
<term>Nutriments (métabolisme)</term>
<term>Nutriments (pharmacologie)</term>
<term>Ribosomes (effets des médicaments et des substances chimiques)</term>
<term>Ribosomes (métabolisme)</term>
<term>Saccharomyces cerevisiae (croissance et développement)</term>
<term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Stress physiologique (MeSH)</term>
<term>Voies et réseaux métaboliques (effets des médicaments et des substances chimiques)</term>
<term>Voies et réseaux métaboliques (génétique)</term>
<term>Évolution biologique (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Lysine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glucose</term>
<term>Nitrogen</term>
</keywords>
<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Metabolic Networks and Pathways</term>
<term>Ribosomes</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Lysine</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
<term>Ribosomes</term>
<term>Saccharomyces cerevisiae</term>
<term>Voies et réseaux métaboliques</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adaptation, Physiological</term>
<term>Autophagy</term>
<term>Metabolic Networks and Pathways</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adaptation physiologique</term>
<term>Autophagie</term>
<term>Saccharomyces cerevisiae</term>
<term>Voies et réseaux métaboliques</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Nutrients</term>
<term>Ribosomes</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Azote</term>
<term>Glucose</term>
<term>Nutriments</term>
<term>Ribosomes</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Azote</term>
<term>Glucose</term>
<term>Lysine</term>
<term>Nutriments</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Glucose</term>
<term>Lysine</term>
<term>Nitrogen</term>
<term>Nutrients</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Biological Evolution</term>
<term>Stress, Physiological</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Stress physiologique</term>
<term>Évolution biologique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">In eukaryotes, conserved mechanisms ensure that cell growth is coordinated with nutrient availability. Overactive growth during nutrient limitation ("nutrient-growth dysregulation") can lead to rapid cell death. Here, we demonstrate that cells can adapt to nutrient-growth dysregulation by evolving major metabolic defects. Specifically, when yeast lysine-auxotrophic mutant lys- encountered lysine limitation, an evolutionarily novel stress, cells suffered nutrient-growth dysregulation. A subpopulation repeatedly evolved to lose the ability to synthesize organosulfurs (lys-orgS-). Organosulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by lys- cells during lysine limitation when growth was dysregulated, but not during glucose limitation when growth was regulated. Limiting organosulfurs conferred a frequency-dependent fitness advantage to lys-orgS- by eliciting a proper slow growth program, including autophagy. Thus, nutrient-growth dysregulation is associated with rapid organosulfur release, which enables the selection of organosulfur auxotrophy to better tune cell growth to the metabolic environment. We speculate that evolutionarily novel stresses can trigger atypical release of certain metabolites, setting the stage for the evolution of new ecological interactions.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32833957</PMID>
<DateCompleted><Year>2020</Year>
<Month>09</Month>
<Day>17</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>09</Month>
<Day>17</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1545-7885</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>18</Volume>
<Issue>8</Issue>
<PubDate><Year>2020</Year>
<Month>08</Month>
</PubDate>
</JournalIssue>
<Title>PLoS biology</Title>
<ISOAbbreviation>PLoS Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect.</ArticleTitle>
<Pagination><MedlinePgn>e3000757</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pbio.3000757</ELocationID>
<Abstract><AbstractText>In eukaryotes, conserved mechanisms ensure that cell growth is coordinated with nutrient availability. Overactive growth during nutrient limitation ("nutrient-growth dysregulation") can lead to rapid cell death. Here, we demonstrate that cells can adapt to nutrient-growth dysregulation by evolving major metabolic defects. Specifically, when yeast lysine-auxotrophic mutant lys- encountered lysine limitation, an evolutionarily novel stress, cells suffered nutrient-growth dysregulation. A subpopulation repeatedly evolved to lose the ability to synthesize organosulfurs (lys-orgS-). Organosulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by lys- cells during lysine limitation when growth was dysregulated, but not during glucose limitation when growth was regulated. Limiting organosulfurs conferred a frequency-dependent fitness advantage to lys-orgS- by eliciting a proper slow growth program, including autophagy. Thus, nutrient-growth dysregulation is associated with rapid organosulfur release, which enables the selection of organosulfur auxotrophy to better tune cell growth to the metabolic environment. We speculate that evolutionarily novel stresses can trigger atypical release of certain metabolites, setting the stage for the evolution of new ecological interactions.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Green</LastName>
