Expression and developmental regulation of the k-FGF oncogene in human and murine embryonal carcinoma cells
Identifieur interne : 001118 ( Istex/Corpus ); précédent : 001117; suivant : 001119Expression and developmental regulation of the k-FGF oncogene in human and murine embryonal carcinoma cells
Auteurs : Jay Tiesman ; Angie RizzinoSource :
- In Vitro Cellular & Developmental Biology [ 0883-8364 ] ; 1989-12-01.
English descriptors
- KwdEn :
- Teeft :
- Bethesda research laboratories, Bfgf, Biol, Bovine, Carcinoma, Cdna, Cell line, Cell lines, Claudio basilico, Current study, Delli bovi, Developmental regulation, Early development, Early mouse embryos, Embryo, Embryonal, Embryonal carcinoma cells, Endonuclease, Ethidium bromide, Fibroblast, Fibroblast growth factor, Fragment, Further evidence, Growth factor, Growth factor activity, Growth factors, Mammalian embryogenesis, Mesoderm formation, Northern blot analysis, Nucleotide sequence, Oligonucleotide, Oligonucleotide primers, Oncogene, Other members, Polymerase, Polymerase chain reaction, Primer, Primer annealing, Reaction mixture, Restriction endonuclease sites, Restriction endonucleases, Restriction enzymes, Rizzino, Similar results, Subsequent studies, Thermal cycling, Tiesman, Transcript, Ultraviolet transilluminator, York university school.
Abstract
Summary: Embryonal carcinoma (EC) cells provide an effective model system for studying growth factor production and regulation during mammalian embryogenesis. Our earlier data indicated that the mouse EC cell lines F9 and PC-13 and the human EC cell line NT2/D1 produce a factor with properties similar to those ascribed to members of the fibroblast growth factor (FGF) family and that production of this FGF-related factor is suppressed when all three EC cell lines are induced to differentiate. Subsequent studies suggested that NT2/D1 EC cells express transcripts for basic FGF (bFGF). The current study confirms and extends these findings using a combination of reverse transcription and polymerase chain reaction (RT-PCR). In this study, the expression of bFGF and other members of the FGF family have been examined in F9 and PC-13 cells in addition to NT2/D1 EC cells. In contrast to NT2/D1 EC cells, bFGF expression could not be detected in F9 and PC-13 EC cells. Additionally, expression of four other members of the FGF family (acidic FGF, int-2, FGF-5, and FGF-6) were not detected in NT2/D1, F9, or PC-13 EC cells. However, expression of another member of the FGF family, the k-FGF oncogene, was detected in NT2/D1, F9, and PC-13 EC cells. Moreover, the expression of this transcript is reduced dramatically when each of the three EC cell lines is induced to differentiate. Taken together, our findings argue that expression of the k-FGF oncogene is predominantly responsible for the FGF-related activity detected in EC cells and that differentiation of these EC cells results in suppression of this oncogene.
Url:
DOI: 10.1007/BF02621274
Links to Exploration step
ISTEX:543D8B8D5E16BD8802107ACB6BCEF5AE9F4E934ALe document en format XML
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Our earlier data indicated that the mouse EC cell lines F9 and PC-13 and the human EC cell line NT2/D1 produce a factor with properties similar to those ascribed to members of the fibroblast growth factor (FGF) family and that production of this FGF-related factor is suppressed when all three EC cell lines are induced to differentiate. Subsequent studies suggested that NT2/D1 EC cells express transcripts for basic FGF (bFGF). The current study confirms and extends these findings using a combination of reverse transcription and polymerase chain reaction (RT-PCR). In this study, the expression of bFGF and other members of the FGF family have been examined in F9 and PC-13 cells in addition to NT2/D1 EC cells. In contrast to NT2/D1 EC cells, bFGF expression could not be detected in F9 and PC-13 EC cells. Additionally, expression of four other members of the FGF family (acidic FGF, int-2, FGF-5, and FGF-6) were not detected in NT2/D1, F9, or PC-13 EC cells. However, expression of another member of the FGF family, the k-FGF oncogene, was detected in NT2/D1, F9, and PC-13 EC cells. Moreover, the expression of this transcript is reduced dramatically when each of the three EC cell lines is induced to differentiate. Taken together, our findings argue that expression of the k-FGF oncogene is predominantly responsible for the FGF-related activity detected in EC cells and that differentiation of these EC cells results in suppression of this oncogene.