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Article: Expression of CLMP, a novel tight junction protein, is mediated via the interaction of GATA with the Kruppel family proteins, KLF4 and Sp1, in mouse TM4 sertoli cells

TitleExpression of CLMP, a novel tight junction protein, is mediated via the interaction of GATA with the Kruppel family proteins, KLF4 and Sp1, in mouse TM4 sertoli cells
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal Of Cellular Physiology, 2008, v. 214 n. 2, p. 334-344 How to Cite?
AbstractRegulation of tight junction protein expressions in Sertoli cells is important for germ cell translocation across the blood-testis-barrier (BTB) during spermatogenesis. In this study, a novel tight junction transmembrane protein, CLMP, found expressed in mouse testis was shown to localize at the BTB along with the tight junction marker ZO-1. By the use of transient transfection assay performed in a mouse Sertoli cell-cell line, TM4 cells, we showed that the minimal CLMP promoter was located between nucleotides -550 and -288 relative to the translation start site. Site-directed mutagenic studies showed that three motifs, namely GATA, KLF4, and SRY, within this region functionally co-operated with one another to regulate CLMP gene transcription. Using specific antibodies in EMSA analysis, a ternary protein complex GATA-1/GATA-6/KLF4 was detected at all the three motifs, suggesting that a looping mechanism might involve in regulating CLMP gene transcription. Interestingly, the ubiquitously expressed transcription factors, Sp1 and Sp3, were also found in this ternary complex over the KLF4 motif. Overexpression of KLF4 significantly increased the promoter activity whilst overexpression of Sp1 or Sp3 exerted an opposite effect. In particular, co-transfection studies showed that Sp1 could significantly abolish the KLF4-induced transactivation of the CLMP gene, suggesting that KLF4 and Sp1 might compete for the same binding site on the CLMP promoter. Taken together, this differential interaction of the transcription factors, GATA-1, GATA-6, KLF4, Sp1, and Sp3, in CLMP gene expression might provide a precise machinery in regulating Sertoli cell tight junction dynamics. © 2007 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/179029
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSze, KLen_US
dc.contributor.authorLee, WMen_US
dc.contributor.authorLui, WYen_US
dc.date.accessioned2012-12-19T09:51:32Z-
dc.date.available2012-12-19T09:51:32Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Cellular Physiology, 2008, v. 214 n. 2, p. 334-344en_US
dc.identifier.issn0021-9541en_US
dc.identifier.urihttp://hdl.handle.net/10722/179029-
dc.description.abstractRegulation of tight junction protein expressions in Sertoli cells is important for germ cell translocation across the blood-testis-barrier (BTB) during spermatogenesis. In this study, a novel tight junction transmembrane protein, CLMP, found expressed in mouse testis was shown to localize at the BTB along with the tight junction marker ZO-1. By the use of transient transfection assay performed in a mouse Sertoli cell-cell line, TM4 cells, we showed that the minimal CLMP promoter was located between nucleotides -550 and -288 relative to the translation start site. Site-directed mutagenic studies showed that three motifs, namely GATA, KLF4, and SRY, within this region functionally co-operated with one another to regulate CLMP gene transcription. Using specific antibodies in EMSA analysis, a ternary protein complex GATA-1/GATA-6/KLF4 was detected at all the three motifs, suggesting that a looping mechanism might involve in regulating CLMP gene transcription. Interestingly, the ubiquitously expressed transcription factors, Sp1 and Sp3, were also found in this ternary complex over the KLF4 motif. Overexpression of KLF4 significantly increased the promoter activity whilst overexpression of Sp1 or Sp3 exerted an opposite effect. In particular, co-transfection studies showed that Sp1 could significantly abolish the KLF4-induced transactivation of the CLMP gene, suggesting that KLF4 and Sp1 might compete for the same binding site on the CLMP promoter. Taken together, this differential interaction of the transcription factors, GATA-1, GATA-6, KLF4, Sp1, and Sp3, in CLMP gene expression might provide a precise machinery in regulating Sertoli cell tight junction dynamics. © 2007 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_US
dc.relation.ispartofJournal of Cellular Physiologyen_US
dc.rightsJournal of Cellular Physiology . Copyright © John Wiley & Sons, Inc.-
dc.subject.meshAnimalsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshChromatin Immunoprecipitationen_US
dc.subject.meshElectrophoretic Mobility Shift Assayen_US
dc.subject.meshFluorescein-5-Isothiocyanateen_US
dc.subject.meshFluorescent Antibody Technique, Indirecten_US
dc.subject.meshFluorescent Dyesen_US
dc.subject.meshGata Transcription Factors - Metabolismen_US
dc.subject.meshGenes, Reporteren_US
dc.subject.meshIndolesen_US
dc.subject.meshKruppel-Like Transcription Factors - Genetics - Metabolismen_US
dc.subject.meshLuciferases - Analysis - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Proteins - Genetics - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMicroscopy, Fluorescenceen_US
dc.subject.meshModels, Geneticen_US
dc.subject.meshMutagenesis, Site-Directeden_US
dc.subject.meshNih 3T3 Cellsen_US
dc.subject.meshSertoli Cells - Metabolismen_US
dc.subject.meshSp1 Transcription Factor - Genetics - Metabolismen_US
dc.subject.meshTransfectionen_US
dc.subject.meshBeta-Galactosidase - Analysis - Metabolismen_US
dc.titleExpression of CLMP, a novel tight junction protein, is mediated via the interaction of GATA with the Kruppel family proteins, KLF4 and Sp1, in mouse TM4 sertoli cellsen_US
dc.typeArticleen_US
dc.identifier.emailLee, WM: hrszlwm@hku.hken_US
dc.identifier.emailLui, WY: wylui@hku.hken_US
dc.identifier.authorityLee, WM=rp00728en_US
dc.identifier.authorityLui, WY=rp00756en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jcp.21201en_US
dc.identifier.pmid17620326-
dc.identifier.scopuseid_2-s2.0-37349012913en_US
dc.identifier.hkuros143831-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37349012913&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume214en_US
dc.identifier.issue2en_US
dc.identifier.spage334en_US
dc.identifier.epage344en_US
dc.identifier.eissn1097-4652-
dc.identifier.isiWOS:000252163400007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSze, KL=12779346400en_US
dc.identifier.scopusauthoridLee, WM=24799156600en_US
dc.identifier.scopusauthoridLui, WY=35220192400en_US

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