Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.
Identifieur interne : 001986 ( Main/Corpus ); précédent : 001985; suivant : 001987Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.
Auteurs : Jennifer J. Tate ; Kathleen H. Cox ; Rajendra Rai ; Terrance G. CooperSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2002.
English descriptors
- KwdEn :
- Base Sequence (MeSH), DNA Primers (MeSH), Fungal Proteins (physiology), Gene Expression Regulation, Fungal (drug effects), Gene Expression Regulation, Fungal (physiology), Genes, Fungal (MeSH), Nitrogen (metabolism), Repressor Proteins (MeSH), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (MeSH), Sirolimus (pharmacology), Transcription Factors (MeSH).
- MESH :
- chemical , metabolism : Nitrogen.
- chemical , pharmacology : Sirolimus.
- chemical , physiology : Fungal Proteins.
- chemical : DNA Primers, Repressor Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- drug effects : Gene Expression Regulation, Fungal.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- physiology : Gene Expression Regulation, Fungal.
- Base Sequence, Genes, Fungal.
Abstract
The Tor1/2p signal transduction pathway regulates nitrogen catabolite repression (NCR)-sensitive (GAP1, GAT1, DAL5) and retrograde (CIT2, DLD3, IDH1/2) gene expression by controlling intracellular localization of the transcription activators, Gln3p and Gat1p, and Rtg1p and Rtg3p, respectively. The accepted pathway for this regulation is NH(3) or excess nitrogen dash, vertical Mks1p dash, vertical Ure2p dash, vertical Gln3p --> DAL5, and rapamycin or limiting nitrogen dash, vertical Torp --> Tap42 dash, vertical Mks1p --> Rtg1/3p --> CIT2, respectively. In current models, Mks1p positively regulates both Gln3p (and DAL5 expression) and Rtg1/3p (and CIT2 expression). Here, in contrast, we show the following. (i) Mks1p is a strong negative regulator of CIT2 expression and does not effect NCR-sensitive expression of DAL5 or GAP1. (ii) Retrograde carbon and NCR-sensitive nitrogen metabolism are not linked by the quality of the nitrogen source, i.e. its ability to elicit NCR, but by the product of its catabolism, i.e. glutamate or ammonia. (iii) In some instances, we can dissociate rapamycin-induced CIT2 expression from Mks1p function, i.e. rapamycin does not suppress Mks1p-mediated down-regulation of CIT2 expression. These findings suggest that currently accepted models of Tor1/2p signal transduction pathway regulation require revision.
DOI: 10.1074/jbc.M200962200
PubMed: 11923302
PubMed Central: PMC4384460
Links to Exploration step
pubmed:11923302Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.</title><author><name sortKey="Tate, Jennifer J" sort="Tate, Jennifer J" uniqKey="Tate J" first="Jennifer J" last="Tate">Jennifer J. Tate</name><affiliation><nlm:affiliation>Department of Molecular Sciences, University of Tennessee, Memphis, Tennessee 38120, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cox, Kathleen H" sort="Cox, Kathleen H" uniqKey="Cox K" first="Kathleen H" last="Cox">Kathleen H. Cox</name></author><author><name sortKey="Rai, Rajendra" sort="Rai, Rajendra" uniqKey="Rai R" first="Rajendra" last="Rai">Rajendra Rai</name></author><author><name sortKey="Cooper, Terrance G" sort="Cooper, Terrance G" uniqKey="Cooper T" first="Terrance G" last="Cooper">Terrance G. Cooper</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:11923302</idno><idno type="pmid">11923302</idno><idno type="doi">10.1074/jbc.M200962200</idno><idno type="pmc">PMC4384460</idno><idno type="wicri:Area/Main/Corpus">001986</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001986</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.</title><author><name sortKey="Tate, Jennifer J" sort="Tate, Jennifer J" uniqKey="Tate J" first="Jennifer J" last="Tate">Jennifer J. Tate</name><affiliation><nlm:affiliation>Department of Molecular Sciences, University of Tennessee, Memphis, Tennessee 38120, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cox, Kathleen H" sort="Cox, Kathleen H" uniqKey="Cox K" first="Kathleen H" last="Cox">Kathleen H. Cox</name></author><author><name sortKey="Rai, Rajendra" sort="Rai, Rajendra" uniqKey="Rai R" first="Rajendra" last="Rai">Rajendra Rai</name></author><author><name sortKey="Cooper, Terrance G" sort="Cooper, Terrance G" uniqKey="Cooper T" first="Terrance G" last="Cooper">Terrance G. Cooper</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="ISSN">0021-9258</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Base Sequence (MeSH)</term><term>DNA Primers (MeSH)</term><term>Fungal Proteins (physiology)</term><term>Gene Expression Regulation, Fungal (drug effects)</term><term>Gene Expression Regulation, Fungal (physiology)</term><term>Genes, Fungal (MeSH)</term><term>Nitrogen (metabolism)</term><term>Repressor Proteins (MeSH)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (metabolism)</term><term>Saccharomyces cerevisiae Proteins (MeSH)</term><term>Sirolimus (pharmacology)</term><term>Transcription