</div></front></TEI><istex><corpusName>springer-journals</corpusName><keywords><teeft><json:string>primer</json:string><json:string>rizzino</json:string><json:string>oncogene</json:string><json:string>tiesman</json:string><json:string>fibroblast</json:string><json:string>northern blot analysis</json:string><json:string>bfgf</json:string><json:string>growth factors</json:string><json:string>growth factor</json:string><json:string>embryonal</json:string><json:string>polymerase</json:string><json:string>oligonucleotide</json:string><json:string>endonuclease</json:string><json:string>cdna</json:string><json:string>biol</json:string><json:string>oligonucleotide primers</json:string><json:string>cell lines</json:string><json:string>cell line</json:string><json:string>other members</json:string><json:string>fibroblast growth factor</json:string><json:string>embryo</json:string><json:string>polymerase chain reaction</json:string><json:string>carcinoma</json:string><json:string>early development</json:string><json:string>nucleotide sequence</json:string><json:string>transcript</json:string><json:string>embryonal carcinoma cells</json:string><json:string>ethidium bromide</json:string><json:string>similar results</json:string><json:string>reaction mixture</json:string><json:string>bovine</json:string><json:string>delli bovi</json:string><json:string>developmental regulation</json:string><json:string>subsequent studies</json:string><json:string>restriction endonuclease sites</json:string><json:string>mesoderm formation</json:string><json:string>mammalian embryogenesis</json:string><json:string>claudio basilico</json:string><json:string>york university school</json:string><json:string>ultraviolet transilluminator</json:string><json:string>restriction enzymes</json:string><json:string>bethesda research laboratories</json:string><json:string>current study</json:string><json:string>thermal cycling</json:string><json:string>primer annealing</json:string><json:string>further evidence</json:string><json:string>growth factor activity</json:string><json:string>restriction endonucleases</json:string><json:string>early mouse embryos</json:string><json:string>fragment</json:string></teeft></keywords><author><json:item><name>Jay Tiesman</name><affiliations><json:string>Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 42nd and Dewey Ave., 68105, Omaha, Nebraska</json:string></affiliations></json:item><json:item><name>Angie Rizzino</name><affiliations><json:string>Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 42nd and Dewey Ave., 68105, Omaha, Nebraska</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>differentiation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>embryonal carcinoma cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FGF family</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>k-FGF</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>polymerase chain reaction</value></json:item></subject><articleId><json:string>BF02621274</json:string><json:string>Art17</json:string></articleId><arkIstex>ark:/67375/1BB-X61XWHLW-0</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>BriefCommunication</json:string></originalGenre><abstract>Summary: Embryonal carcinoma (EC) cells provide an effective model system for studying growth factor production and regulation during mammalian embryogenesis. Our earlier data indicated that the mouse EC cell lines F9 and PC-13 and the human EC cell line NT2/D1 produce a factor with properties similar to those ascribed to members of the fibroblast growth factor (FGF) family and that production of this FGF-related factor is suppressed when all three EC cell lines are induced to differentiate. Subsequent studies suggested that NT2/D1 EC cells express transcripts for basic FGF (bFGF). The current study confirms and extends these findings using a combination of reverse transcription and polymerase chain reaction (RT-PCR). In this study, the expression of bFGF and other members of the FGF family have been examined in F9 and PC-13 cells in addition to NT2/D1 EC cells. In contrast to NT2/D1 EC cells, bFGF expression could not be detected in F9 and PC-13 EC cells. Additionally, expression of four other members of the FGF family (acidic FGF, int-2, FGF-5, and FGF-6) were not detected in NT2/D1, F9, or PC-13 EC cells. However, expression of another member of the FGF family, the k-FGF oncogene, was detected in NT2/D1, F9, and PC-13 EC cells. Moreover, the expression of this transcript is reduced dramatically when each of the three EC cell lines is induced to differentiate. Taken together, our findings argue that expression of the k-FGF oncogene is predominantly responsible for the FGF-related activity detected in EC cells and that differentiation of these EC cells results in suppression of this oncogene.</abstract><qualityIndicators><score>9.974</score><pdfWordCount>4974</pdfWordCount><pdfCharCount>27579</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>258</abstractWordCount><abstractCharCount>1620</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Expression and developmental regulation of the k-FGF oncogene in human and murine embryonal carcinoma cells</title><pmid><json:string>2481673</json:string></pmid><genre><json:string>brief-communication</json:string></genre><host><title>In Vitro Cellular & Developmental Biology</title><language><json:string>unknown</json:string></language><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><issn><json:string>0883-8364</json:string></issn><eissn><json:string>1475-2689</json:string></eissn><journalId><json:string>11627</json:string></journalId><volume>25</volume><issue>12</issue><pages><first>1193</first><last>1198</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Plant Biochemistry</value></json:item><json:item><value>Cell Biology</value></json:item><json:item><value>Developmental Biology</value></json:item><json:item><value>Plant Genetics & Genomics</value></json:item><json:item><value>Plant Physiology</value></json:item></subject></host><namedEntities><unitex><date></date><geogName></geogName><orgName></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName></persName><placeName></placeName><ref_url></ref_url><ref_bibl></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/1BB-X61XWHLW-0</json:string></ark><categories><wos></wos><scienceMetrix></scienceMetrix><scopus><json:string>1 - 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Our earlier data indicated that the mouse EC cell lines F9 and PC-13 and the human EC cell line NT2/D1 produce a factor with properties similar to those ascribed to members of the fibroblast growth factor (FGF) family and that production of this FGF-related factor is suppressed when all three EC cell lines are induced to differentiate. Subsequent studies suggested that NT2/D1 EC cells express transcripts for basic FGF (bFGF). The current study confirms and extends these findings using a combination of reverse transcription and polymerase chain reaction (RT-PCR). In this study, the expression of bFGF and other members of the FGF family have been examined in F9 and PC-13 cells in addition to NT2/D1 EC cells. In contrast to NT2/D1 EC cells, bFGF expression could not be detected in F9 and PC-13 EC cells. Additionally, expression of four other members of the FGF family (acidic FGF, int-2, FGF-5, and FGF-6) were not detected in NT2/D1, F9, or PC-13 EC cells. However, expression of another member of the FGF family, the k-FGF oncogene, was detected in NT2/D1, F9, and PC-13 EC cells. Moreover, the expression of this transcript is reduced dramatically when each of the three EC cell lines is induced to differentiate. Taken together, our findings argue that expression of the k-FGF oncogene is predominantly responsible for the FGF-related activity detected in EC cells and that differentiation of these EC cells results in suppression of this oncogene.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Key words</head><item><term>differentiation</term></item><item><term>embryonal carcinoma cells</term></item><item><term>FGF family</term></item><item><term>k-FGF</term></item><item><term>polymerase chain reaction</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Life Sciences</head><item><term>Plant Biochemistry</term></item><item><term>Cell Biology</term></item><item><term>Developmental Biology</term></item><item><term>Plant Genetics & Genomics</term></item><item><term>Plant Physiology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989-12-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-X61XWHLW-0/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>New York</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>11627</JournalID><JournalPrintISSN>0883-8364</JournalPrintISSN><JournalElectronicISSN>1475-2689</JournalElectronicISSN><JournalTitle>In Vitro Cellular & Developmental Biology</JournalTitle><JournalSubTitle>Journal of the Tissue Culture Association</JournalSubTitle><JournalAbbreviatedTitle>In Vitro Cell Dev Biol</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Life Sciences</JournalSubject><JournalSubject Type="Secondary">Plant Biochemistry</JournalSubject><JournalSubject Type="Secondary">Cell Biology</JournalSubject><JournalSubject Type="Secondary">Developmental Biology</JournalSubject><JournalSubject Type="Secondary">Plant Genetics & Genomics</JournalSubject><JournalSubject Type="Secondary">Plant Physiology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo TocLevels="0" VolumeType="Regular"><VolumeIDStart>25</VolumeIDStart><VolumeIDEnd>25</VolumeIDEnd><VolumeIssueCount>12</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>12</IssueIDStart><IssueIDEnd>12</IssueIDEnd><IssueArticleCount>18</IssueArticleCount><IssueHistory><CoverDate><Year>1989</Year><Month>12</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Tissue Culture Association</CopyrightHolderName><CopyrightYear>1989</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art17"><ArticleInfo ArticleType="BriefCommunication" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>BF02621274</ArticleID><ArticleDOI>10.1007/BF02621274</ArticleDOI><ArticleSequenceNumber>17</ArticleSequenceNumber><ArticleTitle Language="En">Expression and developmental regulation of the k-FGF oncogene in human and murine embryonal carcinoma cells</ArticleTitle><ArticleCategory>Rapid Communications in Cell Biology</ArticleCategory><ArticleFirstPage>1193</ArticleFirstPage><ArticleLastPage>1198</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2007</Year><Month>4</Month><Day>29</Day></RegistrationDate><Accepted><Year>1989</Year><Month>10</Month><Day>3</Day></Accepted></ArticleHistory><ArticleEditorialResponsibility>editor David. W. Barnes</ArticleEditorialResponsibility><ArticleCopyright><CopyrightHolderName>Tissue Culture Association</CopyrightHolderName><CopyrightYear>1989</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>11627</JournalID><VolumeIDStart>25</VolumeIDStart><VolumeIDEnd>25</VolumeIDEnd><IssueIDStart>12</IssueIDStart><IssueIDEnd>12</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Jay</GivenName><FamilyName>Tiesman</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Angie</GivenName><FamilyName>Rizzino</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Eppley Institute for Research in Cancer and Allied Diseases</OrgDivision><OrgName>University of Nebraska Medical Center, 42nd and Dewey Ave.</OrgName><OrgAddress><Postcode>68105</Postcode><City>Omaha</City><State>Nebraska</State></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Embryonal carcinoma (EC) cells provide an effective model system for studying growth factor production and regulation during mammalian embryogenesis. Our earlier data indicated that the mouse EC cell lines F9 and PC-13 and the human EC cell line NT2/D1 produce a factor with properties similar to those ascribed to members of the fibroblast growth factor (FGF) family and that production of this FGF-related factor is suppressed when all three EC cell lines are induced to differentiate. Subsequent studies suggested that NT2/D1 EC cells express transcripts for basic FGF (bFGF). The current study confirms and extends these findings using a combination of reverse transcription and polymerase chain reaction (RT-PCR). In this study, the expression of bFGF and other members of the FGF family have been examined in F9 and PC-13 cells in addition to NT2/D1 EC cells. In contrast to NT2/D1 EC cells, bFGF expression could not be detected in F9 and PC-13 EC cells. Additionally, expression of four other members of the FGF family (acidic FGF, int-2, FGF-5, and FGF-6) were not detected in NT2/D1, F9, or PC-13 EC cells. However, expression of another member of the FGF family, the k-FGF oncogene, was detected in NT2/D1, F9, and PC-13 EC cells. Moreover, the expression of this transcript is reduced dramatically when each of the three EC cell lines is induced to differentiate. Taken together, our findings argue that expression of the k-FGF oncogene is predominantly responsible for the FGF-related activity detected in EC cells and that differentiation of these EC cells results in suppression of this oncogene.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>differentiation</Keyword><Keyword>embryonal carcinoma cells</Keyword><Keyword>FGF family</Keyword><Keyword>k-FGF</Keyword><Keyword>polymerase chain reaction</Keyword></KeywordGroup><ArticleNote Type="Misc"><SimplePara>This work was supported by grants from the National Institute of Child Health and Human Development (HD 19837), the National Cancer Institute (Laboratory Cancer Research Center Support Grant, CA 36727), and the American Cancer Society (ACS SIG-16). Jay Tiesman was supported by a fellowship from the Nebraska Governor’s Research Initiative in Biotechnology.</SimplePara></ArticleNote><ArticleNote Type="Misc"><SimplePara>EDITOR’S STATEMENT In this paper Tiesman and Rizzino utilize a sensitive technique combining reverse transcription and polymerase chain reaction to demonstrate that the k-FGF gene is primarily responsible for the FGF-related growth factor activity produced by embryonal carcinoma cells in culture, and that this activity is supressed upon cell differentiation. Similar processes may occur in early development in normal cells.</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Expression and developmental regulation of the k-FGF oncogene in human and murine embryonal carcinoma cells</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Expression and developmental regulation of the k-FGF oncogene in human and murine embryonal carcinoma cells</title></titleInfo><name type="personal"><namePart type="given">Jay</namePart><namePart type="family">Tiesman</namePart><affiliation>Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 42nd and Dewey Ave., 68105, Omaha, Nebraska</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Angie</namePart><namePart type="family">Rizzino</namePart><affiliation>Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, 42nd and Dewey Ave., 68105, Omaha, Nebraska</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="BriefCommunication" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">1989-12-01</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Summary: Embryonal carcinoma (EC) cells provide an effective model system for studying growth factor production and regulation during mammalian embryogenesis. Our earlier data indicated that the mouse EC cell lines F9 and PC-13 and the human EC cell line NT2/D1 produce a factor with properties similar to those ascribed to members of the fibroblast growth factor (FGF) family and that production of this FGF-related factor is suppressed when all three EC cell lines are induced to differentiate. Subsequent studies suggested that NT2/D1 EC cells express transcripts for basic FGF (bFGF). The current study confirms and extends these findings using a combination of reverse transcription and polymerase chain reaction (RT-PCR). In this study, the expression of bFGF and other members of the FGF family have been examined in F9 and PC-13 cells in addition to NT2/D1 EC cells. In contrast to NT2/D1 EC cells, bFGF expression could not be detected in F9 and PC-13 EC cells. Additionally, expression of four other members of the FGF family (acidic FGF, int-2, FGF-5, and FGF-6) were not detected in NT2/D1, F9, or PC-13 EC cells. However, expression of another member of the FGF family, the k-FGF oncogene, was detected in NT2/D1, F9, and PC-13 EC cells. Moreover, the expression of this transcript is reduced dramatically when each of the three EC cell lines is induced to differentiate. Taken together, our findings argue that expression of the k-FGF oncogene is predominantly responsible for the FGF-related activity detected in EC cells and that differentiation of these EC cells results in suppression of this oncogene.</abstract><note>Rapid Communications in Cell Biology</note><subject lang="en"><genre>Key words</genre><topic>differentiation</topic><topic>embryonal carcinoma cells</topic><topic>FGF family</topic><topic>k-FGF</topic><topic>polymerase chain reaction</topic></subject><relatedItem type="host"><titleInfo><title>In Vitro Cellular & Developmental Biology</title><subTitle>Journal of the Tissue Culture Association</subTitle></titleInfo><titleInfo type="abbreviated"><title>In Vitro Cell Dev Biol</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">1989-12-01</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><subject><genre>Life Sciences</genre><topic>Plant Biochemistry</topic><topic>Cell Biology</topic><topic>Developmental Biology</topic><topic>Plant Genetics & Genomics</topic><topic>Plant Physiology</topic></subject><identifier type="ISSN">0883-8364</identifier><identifier type="eISSN">1475-2689</identifier><identifier type="JournalID">11627</identifier><identifier type="IssueArticleCount">18</identifier><identifier type="VolumeIssueCount">12</identifier><part><date>1989</date><detail type="volume"><number>25</number><caption>vol.</caption></detail><detail type="issue"><number>12</number><caption>no.</caption></detail><extent unit="pages"><start>1193</start><end>1198</end></extent></part><recordInfo><recordOrigin>Tissue Culture Association, 1989</recordOrigin></recordInfo></relatedItem><identifier type="istex">543D8B8D5E16BD8802107ACB6BCEF5AE9F4E934A</identifier><identifier type="ark">ark:/67375/1BB-X61XWHLW-0</identifier><identifier type="DOI">10.1007/BF02621274</identifier><identifier type="ArticleID">BF02621274</identifier><identifier type="ArticleID">Art17</identifier><accessCondition type="use and reproduction" contentType="copyright">Tissue Culture Association, 1989</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Tissue Culture Association, 1989</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-X61XWHLW-0/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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