Introns are mediators of cell response to starvation.
Identifieur interne : 000311 ( Main/Exploration ); précédent : 000310; suivant : 000312Introns are mediators of cell response to starvation.
Auteurs : Julie Parenteau [Canada] ; Laurine Maignon [Canada] ; Mélodie Berthoumieux [Canada] ; Mathieu Catala [Canada] ; Vanessa Gagnon [Canada] ; Sherif Abou Elela [Canada]Source :
- Nature [ 1476-4687 ] ; 2019.
Descripteurs français
- KwdFr :
- Biosynthèse des protéines (MeSH), Complexe-1 cible mécanistique de la rapamycine (métabolisme), Cyclic AMP-Dependent Protein Kinases (métabolisme), Délétion de séquence (génétique), Introns (génétique), Milieux de culture (pharmacologie), Nutriments (déficit), Privation alimentaire (MeSH), Protéines ribosomiques (génétique), Respiration cellulaire (MeSH), Ribosomes (génétique), Ribosomes (métabolisme), Régions 5' non traduites (génétique), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (cytologie), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Transcriptome (génétique), Transduction du signal (MeSH), Viabilité microbienne (effets des médicaments et des substances chimiques), Viabilité microbienne (génétique).
- MESH :
- croissance et développement : Saccharomyces cerevisiae.
- cytologie : Saccharomyces cerevisiae.
- déficit : Nutriments.
- effets des médicaments et des substances chimiques : Saccharomyces cerevisiae, Viabilité microbienne.
- génétique : Délétion de séquence, Introns, Protéines ribosomiques, Ribosomes, Régions 5' non traduites, Saccharomyces cerevisiae, Transcriptome, Viabilité microbienne.
- métabolisme : Complexe-1 cible mécanistique de la rapamycine, Cyclic AMP-Dependent Protein Kinases, Ribosomes.
- pharmacologie : Milieux de culture.
- Biosynthèse des protéines, Privation alimentaire, Respiration cellulaire, Régulation de l'expression des gènes fongiques, Transduction du signal.
English descriptors
- KwdEn :
- 5' Untranslated Regions (genetics), Cell Respiration (MeSH), Culture Media (pharmacology), Cyclic AMP-Dependent Protein Kinases (metabolism), Food Deprivation (MeSH), Gene Expression Regulation, Fungal (MeSH), Introns (genetics), Mechanistic Target of Rapamycin Complex 1 (metabolism), Microbial Viability (drug effects), Microbial Viability (genetics), Nutrients (deficiency), Protein Biosynthesis (MeSH), Ribosomal Proteins (genetics), Ribosomes (genetics), Ribosomes (metabolism), Saccharomyces cerevisiae (cytology), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Sequence Deletion (genetics), Signal Transduction (MeSH), Transcriptome (genetics).
- MESH :
- chemical , genetics : 5' Untranslated Regions, Ribosomal Proteins.
- chemical , metabolism : Cyclic AMP-Dependent Protein Kinases, Mechanistic Target of Rapamycin Complex 1.
- chemical , pharmacology : Culture Media.
- cytology : Saccharomyces cerevisiae.
- deficiency : Nutrients.
- drug effects : Microbial Viability, Saccharomyces cerevisiae.
- genetics : Introns, Microbial Viability, Ribosomes, Saccharomyces cerevisiae, Sequence Deletion, Transcriptome.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Ribosomes.
- Cell Respiration, Food Deprivation, Gene Expression Regulation, Fungal, Protein Biosynthesis, Signal Transduction.
Abstract
Introns are ubiquitous features of all eukaryotic cells. Introns need to be removed from nascent messenger RNA through the process of splicing to produce functional proteins. Here we show that the physical presence of introns in the genome promotes cell survival under starvation conditions. A systematic deletion set of all known introns in budding yeast genes indicates that, in most cases, cells with an intron deletion are impaired when nutrients are depleted. This effect of introns on growth is not linked to the expression of the host gene, and was reproduced even when translation of the host mRNA was blocked. Transcriptomic and genetic analyses indicate that introns promote resistance to starvation by enhancing the repression of ribosomal protein genes that are downstream of the nutrient-sensing TORC1 and PKA pathways. Our results reveal functions of introns that may help to explain their evolutionary preservation in genes, and uncover regulatory mechanisms of cell adaptations to starvation.
