TOR and RAS pathways regulate desiccation tolerance in Saccharomyces cerevisiae.
Identifieur interne : 000F72 ( Main/Exploration ); précédent : 000F71; suivant : 000F73TOR and RAS pathways regulate desiccation tolerance in Saccharomyces cerevisiae.
Auteurs : Aaron Z. Welch [États-Unis] ; Patrick A. Gibney ; David Botstein ; Douglas E. KoshlandSource :
- Molecular biology of the cell [ 1939-4586 ] ; 2013.
Descripteurs français
- KwdFr :
- Adaptation physiologique (MeSH), Cyclic AMP-Dependent Protein Kinases (métabolisme), Déshydratation (MeSH), Facteurs de transcription (antagonistes et inhibiteurs), Facteurs de transcription (métabolisme), Grande sous-unité du ribosome des eucaryotes (métabolisme), Milieux de culture (MeSH), Phosphatidylinositol 3-kinases (métabolisme), Protéines G ras (génétique), Protéines G ras (métabolisme), Protéines de Saccharomyces cerevisiae (antagonistes et inhibiteurs), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (métabolisme), Saccharomyces cerevisiae (physiologie), Sirolimus (pharmacologie), Stress physiologique (MeSH), Techniques de knock-out de gènes (MeSH), Transduction du signal (MeSH).
- MESH :
- antagonistes et inhibiteurs : Facteurs de transcription, Protéines de Saccharomyces cerevisiae.
- croissance et développement : Saccharomyces cerevisiae.
- génétique : Protéines G ras, Protéines de Saccharomyces cerevisiae.
- métabolisme : Cyclic AMP-Dependent Protein Kinases, Facteurs de transcription, Grande sous-unité du ribosome des eucaryotes, Phosphatidylinositol 3-kinases, Protéines G ras, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- pharmacologie : Sirolimus.
- physiologie : Saccharomyces cerevisiae.
- Adaptation physiologique, Déshydratation, Milieux de culture, Stress physiologique, Techniques de knock-out de gènes, Transduction du signal.
English descriptors
- KwdEn :
- Adaptation, Physiological (MeSH), Culture Media (MeSH), Cyclic AMP-Dependent Protein Kinases (metabolism), Dehydration (MeSH), Gene Knockout Techniques (MeSH), Phosphatidylinositol 3-Kinases (metabolism), Ribosome Subunits, Large, Eukaryotic (metabolism), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (antagonists & inhibitors), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), Stress, Physiological (MeSH), Transcription Factors (antagonists & inhibitors), Transcription Factors (metabolism), ras Proteins (genetics), ras Proteins (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , genetics : Saccharomyces cerevisiae Proteins, ras Proteins.
- chemical , metabolism : Cyclic AMP-Dependent Protein Kinases, Phosphatidylinositol 3-Kinases, Saccharomyces cerevisiae Proteins, Transcription Factors, ras Proteins.
- chemical , pharmacology : Sirolimus.
- chemical : Culture Media.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Ribosome Subunits, Large, Eukaryotic, Saccharomyces cerevisiae.
- physiology : Saccharomyces cerevisiae.
- Adaptation, Physiological, Dehydration, Gene Knockout Techniques, Signal Transduction, Stress, Physiological.
Abstract
Tolerance to desiccation in cultures of Saccharomyces cerevisiae is inducible; only one in a million cells from an exponential culture survive desiccation compared with one in five cells in stationary phase. Here we exploit the desiccation sensitivity of exponentially dividing cells to understand the stresses imposed by desiccation and their stress response pathways. We found that induction of desiccation tolerance is cell autonomous and that there is an inverse correlation between desiccation tolerance and growth rate in glucose-, ammonia-, or phosphate-limited continuous cultures. A transient heat shock induces a 5000-fold increase in desiccation tolerance, whereas hyper-ionic, -reductive, -oxidative, or -osmotic stress induced much less. Furthermore, we provide evidence that the Sch9p-regulated branch of the TOR and Ras-cAMP pathway inhibits desiccation tolerance by inhibiting the stress response transcription factors Gis1p, Msn2p, and Msn4p and by activating Sfp1p, a ribosome biogenesis transcription factor. Among 41 mutants defective in ribosome biogenesis, a subset defective in 60S showed a dramatic increase in desiccation tolerance independent of growth rate. We suggest that reduction of a specific intermediate in 60S biogenesis, resulting from conditions such as heat shock and nutrient deprivation, increases desiccation tolerance.
