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Article: Dual transcriptional control of claudin-11 via an overlapping GATA/NF-Y motif: Positive regulation through the interaction of GATA, NF-YA, and CREB and negative regulation through the interaction of Smad, HDAC1, and mSin3A

TitleDual transcriptional control of claudin-11 via an overlapping GATA/NF-Y motif: Positive regulation through the interaction of GATA, NF-YA, and CREB and negative regulation through the interaction of Smad, HDAC1, and mSin3A
Authors
Issue Date2007
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, 2007, v. 211 n. 3, p. 638-648 How to Cite?
AbstractThe expression of claudin-11, a key integral tight junction protein, is tightly regulated to ensure that the integrity of the seminiferous epithelium could be maintained during the translocation of spermatocytes at the blood-testis barrier at stages VIII-IX. In this study, we elucidate how the overlapping GATA/NF-Y motif within the core promoter of claudin-11 gene is modulated by differential binding of various transcription factors, resulting in dual transcriptional control. Using electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay, we confirmed that GATA, nuclear factor YA (NF-YA), and cAMP response element-binding protein (CREB) form a complex in vivo and bind to the GATA/NF-Y region to promote claudin-11 gene transcription. Such gene activations were significantly reduced in the presence of siRNA specific to these transcription factors. GATA and CREB transactivation could be further modulated by the presence of Smad3 and Smad4 proteins. Binding of Smad proteins at the GATA/NF-Y motif could repress the GATA and CREB transactivation of claudin-11 gene. Such repression which required the recruitment and physical interactions of histone deacetylase I and its co-repressor, mSin3A with Smad proteins, was abolished by treatment with Trichostatin A, thus suggesting the involvement of histone deacetylation at the site of the promoter region. It is believed that cyclic changes in the ratio of positive regulators (GATA, NF-Y, and CREB) to negative regulators (Smads) in the seminiferous epithelium during the spermatogenic cycle might provide a precise control in claudin-11 gene transcription. © 2007 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/84938
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLui, WYen_HK
dc.contributor.authorWong, EWPen_HK
dc.contributor.authorGuan, Yen_HK
dc.contributor.authorLee, WMen_HK
dc.date.accessioned2010-09-06T08:58:52Z-
dc.date.available2010-09-06T08:58:52Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Cellular Physiology, 2007, v. 211 n. 3, p. 638-648en_HK
dc.identifier.issn0021-9541en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84938-
dc.description.abstractThe expression of claudin-11, a key integral tight junction protein, is tightly regulated to ensure that the integrity of the seminiferous epithelium could be maintained during the translocation of spermatocytes at the blood-testis barrier at stages VIII-IX. In this study, we elucidate how the overlapping GATA/NF-Y motif within the core promoter of claudin-11 gene is modulated by differential binding of various transcription factors, resulting in dual transcriptional control. Using electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay, we confirmed that GATA, nuclear factor YA (NF-YA), and cAMP response element-binding protein (CREB) form a complex in vivo and bind to the GATA/NF-Y region to promote claudin-11 gene transcription. Such gene activations were significantly reduced in the presence of siRNA specific to these transcription factors. GATA and CREB transactivation could be further modulated by the presence of Smad3 and Smad4 proteins. Binding of Smad proteins at the GATA/NF-Y motif could repress the GATA and CREB transactivation of claudin-11 gene. Such repression which required the recruitment and physical interactions of histone deacetylase I and its co-repressor, mSin3A with Smad proteins, was abolished by treatment with Trichostatin A, thus suggesting the involvement of histone deacetylation at the site of the promoter region. It is believed that cyclic changes in the ratio of positive regulators (GATA, NF-Y, and CREB) to negative regulators (Smads) in the seminiferous epithelium during the spermatogenic cycle might provide a precise control in claudin-11 gene transcription. © 2007 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_HK
dc.relation.ispartofJournal of Cellular Physiologyen_HK
dc.rightsJournal of Cellular Physiology. Copyright © John Wiley & Sons, Inc.en_HK
dc.titleDual transcriptional control of claudin-11 via an overlapping GATA/NF-Y motif: Positive regulation through the interaction of GATA, NF-YA, and CREB and negative regulation through the interaction of Smad, HDAC1, and mSin3Aen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9541&volume=211&spage=638&epage=648&date=2007&atitle=Dual+transcriptional+control+of+claudin-11+via+an+overlapping+GATA/NF-Y+motif:+Positive+regulation+through+the+interaction+of+GATA,+NF-YA,+and+CREB+and+negative+regulation+through+the+interaction+of+Smad,+HDAC1,+and+mSin3Aen_HK
dc.identifier.emailLui, WY: wylui@hku.hken_HK
dc.identifier.emailLee, WM: hrszlwm@hku.hken_HK
dc.identifier.authorityLui, WY=rp00756en_HK
dc.identifier.authorityLee, WM=rp00728en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jcp.20970en_HK
dc.identifier.pmid17226765-
dc.identifier.scopuseid_2-s2.0-34247621696en_HK
dc.identifier.hkuros126262en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247621696&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume211en_HK
dc.identifier.issue3en_HK
dc.identifier.spage638en_HK
dc.identifier.epage648en_HK
dc.identifier.eissn1097-4652-
dc.identifier.isiWOS:000246165100009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLui, WY=35220192400en_HK
dc.identifier.scopusauthoridWong, EWP=23029194700en_HK
dc.identifier.scopusauthoridGuan, Y=24802016400en_HK
dc.identifier.scopusauthoridLee, WM=24799156600en_HK

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