DOI: 10.1038/s41586-018-0859-7
PubMed: 30651641
Affiliations:
Links toward previous steps (curation, corpus...)
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(drug effects)</term><term>Microbial Viability (genetics)</term><term>Nutrients (deficiency)</term><term>Protein Biosynthesis (MeSH)</term><term>Ribosomal Proteins (genetics)</term><term>Ribosomes (genetics)</term><term>Ribosomes (metabolism)</term><term>Saccharomyces cerevisiae (cytology)</term><term>Saccharomyces cerevisiae (drug effects)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (growth & development)</term><term>Sequence Deletion (genetics)</term><term>Signal Transduction (MeSH)</term><term>Transcriptome (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Biosynthèse des protéines (MeSH)</term><term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term><term>Cyclic AMP-Dependent Protein Kinases (métabolisme)</term><term>Délétion de séquence (génétique)</term><term>Introns (génétique)</term><term>Milieux de culture (pharmacologie)</term><term>Nutriments (déficit)</term><term>Privation alimentaire (MeSH)</term><term>Protéines ribosomiques (génétique)</term><term>Respiration cellulaire (MeSH)</term><term>Ribosomes (génétique)</term><term>Ribosomes (métabolisme)</term><term>Régions 5' non traduites (génétique)</term><term>Régulation de l'expression des gènes fongiques (MeSH)</term><term>Saccharomyces cerevisiae (croissance et développement)</term><term>Saccharomyces cerevisiae (cytologie)</term><term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Transcriptome (génétique)</term><term>Transduction du signal (MeSH)</term><term>Viabilité microbienne (effets des médicaments et des substances chimiques)</term><term>Viabilité microbienne (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>5' Untranslated Regions</term><term>Ribosomal Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" 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xml:lang="fr"><term>Saccharomyces cerevisiae</term><term>Viabilité microbienne</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Introns</term><term>Microbial Viability</term><term>Ribosomes</term><term>Saccharomyces cerevisiae</term><term>Sequence Deletion</term><term>Transcriptome</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>Délétion de séquence</term><term>Introns</term><term>Protéines ribosomiques</term><term>Ribosomes</term><term>Régions 5' non traduites</term><term>Saccharomyces cerevisiae</term><term>Transcriptome</term><term>Viabilité microbienne</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Ribosomes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Cyclic AMP-Dependent Protein Kinases</term><term>Ribosomes</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Milieux de culture</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Respiration</term><term>Food Deprivation</term><term>Gene Expression Regulation, Fungal</term><term>Protein Biosynthesis</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Biosynthèse des protéines</term><term>Privation alimentaire</term><term>Respiration cellulaire</term><term>Régulation de l'expression des gènes fongiques</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Introns are ubiquitous features of all eukaryotic cells. Introns need to be removed from nascent messenger RNA through the process of splicing to produce functional proteins. Here we show that the physical presence of introns in the genome promotes cell survival under starvation conditions. A systematic deletion set of all known introns in budding yeast genes indicates that, in most cases, cells with an intron deletion are impaired when nutrients are depleted. This effect of introns on growth is not linked to the expression of the host gene, and was reproduced even when translation of the host mRNA was blocked. Transcriptomic and genetic analyses indicate that introns promote resistance to starvation by enhancing the repression of ribosomal protein genes that are downstream of the nutrient-sensing TORC1 and PKA pathways. Our results reveal functions of introns that may help to explain their evolutionary preservation in genes, and uncover regulatory mechanisms of cell adaptations to starvation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30651641</PMID><DateCompleted><Year>2019</Year><Month>06</Month><Day>19</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-4687</ISSN><JournalIssue CitedMedium="Internet"><Volume>565</Volume><Issue>7741</Issue><PubDate><Year>2019</Year><Month>01</Month></PubDate></JournalIssue><Title>Nature</Title><ISOAbbreviation>Nature</ISOAbbreviation></Journal><ArticleTitle>Introns are mediators of cell response to starvation.