DOI: 10.1091/mbc.E12-07-0524
PubMed: 23171550
PubMed Central: PMC3541959
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Here we exploit the desiccation sensitivity of exponentially dividing cells to understand the stresses imposed by desiccation and their stress response pathways. We found that induction of desiccation tolerance is cell autonomous and that there is an inverse correlation between desiccation tolerance and growth rate in glucose-, ammonia-, or phosphate-limited continuous cultures. A transient heat shock induces a 5000-fold increase in desiccation tolerance, whereas hyper-ionic, -reductive, -oxidative, or -osmotic stress induced much less. Furthermore, we provide evidence that the Sch9p-regulated branch of the TOR and Ras-cAMP pathway inhibits desiccation tolerance by inhibiting the stress response transcription factors Gis1p, Msn2p, and Msn4p and by activating Sfp1p, a ribosome biogenesis transcription factor. Among 41 mutants defective in ribosome biogenesis, a subset defective in 60S showed a dramatic increase in desiccation tolerance independent of growth rate. We suggest that reduction of a specific intermediate in 60S biogenesis, resulting from conditions such as heat shock and nutrient deprivation, increases desiccation tolerance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23171550</PMID><DateCompleted><Year>2013</Year><Month>06</Month><Day>17</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1939-4586</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>2</Issue><PubDate><Year>2013</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Molecular biology of the cell</Title><ISOAbbreviation>Mol Biol Cell</ISOAbbreviation></Journal><ArticleTitle>TOR and RAS pathways regulate desiccation tolerance in Saccharomyces cerevisiae.</ArticleTitle><Pagination><MedlinePgn>115-28</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1091/mbc.E12-07-0524</ELocationID><Abstract><AbstractText>Tolerance to desiccation in cultures of Saccharomyces cerevisiae is inducible; only one in a million cells from an exponential culture survive desiccation compared with one in five cells in stationary phase. Here we exploit the desiccation sensitivity of exponentially dividing cells to understand the stresses imposed by desiccation and their stress response pathways. We found that induction of desiccation tolerance is cell autonomous and that there is an inverse correlation between desiccation tolerance and growth rate in glucose-, ammonia-, or phosphate-limited continuous cultures. A transient heat shock induces a 5000-fold increase in desiccation tolerance, whereas hyper-ionic, -reductive, -oxidative, or -osmotic stress induced much less. Furthermore, we provide evidence that the Sch9p-regulated branch of the TOR and Ras-cAMP pathway inhibits desiccation tolerance by inhibiting the stress response transcription factors Gis1p, Msn2p, and Msn4p and by activating Sfp1p, a ribosome biogenesis transcription factor. Among 41 mutants defective in ribosome biogenesis, a subset defective in 60S showed a dramatic increase in desiccation tolerance independent of growth rate. We suggest that reduction of a specific intermediate in 60S biogenesis, resulting from conditions such as heat shock and nutrient deprivation, increases desiccation tolerance.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Welch</LastName><ForeName>Aaron Z</ForeName><Initials>AZ</Initials><AffiliationInfo><Affiliation>Department of Biology, Johns Hopkins University, Baltimore, MD 21218, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gibney</LastName><ForeName>Patrick A</ForeName><Initials>PA</Initials></Author><Author ValidYN="Y"><LastName>Botstein</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Koshland</LastName><ForeName>Douglas E</ForeName><Initials>DE</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 GM046406</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 GM046406</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>GM097852</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>F32 GM097852</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 GM071508</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><Agency>Howard Hughes Medical Institute</Agency><Country>United