Factors (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nitrogen</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Fungal Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>DNA Primers</term><term>Repressor Proteins</term><term>Saccharomyces cerevisiae Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation, Fungal</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation, Fungal</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Base Sequence</term><term>Genes, Fungal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Tor1/2p signal transduction pathway regulates nitrogen catabolite repression (NCR)-sensitive (GAP1, GAT1, DAL5) and retrograde (CIT2, DLD3, IDH1/2) gene expression by controlling intracellular localization of the transcription activators, Gln3p and Gat1p, and Rtg1p and Rtg3p, respectively. The accepted pathway for this regulation is NH(3) or excess nitrogen dash, vertical Mks1p dash, vertical Ure2p dash, vertical Gln3p --> DAL5, and rapamycin or limiting nitrogen dash, vertical Torp --> Tap42 dash, vertical Mks1p --> Rtg1/3p --> CIT2, respectively. In current models, Mks1p positively regulates both Gln3p (and DAL5 expression) and Rtg1/3p (and CIT2 expression). Here, in contrast, we show the following. (i) Mks1p is a strong negative regulator of CIT2 expression and does not effect NCR-sensitive expression of DAL5 or GAP1. (ii) Retrograde carbon and NCR-sensitive nitrogen metabolism are not linked by the quality of the nitrogen source, i.e. its ability to elicit NCR, but by the product of its catabolism, i.e. glutamate or ammonia. (iii) In some instances, we can dissociate rapamycin-induced CIT2 expression from Mks1p function, i.e. rapamycin does not suppress Mks1p-mediated down-regulation of CIT2 expression. These findings suggest that currently accepted models of Tor1/2p signal transduction pathway regulation require revision.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11923302</PMID><DateCompleted><Year>2002</Year><Month>07</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0021-9258</ISSN><JournalIssue CitedMedium="Print"><Volume>277</Volume><Issue>23</Issue><PubDate><Year>2002</Year><Month>Jun</Month><Day>07</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.</ArticleTitle><Pagination><MedlinePgn>20477-82</MedlinePgn></Pagination><Abstract><AbstractText>The Tor1/2p signal transduction pathway regulates nitrogen catabolite repression (NCR)-sensitive (GAP1, GAT1, DAL5) and retrograde (CIT2, DLD3, IDH1/2) gene expression by controlling intracellular localization of the transcription activators, Gln3p and Gat1p, and Rtg1p and Rtg3p, respectively. The accepted pathway for this regulation is NH(3) or excess nitrogen dash, vertical Mks1p dash, vertical Ure2p dash, vertical Gln3p --> DAL5, and rapamycin or limiting nitrogen dash, vertical Torp --> Tap42 dash, vertical Mks1p --> Rtg1/3p --> CIT2, respectively. In current models, Mks1p positively regulates both Gln3p (and DAL5 expression) and Rtg1/3p (and CIT2 expression). Here, in contrast, we show the following. (i) Mks1p is a strong negative regulator of CIT2 expression and does not effect NCR-sensitive expression of DAL5 or GAP1. (ii) Retrograde carbon and NCR-sensitive nitrogen metabolism are not linked by the quality of the nitrogen source, i.e. its ability to elicit NCR, but by the product of its catabolism, i.e. glutamate or ammonia. (iii) In some instances, we can dissociate rapamycin-induced CIT2 expression from Mks1p function, i.e. rapamycin does not suppress Mks1p-mediated down-regulation of CIT2 expression. These findings suggest that currently accepted models of Tor1/2p signal transduction pathway regulation require revision.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tate</LastName><ForeName>Jennifer J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Molecular Sciences, University of Tennessee, Memphis, Tennessee 38120, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cox</LastName><ForeName>Kathleen H</ForeName><Initials>KH</Initials></Author><Author ValidYN="Y"><LastName>Rai</LastName><ForeName>Rajendra</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Cooper</LastName><ForeName>Terrance G</ForeName><Initials>TG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 GM035642</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>GM-35642</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2002</Year><Month>03</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C080921">MKS1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012097">Repressor Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</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="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017931" MajorTopicYN="N">DNA Primers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005800" MajorTopicYN="Y">Genes, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009584" MajorTopicYN="N">Nitrogen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012097" MajorTopicYN="Y">Repressor Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="Y">Saccharomyces