<ForeName>Robin</ForeName>
<Initials>R</Initials>
<Identifier Source="ORCID">0000-0001-7411-0593</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sonal</LastName>
<Identifier Source="ORCID">0000-0002-2361-4131</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Lin</ForeName>
<Initials>L</Initials>
<Identifier Source="ORCID">0000-0002-9370-6891</Identifier>
<AffiliationInfo><Affiliation>Department of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hart</LastName>
<ForeName>Samuel F M</ForeName>
<Initials>SFM</Initials>
<Identifier Source="ORCID">0000-0002-5068-2199</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lu</LastName>
<ForeName>Wenyun</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Skelding</LastName>
<ForeName>David</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Burton</LastName>
<ForeName>Justin C</ForeName>
<Initials>JC</Initials>
<Identifier Source="ORCID">0000-0002-4797-8968</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mi</LastName>
<ForeName>Hanbing</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Capel</LastName>
<ForeName>Aric</ForeName>
<Initials>A</Initials>
<Identifier Source="ORCID">0000-0002-2748-379X</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Hung Alex</ForeName>
<Initials>HA</Initials>
<Identifier Source="ORCID">0000-0001-5119-6208</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Aaron</ForeName>
<Initials>A</Initials>
<Identifier Source="ORCID">0000-0002-6006-0908</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Subramaniam</LastName>
<ForeName>Arvind R</ForeName>
<Initials>AR</Initials>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rabinowitz</LastName>
<ForeName>Joshua D</ForeName>
<Initials>JD</Initials>
<Identifier Source="ORCID">0000-0002-1247-4727</Identifier>
<AffiliationInfo><Affiliation>Department of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shou</LastName>
<ForeName>Wenying</ForeName>
<Initials>W</Initials>
<Identifier Source="ORCID">0000-0001-5693-381X</Identifier>
<AffiliationInfo><Affiliation>Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 GM124128</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>DP2 OD006498</GrantID>
<Acronym>OD</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R35 GM119835</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R50 CA211437</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>1917258 </GrantID>
<Acronym>BB_</Acronym>
<Agency>Biotechnology and Biological Sciences Research Council</Agency>
<Country>United Kingdom</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>08</Month>
<Day>24</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS Biol</MedlineTA>
<NlmUniqueID>101183755</NlmUniqueID>
<ISSNLinking>1544-9173</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber>
<NameOfSubstance UI="D005947">Glucose</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>K3Z4F929H6</RegistryNumber>
<NameOfSubstance UI="D008239">Lysine</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>N762921K75</RegistryNumber>
<NameOfSubstance UI="D009584">Nitrogen</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber>
<NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000222" MajorTopicYN="N">Adaptation, Physiological</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005075" MajorTopicYN="N">Biological Evolution</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008239" MajorTopicYN="N">Lysine</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053858" MajorTopicYN="N">Metabolic Networks and Pathways</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009584" MajorTopicYN="N">Nitrogen</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000078622" MajorTopicYN="N">Nutrients</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012270" MajorTopicYN="N">Ribosomes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<CoiStatement>The authors have declared that no competing interests exist.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>02</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2020</Year>
<Month>07</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2020</Year>
<Month>09</Month>
<Day>03</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2020</Year>
<Month>8</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>9</Month>
<Day>18</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2020</Year>
<Month>8</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<ArticleId IdType="doi">10.1371/journal.pbio.3000757</ArticleId>
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<ArticleId IdType="pmc">PMC7470746</ArticleId>
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<name sortKey="Mi, Hanbing" sort="Mi, Hanbing" uniqKey="Mi H" first="Hanbing" last="Mi">Hanbing Mi</name>
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	Serveur d'exploration sur la rapamycine et les champignons
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Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect.

Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect.

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