States</Country></Grant><Grant><GrantID>GM071508</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>11</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Biol Cell</MedlineTA><NlmUniqueID>9201390</NlmUniqueID><ISSNLinking>1059-1524</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003470">Culture Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C561842">TORC1 protein complex, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber><NameOfSubstance UI="C083324">TOR1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.11</RegistryNumber><NameOfSubstance UI="D017868">Cyclic AMP-Dependent Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber><NameOfSubstance UI="C489014">RAS1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber><NameOfSubstance UI="C489015">RAS2 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber><NameOfSubstance UI="D018631">ras Proteins</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></MeshHeading><MeshHeading><DescriptorName UI="D003470" MajorTopicYN="N">Culture Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017868" MajorTopicYN="N">Cyclic AMP-Dependent Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003681" MajorTopicYN="N">Dehydration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055786" MajorTopicYN="N">Gene Knockout Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054683" MajorTopicYN="N">Ribosome Subunits, Large, Eukaryotic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, 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IdType="pubmed">15253933</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 2010 Jan 29;327(5965):546</Citation><ArticleIdList><ArticleId IdType="pubmed">20110497</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2004 May 28;117(5):637-48</Citation><ArticleIdList><ArticleId IdType="pubmed">15163411</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2009 Feb;20(3):891-903</Citation><ArticleIdList><ArticleId IdType="pubmed">19056679</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbiol Mol Biol Rev. 2012 Jun;76(2):115-58</Citation><ArticleIdList><ArticleId IdType="pubmed">22688810</ArticleId></ArticleIdList></Reference><Reference><Citation>Genome Res. 2007 Apr;17(4):536-43</Citation><ArticleIdList><ArticleId IdType="pubmed">17322287</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 1989 Feb;9(2):390-5</Citation><ArticleIdList><ArticleId IdType="pubmed">2651897</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2004 May 14;279(20):20663-71</Citation><ArticleIdList><ArticleId IdType="pubmed">15016820</ArticleId></ArticleIdList></Reference><Reference><Citation>FEBS Lett. 2009 Dec 17;583(24):4025-9</Citation><ArticleIdList><ArticleId IdType="pubmed">19878680</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Physiol. 1992;54:579-99</Citation><ArticleIdList><ArticleId IdType="pubmed">1562184</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2011 Nov;22(21):4192-204</Citation><ArticleIdList><ArticleId IdType="pubmed">21900497</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1950 Dec 15;112(2920):715-6</Citation><ArticleIdList><ArticleId IdType="pubmed">14787503</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2008 Nov;19(11):4580-7</Citation><ArticleIdList><ArticleId IdType="pubmed">18753408</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2004 Oct 5;101(40):14315-22</Citation><ArticleIdList><ArticleId IdType="pubmed">15353587</ArticleId></ArticleIdList></Reference><Reference><Citation>Res Microbiol. 2002 Jan-Feb;153(1):7-12</Citation><ArticleIdList><ArticleId IdType="pubmed">11881900</ArticleId></ArticleIdList></Reference><Reference><Citation>FEMS Yeast Res. 2006 Sep;6(6):902-13</Citation><ArticleIdList><ArticleId IdType="pubmed">16911512</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2000 Dec;11(12):4241-57</Citation><ArticleIdList><ArticleId IdType="pubmed">11102521</ArticleId></ArticleIdList></Reference><Reference><Citation>Naturwissenschaften. 2007 Oct;94(10):791-812</Citation><ArticleIdList><ArticleId IdType="pubmed">17479232</ArticleId></ArticleIdList></Reference><Reference><Citation>Enzyme Microb Technol. 2000 Jun 1;26(9-10):724-736</Citation><ArticleIdList><ArticleId IdType="pubmed">10862878</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2008;3(2):e1598</Citation><ArticleIdList><ArticleId IdType="pubmed">18270585</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Genet. 2008;42:27-81</Citation><ArticleIdList><ArticleId IdType="pubmed">18303986</ArticleId></ArticleIdList></Reference><Reference><Citation>Microbiol Rev. 1994 Dec;58(4):755-805</Citation><ArticleIdList><ArticleId IdType="pubmed">7854254</ArticleId></ArticleIdList></Reference><Reference><Citation>Genetics. 2005 Jul;170(3):1009-21</Citation><ArticleIdList><ArticleId IdType="pubmed">15879503</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochim Biophys Acta. 2008 Nov;1780(11):1217-35</Citation><ArticleIdList><ArticleId IdType="pubmed">18178164</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Genet. 2009 May;5(5):e1000467</Citation><ArticleIdList><ArticleId IdType="pubmed">19424415</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2002 Jul 25;418(6896):387-91</Citation><ArticleIdList><ArticleId IdType="pubmed">12140549</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Biol. 2011 Aug 9;21(15):1331-6</Citation><ArticleIdList><ArticleId IdType="pubmed">21782434</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2008 Apr 18;133(2):292-302</Citation><ArticleIdList><ArticleId IdType="pubmed">18423200</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2008 Jan;19(1):352-67</Citation><ArticleIdList><ArticleId IdType="pubmed">17959824</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Biotechnol. 2011 Apr;29(4):361-7</Citation><ArticleIdList><ArticleId IdType="pubmed">21441928</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS Genet. 2008 Jan;4(1):e13</Citation><ArticleIdList><ArticleId IdType="pubmed">18225956</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Chem Biol. 2006 Feb;2(2):103-9</Citation><ArticleIdList><ArticleId IdType="pubmed">16415861</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 2001 Mar;21(5):1784-94</Citation><ArticleIdList><ArticleId IdType="pubmed">11238915</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biosyst. 2011 Jan;7(1):139-49</Citation><ArticleIdList><ArticleId IdType="pubmed">20963216</ArticleId></ArticleIdList></Reference><Reference><Citation>Aging Cell. 2007 Feb;6(1):95-110</Citation><ArticleIdList><ArticleId IdType="pubmed">17266679</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Stress Chaperones. 2005 Autumn;10(3):167-70</Citation><ArticleIdList><ArticleId IdType="pubmed">16184761</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2007 Nov 13;104(46):18073-8</Citation><ArticleIdList><ArticleId IdType="pubmed">17984052</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Signal. 2005 Oct;17(10):1183-93</Citation><ArticleIdList><ArticleId IdType="pubmed">15982853</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Microbiol. 2001;55:165-99</Citation><ArticleIdList><ArticleId IdType="pubmed">11544353</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Genet. 2000 Aug;38(2):60-70</Citation><ArticleIdList><ArticleId IdType="pubmed">10975254</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 1987 Apr;7(4):1371-7</Citation><ArticleIdList><ArticleId IdType="pubmed">3037314</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO Rep. 2007 Sep;8(9):864-70</Citation><ArticleIdList><ArticleId IdType="pubmed">17721444</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2006 May 1;20(9):1150-61</Citation><ArticleIdList><ArticleId IdType="pubmed">16618799</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2001 Feb;12(2):323-37</Citation><ArticleIdList><ArticleId IdType="pubmed">11179418</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Botstein, David" sort="Botstein, David" uniqKey="Botstein D" first="David" last="Botstein">David Botstein</name><name sortKey="Gibney, Patrick A" sort="Gibney, Patrick A" uniqKey="Gibney P" first="Patrick A" last="Gibney">Patrick A. Gibney</name><name sortKey="Koshland, Douglas E" sort="Koshland, Douglas E" uniqKey="Koshland D" first="Douglas E" last="Koshland">Douglas E. Koshland</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Welch, Aaron Z" sort="Welch, Aaron Z" uniqKey="Welch A" first="Aaron Z" last="Welch">Aaron Z. Welch</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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