Impaired mitochondrial Fe-S cluster biogenesis activates the DNA damage response through different signaling mediators.
Identifieur interne : 000542 ( Main/Exploration ); précédent : 000541; suivant : 000543Impaired mitochondrial Fe-S cluster biogenesis activates the DNA damage response through different signaling mediators.
Auteurs : Jordi Pijuan [Espagne] ; Carlos María [Espagne] ; Enrique Herrero [Espagne] ; Gemma Bellí [Autriche]Source :
- Journal of cell science [ 1477-9137 ] ; 2015.
Descripteurs français
- KwdFr :
- Altération de l'ADN (MeSH), Checkpoint kinase 1 (MeSH), Ferrosulfoprotéines (génétique), Ferrosulfoprotéines (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Mitochondries (génétique), Mitochondries (métabolisme), Protein kinases (génétique), Protein kinases (métabolisme), Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (métabolisme), Protéine Rad52 de réparation-recombinaison de l'ADN (génétique), Protéine Rad52 de réparation-recombinaison de l'ADN (métabolisme), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines du cycle cellulaire (génétique), Protéines du cycle cellulaire (métabolisme), Protéines et peptides de signalisation intracellulaire (génétique), Protéines et peptides de signalisation intracellulaire (métabolisme), Protéines mitochondriales (génétique), Protéines mitochondriales (métabolisme), Ribonucleotide reductases (génétique), Ribonucleotide reductases (métabolisme), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Transduction du signal (MeSH).
- MESH :
- génétique : Ferrosulfoprotéines, Glutarédoxines, Mitochondries, Protein kinases, Protein-Serine-Threonine Kinases, Protéine Rad52 de réparation-recombinaison de l'ADN, Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire, Protéines et peptides de signalisation intracellulaire, Protéines mitochondriales, Ribonucleotide reductases, Saccharomyces cerevisiae.
- métabolisme : Ferrosulfoprotéines, Glutarédoxines, Mitochondries, Protein kinases, Protein-Serine-Threonine Kinases, Protéine Rad52 de réparation-recombinaison de l'ADN, Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire, Protéines et peptides de signalisation intracellulaire, Protéines mitochondriales, Ribonucleotide reductases, Saccharomyces cerevisiae.
- Altération de l'ADN, Checkpoint kinase 1, Transduction du signal.
English descriptors
- KwdEn :
- Cell Cycle Proteins (genetics), Cell Cycle Proteins (metabolism), Checkpoint Kinase 1 (MeSH), DNA Damage (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Intracellular Signaling Peptides and Proteins (genetics), Intracellular Signaling Peptides and Proteins (metabolism), Iron-Sulfur Proteins (genetics), Iron-Sulfur Proteins (metabolism), Mitochondria (genetics), Mitochondria (metabolism), Mitochondrial Proteins (genetics), Mitochondrial Proteins (metabolism), Protein Kinases (genetics), Protein Kinases (metabolism), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Rad52 DNA Repair and Recombination Protein (genetics), Rad52 DNA Repair and Recombination Protein (metabolism), Ribonucleotide Reductases (genetics), Ribonucleotide Reductases (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , genetics : Cell Cycle Proteins, Glutaredoxins, Intracellular Signaling Peptides and Proteins, Iron-Sulfur Proteins, Mitochondrial Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Rad52 DNA Repair and Recombination Protein, Ribonucleotide Reductases, Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Cell Cycle Proteins, Glutaredoxins, Intracellular Signaling Peptides and Proteins, Iron-Sulfur Proteins, Mitochondrial Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Rad52 DNA Repair and Recombination Protein, Ribonucleotide Reductases, Saccharomyces cerevisiae Proteins.
- chemical : Checkpoint Kinase 1.
- genetics : Mitochondria, Saccharomyces cerevisiae.
- metabolism : Mitochondria, Saccharomyces cerevisiae.
- DNA Damage, Signal Transduction.
Abstract
Fe-S cluster biogenesis machinery is required for multiple DNA metabolism processes. In this work, we show that, in Saccharomyces cerevisiae, defects at different stages of the mitochondrial Fe-S cluster assembly machinery (ISC) result in increased spontaneous mutation rate and hyper-recombination, accompanied by an increment in Rad52-associated DNA repair foci and a higher phosphorylated state of γH2A histone, altogether supporting the presence of constitutive DNA lesions. Furthermore, ISC assembly machinery deficiency elicits a DNA damage response that upregulates ribonucleotide reductase activity by promoting the reduction of Sml1 levels and the cytosolic redistribution of Rnr2 and Rnr4 enzyme subunits. Depending on the impaired stage of the ISC machinery, different signaling pathway mediators contribute to such a response, converging on Dun1. Thus, cells lacking the glutaredoxin Grx5, which are compromised at the core ISC system, show Mec1- and Rad53-independent Dun1 activation, whereas both Mec1 and Chk1 are required when the non-core ISC member Iba57 is absent. Grx5-null cells exhibit a strong dependence on the error-free post-replication repair and the homologous recombination pathways, demonstrating that a DNA damage response needs to be activated upon ISC impairment to preserve cell viability.
DOI: 10.1242/jcs.178046
PubMed: 26567217
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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IRBLleida, University of Lleida, Lleida 25198, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198</wicri:regionArea><placeName><region nuts="2" type="communauté">Catalogne</region></placeName></affiliation></author><author><name sortKey="Herrero, Enrique" sort="Herrero, Enrique" uniqKey="Herrero E" first="Enrique" last="Herrero">Enrique Herrero</name><affiliation wicri:level="2"><nlm:affiliation>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198</wicri:regionArea><placeName><region nuts="2" type="communauté">Catalogne</region></placeName></affiliation></author><author><name sortKey="Belli, Gemma" sort="Belli, Gemma" uniqKey="Belli G" first="Gemma" last="Bellí">Gemma Bellí</name><affiliation wicri:level="1"><nlm:affiliation>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198, Spain gemma.belli@cmb.udl.cat.</nlm:affiliation><country wicri:rule="url">Autriche</country><wicri:regionArea>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198</wicri:regionArea><wicri:noRegion>Lleida 25198</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of cell science</title><idno type="eISSN">1477-9137</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Cycle Proteins (genetics)</term><term>Cell Cycle Proteins (metabolism)</term><term>Checkpoint Kinase 1 (MeSH)</term><term>DNA Damage (MeSH)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Intracellular Signaling Peptides and Proteins (genetics)</term><term>Intracellular Signaling Peptides and Proteins (metabolism)</term><term>Iron-Sulfur Proteins (genetics)</term><term>Iron-Sulfur Proteins (metabolism)</term><term>Mitochondria (genetics)</term><term>Mitochondria (metabolism)</term><term>Mitochondrial Proteins (genetics)</term><term>Mitochondrial Proteins (metabolism)</term><term>Protein Kinases (genetics)</term><term>Protein Kinases (metabolism)</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Protein-Serine-Threonine Kinases (metabolism)</term><term>Rad52 DNA Repair and Recombination Protein (genetics)</term><term>Rad52 DNA Repair and Recombination Protein (metabolism)</term><term>Ribonucleotide Reductases (genetics)</term><term>Ribonucleotide Reductases (metabolism)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (metabolism)</term><term>Saccharomyces cerevisiae Proteins (genetics)</term><term>Saccharomyces cerevisiae Proteins (metabolism)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Altération de l'ADN (MeSH)</term><term>Checkpoint kinase 1 (MeSH)</term><term>Ferrosulfoprotéines (génétique)</term><term>Ferrosulfoprotéines (métabolisme)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Mitochondries (génétique)</term><term>Mitochondries (métabolisme)</term><term>Protein kinases (génétique)</term><term>Protein kinases (métabolisme)</term><term>Protein-Serine-Threonine Kinases (génétique)</term><term>Protein-Serine-Threonine Kinases (métabolisme)</term><term>Protéine Rad52 de réparation-recombinaison de l'ADN (génétique)</term><term>Protéine Rad52 de réparation-recombinaison de l'ADN (métabolisme)</term><term>Protéines de Saccharomyces cerevisiae (génétique)</term><term>Protéines de Saccharomyces cerevisiae (métabolisme)</term><term>Protéines du cycle cellulaire (génétique)</term><term>Protéines du cycle cellulaire (métabolisme)</term><term>Protéines et peptides de signalisation intracellulaire (génétique)</term><term>Protéines et peptides de signalisation intracellulaire (métabolisme)</term><term>Protéines mitochondriales (génétique)</term><term>Protéines mitochondriales (métabolisme)</term><term>Ribonucleotide reductases (génétique)</term><term>Ribonucleotide reductases (métabolisme)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Saccharomyces cerevisiae (métabolisme)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cell Cycle Proteins</term><term>Glutaredoxins</term><term>Intracellular Signaling Peptides and Proteins</term><term>Iron-Sulfur Proteins</term><term>Mitochondrial Proteins</term><term>Protein Kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Rad52 DNA Repair and Recombination Protein</term><term>Ribonucleotide Reductases</term><term>Saccharomyces cerevisiae Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cell Cycle Proteins</term><term>Glutaredoxins</term><term>Intracellular Signaling Peptides and Proteins</term><term>Iron-Sulfur Proteins</term><term>Mitochondrial Proteins</term><term>Protein Kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Rad52 DNA Repair and Recombination Protein</term><term>Ribonucleotide Reductases</term><term>Saccharomyces cerevisiae Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Checkpoint Kinase 1</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mitochondria</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Ferrosulfoprotéines</term><term>Glutarédoxines</term><term>Mitochondries</term><term>Protein kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Protéine Rad52 de réparation-recombinaison de l'ADN</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines du cycle cellulaire</term><term>Protéines et peptides de signalisation intracellulaire</term><term>Protéines mitochondriales</term><term>Ribonucleotide reductases</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Ferrosulfoprotéines</term><term>Glutarédoxines</term><term>Mitochondries</term><term>Protein kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Protéine Rad52 de réparation-recombinaison de l'ADN</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines du cycle cellulaire</term><term>Protéines et peptides de signalisation intracellulaire</term><term>Protéines mitochondriales</term><term>Ribonucleotide reductases</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" xml:lang="en"><term>DNA Damage</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Altération de l'ADN</term><term>Checkpoint kinase 1</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fe-S cluster biogenesis machinery is required for multiple DNA metabolism processes. In this work, we show that, in Saccharomyces cerevisiae, defects at different stages of the mitochondrial Fe-S cluster assembly machinery (ISC) result in increased spontaneous mutation rate and hyper-recombination, accompanied by an increment in Rad52-associated DNA repair foci and a higher phosphorylated state of γH2A histone, altogether supporting the presence of constitutive DNA lesions. Furthermore, ISC assembly machinery deficiency elicits a DNA damage response that upregulates ribonucleotide reductase activity by promoting the reduction of Sml1 levels and the cytosolic redistribution of Rnr2 and Rnr4 enzyme subunits. Depending on the impaired stage of the ISC machinery, different signaling pathway mediators contribute to such a response, converging on Dun1. Thus, cells lacking the glutaredoxin Grx5, which are compromised at the core ISC system, show Mec1- and Rad53-independent Dun1 activation, whereas both Mec1 and Chk1 are required when the non-core ISC member Iba57 is absent. Grx5-null cells exhibit a strong dependence on the error-free post-replication repair and the homologous recombination pathways, demonstrating that a DNA damage response needs to be activated upon ISC impairment to preserve cell viability. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26567217</PMID><DateCompleted><Year>2016</Year><Month>09</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1477-9137</ISSN><JournalIssue CitedMedium="Internet"><Volume>128</Volume><Issue>24</Issue><PubDate><Year>2015</Year><Month>Dec</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of cell science</Title><ISOAbbreviation>J Cell Sci</ISOAbbreviation></Journal><ArticleTitle>Impaired mitochondrial Fe-S cluster biogenesis activates the DNA damage response through different signaling mediators.