</ArticleTitle><Pagination><MedlinePgn>612-617</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41586-018-0859-7</ELocationID><Abstract><AbstractText>Introns are ubiquitous features of all eukaryotic cells. Introns need to be removed from nascent messenger RNA through the process of splicing to produce functional proteins. Here we show that the physical presence of introns in the genome promotes cell survival under starvation conditions. A systematic deletion set of all known introns in budding yeast genes indicates that, in most cases, cells with an intron deletion are impaired when nutrients are depleted. This effect of introns on growth is not linked to the expression of the host gene, and was reproduced even when translation of the host mRNA was blocked. Transcriptomic and genetic analyses indicate that introns promote resistance to starvation by enhancing the repression of ribosomal protein genes that are downstream of the nutrient-sensing TORC1 and PKA pathways. Our results reveal functions of introns that may help to explain their evolutionary preservation in genes, and uncover regulatory mechanisms of cell adaptations to starvation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Parenteau</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>RNA Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maignon</LastName><ForeName>Laurine</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>RNA Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Berthoumieux</LastName><ForeName>Mélodie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>RNA Group, Département de Biochimie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Catala</LastName><ForeName>Mathieu</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>RNA Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gagnon</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>RNA Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abou Elela</LastName><ForeName>Sherif</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>RNA Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada. Sherif.Abou.Elela@USherbrooke.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>01</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nature</MedlineTA><NlmUniqueID>0410462</NlmUniqueID><ISSNLinking>0028-0836</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020121">5' Untranslated Regions</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003470">Culture Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012269">Ribosomal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.11</RegistryNumber><NameOfSubstance UI="D017868">Cyclic AMP-Dependent Protein Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Nature. 2019 Jan;565(7741):578-579</RefSource><PMID Version="1">30683935</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D020121" MajorTopicYN="N">5' Untranslated Regions</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019069" MajorTopicYN="N">Cell Respiration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003470" MajorTopicYN="N">Culture Media</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017868" MajorTopicYN="N">Cyclic AMP-Dependent Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005508" MajorTopicYN="N">Food Deprivation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007438" MajorTopicYN="N">Introns</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050296" MajorTopicYN="N">Microbial Viability</DescriptorName><QualifierName UI="Q000187" 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MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017384" MajorTopicYN="N">Sequence Deletion</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>02</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>12</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>1</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>1</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30651641</ArticleId><ArticleId IdType="doi">10.1038/s41586-018-0859-7</ArticleId><ArticleId IdType="pii">10.1038/s41586-018-0859-7</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Parenteau, Julie" sort="Parenteau, Julie" uniqKey="Parenteau J" first="Julie" last="Parenteau">Julie Parenteau</name></noRegion><name sortKey="Abou Elela, Sherif" sort="Abou Elela, Sherif" uniqKey="Abou Elela S" first="Sherif" last="Abou Elela">Sherif Abou Elela</name><name sortKey="Berthoumieux, Melodie" sort="Berthoumieux, Melodie" uniqKey="Berthoumieux M" first="Mélodie" last="Berthoumieux">Mélodie Berthoumieux</name><name sortKey="Catala, Mathieu" sort="Catala, Mathieu" uniqKey="Catala M" first="Mathieu" last="Catala">Mathieu Catala</name><name sortKey="Gagnon, Vanessa" sort="Gagnon, Vanessa" uniqKey="Gagnon V" first="Vanessa" last="Gagnon">Vanessa Gagnon</name><name sortKey="Maignon, Laurine" sort="Maignon, Laurine" uniqKey="Maignon L" first="Laurine" last="Maignon">Laurine Maignon</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000311 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000311 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:30651641
|texte= Introns are mediators of cell response to starvation.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:30651641" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |