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Gene CD58 Human Basis for Alternative Mrna Splicing of The Gene Structure, Promoter Characterization, and Basis for Alternative mRNA Splicing of the Human CD58 Gene This information is current as Reinhard Wallich, Christiane Brenner, Yvonne Brand, Matthias of September 23, 2021. Roux, Manuel Reister and Stefan Meuer J Immunol 1998; 160:2862-2871; ; http://www.jimmunol.org/content/160/6/2862 Downloaded from References This article cites 60 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/160/6/2862.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 23, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Gene Structure, Promoter Characterization, and Basis for Alternative mRNA Splicing of the Human CD58 Gene1 Reinhard Wallich,2 Christiane Brenner, Yvonne Brand, Matthias Roux, Manuel Reister, and Stefan Meuer The 60-kDa lymphocyte function-associated Ag-3 (LFA-3/CD58), a highly glycosylated adhesion molecule that serves as ligand for the T cell-restricted glycoprotein CD2, is encoded by a gene at the human chromosome locus 1p13. We have elucidated the exon-intron organization of the entire human CD58 gene, including ;2.5 kilobases (kb) of 5*-flanking DNA. Four overlapping genomic clones, spanning ;65 kb, contained the entire ;1-kb coding sequence of CD58 and consisted of six separate exons, which varied from 72 to 294 bp in size. At least two different CD58 mRNA precursors can be generated from the human gene as a result of alternative choice of one of the two acceptor splice sites located within exon 5. DNA sequence analysis of about 2.5 kb of Downloaded from 5*-flanking sequence of the CD58 gene indicated the absence of a CAAT box. However, potential binding sites for the transcrip- tional activators AP-2, GATA, PU.1, and Sp-1 are present. Two consensus TATAA elements, located ;2.4 kb upstream of the transcriptional start site, have been identified. The 2.5-kb CD58 promoter sequence displayed functional activity in transient transfection assays in the hepatocellular carcinoma cell line HepG2. Comparing the response of CD58 promoter-driven luciferase plasmids to several cytokines and other agents suggests that the CD58 promoter is regulated by up-regulatory, enhancer-like and down-regulatory, silencer-like elements. Further analysis of this region should allow researchers to gain insight into the molecular http://www.jimmunol.org/ mechanisms by which this gene is regulated, e.g., during inflammatory responses. The Journal of Immunology, 1998, 160: 2862–2871. uman CD58 (lymphocyte function-associated Ag-3) rep- human CD58 (LFA-3) gene. There is one copy of the CD58 gene resents an accessory molecule for costimulation of T per human haploid genome. This gene encompasses about 65 ki- H cells via binding to its receptor CD2 (1–6). The inter- lobases (kb) and contains six exons. The general distribution of action of CD2 on T lymphocytes with CD58 on the surface of exons and intervening sequences reflects the structural and func- endothelial cells, thymic epithelium, erythrocytes, fibroblasts, and tional organization of the protein sequence. We suggest that the APCs is critical for the regulation and effector function of T lym- two forms of CD58 observed in humans, the transmembrane and by guest on September 23, 2021 phocytes (2, 7). CD58 is expressed on the cell surface of nucleated the GPI-linked form, arise from an alternatively spliced common cells in both a transmembrane and a glycosylphosphatidylinositol pre-mRNA by the choice of one of the two splice acceptor sites in (GPI3)-anchored form (8–10). The biologic significance of these exon 5. Characterization of the corresponding cDNAs has shown variants and the signals regulating their expression are unresolved. that the two mRNAs differ by 35 bases in the 39 region. However, marked up-regulation at sites of inflammation (11, 12) Expression of CD58 mRNA has been studied in various tissues and down-regulation of CD58 in at least some tumor cells have and cell lines (9, 10). To investigate the basis of regulation of been observed (13–20). Moreover, the existence of a soluble form CD58 gene expression and to provide a foundation upon which to of the adhesion receptor CD58 in infectious and autoimmune dis- examine the relationship between T lymphocyte activation via eases was described (21–23). It has been postulated that CD2 and CD2 and CD58 expression, we also identified and characterized CD58 may have evolved from a common ancestor by gene dupli- the promoter region of CD58. In transient transfection assays, a cation, which is supported by the fact that human CD2 and CD58 2.5-kb fragment comprising the 59-flanking