cerevisiae Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="Y">Transcription Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>3</Month><Day>30</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>7</Month><Day>13</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>3</Month><Day>30</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11923302</ArticleId><ArticleId IdType="doi">10.1074/jbc.M200962200</ArticleId><ArticleId IdType="pii">M200962200</ArticleId><ArticleId IdType="pmc">PMC4384460</ArticleId><ArticleId IdType="mid">NIHMS674992</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>FEMS Microbiol Rev. 2000 Jan;24(1):67-83</Citation><ArticleIdList><ArticleId IdType="pubmed">10640599</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 1989 Feb;9(2):602-8</Citation><ArticleIdList><ArticleId IdType="pubmed">2651902</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6625-9</Citation><ArticleIdList><ArticleId IdType="pubmed">10823922</ArticleId></ArticleIdList></Reference><Reference><Citation>J Bacteriol. 1972 Jan;109(1):203-8</Citation><ArticleIdList><ArticleId IdType="pubmed">4550662</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Biol. 2000 Nov 13;151(4):863-78</Citation><ArticleIdList><ArticleId IdType="pubmed">11076970</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO J. 1999 May 17;18(10 ):2782-92</Citation><ArticleIdList><ArticleId IdType="pubmed">10329624</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Gen Genet. 1985;200(2):291-4</Citation><ArticleIdList><ArticleId IdType="pubmed">3929019</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Biol. 2000 Dec 14-28;10(24):1574-81</Citation><ArticleIdList><ArticleId IdType="pubmed">11137008</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 1999 Oct;19(10):6720-8</Citation><ArticleIdList><ArticleId IdType="pubmed">10490611</ArticleId></ArticleIdList></Reference><Reference><Citation>Yeast. 1997 Nov;13(14 ):1337-46</Citation><ArticleIdList><ArticleId IdType="pubmed">9392078</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2000 Nov 17;275(46):35727-33</Citation><ArticleIdList><ArticleId IdType="pubmed">10940301</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1999 Dec 9;402(6762):689-92</Citation><ArticleIdList><ArticleId IdType="pubmed">10604478</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2000 Jun;11(6):2103-15</Citation><ArticleIdList><ArticleId IdType="pubmed">10848632</ArticleId></ArticleIdList></Reference><Reference><Citation>Genetics. 1999 Oct;153(2):585-94</Citation><ArticleIdList><ArticleId IdType="pubmed">10511541</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biotechnol. 1999 Aug;12(1):35-73</Citation><ArticleIdList><ArticleId IdType="pubmed">10554772</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Gen Genet. 1993 Apr;238(1-2):6-16</Citation><ArticleIdList><ArticleId IdType="pubmed">8386801</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2000 Jun 9;275(23):17611-8</Citation><ArticleIdList><ArticleId IdType="pubmed">10748041</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14866-70</Citation><ArticleIdList><ArticleId IdType="pubmed">10611304</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 1999 Dec 15;13(24):3271-9</Citation><ArticleIdList><ArticleId IdType="pubmed">10617575</ArticleId></ArticleIdList></Reference><Reference><Citation>J Bacteriol. 1946 Sep;52(3):293-301</Citation><ArticleIdList><ArticleId IdType="pubmed">16561177</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):13213-8</Citation><ArticleIdList><ArticleId IdType="pubmed">11687605</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochem Biophys Res Commun. 1973 Jul 17;53(2):367-72</Citation><ArticleIdList><ArticleId IdType="pubmed">4146147</ArticleId></ArticleIdList></Reference><Reference><Citation>J Bacteriol. 1987 Jun;169(6):2598-600</Citation><ArticleIdList><ArticleId IdType="pubmed">3294799</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2000 Oct 13;103(2):253-62</Citation><ArticleIdList><ArticleId IdType="pubmed">11057898</ArticleId></ArticleIdList></Reference><Reference><Citation>Yeast. 1999 Jun 15;15(8):703-13</Citation><ArticleIdList><ArticleId IdType="pubmed">10392447</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 1996 Jan;7(1):25-42</Citation><ArticleIdList><ArticleId IdType="pubmed">8741837</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Opin Genet Dev. 1999 Feb;9(1):49-54</Citation><ArticleIdList><ArticleId IdType="pubmed">10072357</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2001 Mar 30;276(13):9583-6</Citation><ArticleIdList><ArticleId IdType="pubmed">11266435</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001986 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 001986 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:11923302
|texte= Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:11923302" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |