Sequences upstream from the mouse c-mos oncogene may function as a transcription termination signal
A region upstream from the mouse c-mos proto-oncogene, termed upstream mouse sequence (UMS), prevents expression of mos transforming activity. Previous studies suggested that the UMS prevented transcription readthrough. In this study, we constructed a recombinant DNA clone, pHTS3MS, with the UMS ins...
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Veröffentlicht in: | DNA (New York, N.Y.) N.Y.), 1986-08, Vol.5 (4), p.289-298 |
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creator | McGeady, M L Wood, T G Maizel, J V Vande Woude, G F |
description | A region upstream from the mouse c-mos proto-oncogene, termed upstream mouse sequence (UMS), prevents expression of mos transforming activity. Previous studies suggested that the UMS prevented transcription readthrough. In this study, we constructed a recombinant DNA clone, pHTS3MS, with the UMS inserted downstream from both the mos gene and a truncated long terminal repeat containing only the U3 enhancer region. In this position UMS did not inhibit mos transforming activity. We examined cells transformed by pHTS3MS for RNA expression. S1 nuclease analysis showed that the UMS provides two polyadenylation signals to mos-containing RNA and nuclear run-on transcription showed that the primary transcripts terminate in UMS. In addition, using portions of the UMS, we found that a 360-bp fragment containing the UMS polyadenylation signals and sites inserted between the herpes simplex virus type 1 (HSV-1) thymidine kinase gene (tk) and its promoter inhibits tk transforming activity by 99% and prevents detectable expression of this construct in transient expression assays. Thus, the UMS must contain signals for polyadenylation and appears to function as a transcription terminator. |
doi_str_mv | 10.1089/dna.1986.5.289 |
format | Article |
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Previous studies suggested that the UMS prevented transcription readthrough. In this study, we constructed a recombinant DNA clone, pHTS3MS, with the UMS inserted downstream from both the mos gene and a truncated long terminal repeat containing only the U3 enhancer region. In this position UMS did not inhibit mos transforming activity. We examined cells transformed by pHTS3MS for RNA expression. S1 nuclease analysis showed that the UMS provides two polyadenylation signals to mos-containing RNA and nuclear run-on transcription showed that the primary transcripts terminate in UMS. In addition, using portions of the UMS, we found that a 360-bp fragment containing the UMS polyadenylation signals and sites inserted between the herpes simplex virus type 1 (HSV-1) thymidine kinase gene (tk) and its promoter inhibits tk transforming activity by 99% and prevents detectable expression of this construct in transient expression assays. Thus, the UMS must contain signals for polyadenylation and appears to function as a transcription terminator.</description><identifier>ISSN: 0198-0238</identifier><identifier>DOI: 10.1089/dna.1986.5.289</identifier><identifier>PMID: 3017657</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Base Sequence ; Cell Nucleus - physiology ; Cell Transformation, Viral ; Chromosome Mapping ; Cloning, Molecular ; Endonucleases ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Regulator ; Mice ; Nucleic Acid Conformation ; Oncogenes ; Poly A - genetics ; Proto-Oncogene Proteins - genetics ; Single-Strand Specific DNA and RNA Endonucleases ; Terminator Regions, Genetic ; Thymidine Kinase - genetics ; Transcription, Genetic</subject><ispartof>DNA (New York, N.Y.), 1986-08, Vol.5 (4), p.289-298</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c321t-ee76874fa32b72687dcd09ba2c5107c57b1915b55ba4ce40369b68a0745d6d5a3</citedby><cites>FETCH-LOGICAL-c321t-ee76874fa32b72687dcd09ba2c5107c57b1915b55ba4ce40369b68a0745d6d5a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3040,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3017657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McGeady, M L</creatorcontrib><creatorcontrib>Wood, T G</creatorcontrib><creatorcontrib>Maizel, J V</creatorcontrib><creatorcontrib>Vande Woude, G F</creatorcontrib><title>Sequences upstream from the mouse c-mos oncogene may function as a transcription termination signal</title><title>DNA (New York, N.Y.)