sequence of the CD58 genes as well as CD106 (VCAM-1) are located on chromosome 1p gene demonstrated functional activity when transfected into the and are structurally related (24–27). hepatoma cell line HepG2. To seek evidence for these postulated evolutionary events and to better assess the role of differential expression of CD58 molecules, Materials and Methods we report here on the cloning and characterization of the complete Isolation and characterization of CD58 genomic clones We have screened a human T cell genomic library in l EMBL3 phage vector (Stratagene, Heidelberg, Germany) representing partially MboI-di- Institute of Immunology, University of Heidelberg, Heidelberg, Germany gested DNA. Approximately 1 3 106 clones in Escherichia coli P2/392 32 ' Received for publication September 9, 1997. Accepted for publication November were probed with five overlapping P-labeled 0.3-kb fragments of the 24, 1997. CD58 cDNA. In addition, a human cosmid genomic library constructed in pcos2EMBL (a gift of A. Poustka, German Cancer Research Center, Hei- The costs of publication of this article were defrayed in part by the payment of page delberg, Germany) (28) and a human chromosome 1-specific genomic cos- charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. mid library constructed in Lawrist4 (library no. 112, library name L4/FS1 from the Reference Library DataBase at the MPI for Molecular Genetics, 1 The nucleotide sequences reported here have been submitted to EMBL/GenBank Berlin, Germany) (29) were screened. Approximately 1 3 106 cosmid under accession nos. Y14780, Y14781, Y14782, Y14783, Y14784, and Y14785. clones were separately screened with overlapping CD58 cDNA probes. 2 Address correspondence and reprint requests to Dr. Reinhard Wallich, Institute of Four overlapping clones were selected for further analysis: l4-1 contains Immunology, University of Heidelberg, Im Neuenheimer Feld 305, 69120 Heidel- the 59 end of the gene, ICRFc112D0797Q6 contains exons 1 and 2, l1-2 berg, Germany. E-mail address: [email protected] contains exon 2, and pcosII 3-4 contains the 39 end-harboring exons 3, 4, 3 Abbreviations used in this paper: GPI, glycosylphosphatidylinositol; kb, kilobases. 5, and 6. The recombinant genomic clones were purified, and the inserts Copyright © 1998 by The American Association of Immunologists 0022-1767/98/$02.00 The Journal of Immunology 2863 were characterized by restriction enzyme digestions and by Southern blot DNA transfection and transient expression analysis with synthetic oligonucleotides based on sequences derived from the CD58 cDNA. The endonuclease digestion products were fractionated The promoter/luciferase constructs, as well as pGL-Enhancer (a negative m 2 by electrophoresis on 1% agarose gels, and their size estimated by com- control) and pGL2-Control (a positive control), 5 g/28-cm plate, were parison with standard DNA markers (New England Biolabs GmbH, used in transient transfections of the human hepatoma cell line HepG2 Schwalbach, Germany). Appropriate DNA fragments were isolated by gel (HB-8065; American Type Culture Collection, Rockville, MD) cultured in electrophoresis and subcloned into the Bluescript vector (Stratagene) for RPMI 1640 medium (Life Technologies, Eggenstein, Germany) supple- 3 5 sequencing. mented with 10% FCS. Approximately 4 10 cells/plate were cultured 24 h before transfection. The transfections were performed in serum-free RPMI 1640 with a commercial kit (LipofectAMINE; Life Technologies) DNA sequencing according to the manufacturer’s instructions. To control for variations in transfection efficiency, plasmid pUHD16.1 (a gift of H. Bujard, ZMBH, Exons and the junctions between exons and intervening sequences were University of Heidelberg), containing the SV40 promoter and the Esche- sequenced (30) after subcloning of appropriate fragments into pBlue- 1 richia coli lacZ gene, was cotransfected and the amount of cell extracts was scriptII SK (Stratagene). Specific oligonucleotides chosen from the cod- adjusted according to the b-galactosidase activity. Following an overnight ing sequence of the CD58 cDNA were used. The complete CD58 cDNA incubation, cells were washed and transferred to RPMI 1640/10% FCS for sequences have already been published (9, 10) and have been deposited in 24 h. the EMBL/GenBank database (accession nos.: X06296 and Y00636).1 DNA sequence was determined using a T7 DNA sequencing kit (Pharma- Luciferase and b-galactosidase assays cia, Freiburg, Germany) in accordance with the manufacturer’s recommendation (31). Forty hours after transfection, cells were pelleted and washed twice with PBS.
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