</ArticleTitle><Pagination><MedlinePgn>4653-65</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1242/jcs.178046</ELocationID><Abstract><AbstractText>Fe-S cluster biogenesis machinery is required for multiple DNA metabolism processes. In this work, we show that, in Saccharomyces cerevisiae, defects at different stages of the mitochondrial Fe-S cluster assembly machinery (ISC) result in increased spontaneous mutation rate and hyper-recombination, accompanied by an increment in Rad52-associated DNA repair foci and a higher phosphorylated state of γH2A histone, altogether supporting the presence of constitutive DNA lesions. Furthermore, ISC assembly machinery deficiency elicits a DNA damage response that upregulates ribonucleotide reductase activity by promoting the reduction of Sml1 levels and the cytosolic redistribution of Rnr2 and Rnr4 enzyme subunits. Depending on the impaired stage of the ISC machinery, different signaling pathway mediators contribute to such a response, converging on Dun1. Thus, cells lacking the glutaredoxin Grx5, which are compromised at the core ISC system, show Mec1- and Rad53-independent Dun1 activation, whereas both Mec1 and Chk1 are required when the non-core ISC member Iba57 is absent. Grx5-null cells exhibit a strong dependence on the error-free post-replication repair and the homologous recombination pathways, demonstrating that a DNA damage response needs to be activated upon ISC impairment to preserve cell viability. </AbstractText><CopyrightInformation>© 2015. Published by The Company of Biologists Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pijuan</LastName><ForeName>Jordi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>María</LastName><ForeName>Carlos</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrero</LastName><ForeName>Enrique</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bellí</LastName><ForeName>Gemma</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Basic Medical Sciences, IRBLleida, University of Lleida, Lleida 25198, Spain gemma.belli@cmb.udl.cat.</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>2015</Year><Month>11</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Cell Sci</MedlineTA><NlmUniqueID>0052457</NlmUniqueID><ISSNLinking>0021-9533</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018797">Cell Cycle Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C528773">Grx5 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C527305">Iba57 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007506">Iron-Sulfur Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D024101">Mitochondrial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C497197">RAD52 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051721">Rad52 DNA Repair and Recombination Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C115052">SML1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.17.4.-</RegistryNumber><NameOfSubstance UI="C570014">RNR2 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.17.4.-</RegistryNumber><NameOfSubstance UI="D012264">Ribonucleotide Reductases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.-</RegistryNumber><NameOfSubstance UI="D011494">Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="C104169">DUN1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000071877">Checkpoint Kinase 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C088937">MEC1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D018797" MajorTopicYN="N">Cell Cycle Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071877" MajorTopicYN="N">Checkpoint Kinase 1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004249" MajorTopicYN="Y">DNA Damage</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007506" MajorTopicYN="N">Iron-Sulfur Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D024101" MajorTopicYN="N">Mitochondrial Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051721" MajorTopicYN="N">Rad52 DNA Repair and Recombination Protein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012264" MajorTopicYN="N">Ribonucleotide Reductases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DNA damage response checkpoint</Keyword><Keyword MajorTopicYN="N">Fe-S cluster biogenesis</Keyword><Keyword MajorTopicYN="N">Glutaredoxin</Keyword><Keyword MajorTopicYN="N">Post-replication repair</Keyword><Keyword MajorTopicYN="N">Ribonucleotide reductase</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>07</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>11</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>11</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>9</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26567217</ArticleId><ArticleId IdType="pii">jcs.178046</ArticleId><ArticleId IdType="doi">10.1242/jcs.178046</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Autriche</li><li>Espagne</li></country><region><li>Catalogne</li></region></list><tree><country name="Espagne"><region name="Catalogne"><name sortKey="Pijuan, Jordi" sort="Pijuan, Jordi" uniqKey="Pijuan J" first="Jordi" last="Pijuan">Jordi Pijuan</name></region><name sortKey="Herrero, Enrique" sort="Herrero, Enrique" uniqKey="Herrero E" first="Enrique" last="Herrero">Enrique Herrero</name><name sortKey="Maria, Carlos" sort="Maria, Carlos" uniqKey="Maria C" first="Carlos" last="María">Carlos María</name></country><country name="Autriche"><noRegion><name sortKey="Belli, Gemma" sort="Belli, Gemma" uniqKey="Belli G" first="Gemma" last="Bellí">Gemma Bellí</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Impaired mitochondrial Fe-S cluster biogenesis activates the DNA damage response through different signaling mediators.
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