</title><addtitle>DNA</addtitle><description>A region upstream from the mouse c-mos proto-oncogene, termed upstream mouse sequence (UMS), prevents expression of mos transforming activity. Previous studies suggested that the UMS prevented transcription readthrough. In this study, we constructed a recombinant DNA clone, pHTS3MS, with the UMS inserted downstream from both the mos gene and a truncated long terminal repeat containing only the U3 enhancer region. In this position UMS did not inhibit mos transforming activity. We examined cells transformed by pHTS3MS for RNA expression. S1 nuclease analysis showed that the UMS provides two polyadenylation signals to mos-containing RNA and nuclear run-on transcription showed that the primary transcripts terminate in UMS. In addition, using portions of the UMS, we found that a 360-bp fragment containing the UMS polyadenylation signals and sites inserted between the herpes simplex virus type 1 (HSV-1) thymidine kinase gene (tk) and its promoter inhibits tk transforming activity by 99% and prevents detectable expression of this construct in transient expression assays. Thus, the UMS must contain signals for polyadenylation and appears to function as a transcription terminator.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Cell Nucleus - physiology</subject><subject>Cell Transformation, Viral</subject><subject>Chromosome Mapping</subject><subject>Cloning, Molecular</subject><subject>Endonucleases</subject><subject>Enhancer Elements, Genetic</subject><subject>Gene Expression Regulation</subject><subject>Genes, Regulator</subject><subject>Mice</subject><subject>Nucleic Acid Conformation</subject><subject>Oncogenes</subject><subject>Poly A - genetics</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Single-Strand Specific DNA and RNA Endonucleases</subject><subject>Terminator Regions, Genetic</subject><subject>Thymidine Kinase - genetics</subject><subject>Transcription, Genetic</subject><issn>0198-0238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkDtPxDAQhF2AjuOgpUNyRZdgx7GdlOjESzqJAqitjeMcQbEd7KS4f4_vIVqqnR3NjrQfQjeU5JRU9X3rIKd1JXKeF1V9hpYkbRkpWHWBLmP8JoSRktMFWjBCpeByifS7-ZmN0ybieYxTMGBxF7zF05fB1s_RYJ1ZH7F32m-NSybscDc7PfXeYYgY8BTARR368WBNJtjewUHHfutguELnHQzRXJ_mCn0-PX6sX7LN2_Pr-mGTaVbQKTNGikqWHbCikUWSrW5J3UChOSVSc9nQmvKG8wZKbUrCRN2ICogseStaDmyF7o69Y_DpqTgp20dthgGcSZ8oKQkhnFf_BmnJhRQ1TcH8GNTBxxhMp8bQWwg7RYnaI1cJudojV1wl5Ong9tQ8N9a0f_ETb_YLXxKAEg</recordid><startdate>19860801</startdate><enddate>19860801</enddate><creator>McGeady, M L</creator><creator>Wood, T G</creator><creator>Maizel, J V</creator><creator>Vande Woude, G F</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19860801</creationdate><title>Sequences upstream from the mouse c-mos oncogene may function as a transcription termination signal</title><author>McGeady, M L ; Wood, T G ; Maizel, J V ; Vande Woude, G F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c321t-ee76874fa32b72687dcd09ba2c5107c57b1915b55ba4ce40369b68a0745d6d5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Cell Nucleus - physiology</topic><topic>Cell Transformation, Viral</topic><topic>Chromosome Mapping</topic><topic>Cloning, Molecular</topic><topic>Endonucleases</topic><topic>Enhancer Elements, Genetic</topic><topic>Gene Expression Regulation</topic><topic>Genes, Regulator</topic><topic>Mice</topic><topic>Nucleic Acid Conformation</topic><topic>Oncogenes</topic><topic>Poly A - genetics</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Single-Strand Specific DNA and RNA Endonucleases</topic><topic>Terminator Regions, Genetic</topic><topic>Thymidine Kinase - genetics</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McGeady, M L</creatorcontrib><creatorcontrib>Wood, T G</creatorcontrib><creatorcontrib>Maizel, J V</creatorcontrib><creatorcontrib>Vande Woude, G F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>DNA (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McGeady, M L</au><au>Wood, T G</au><au>Maizel, J V</au><au>Vande Woude, G F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sequences upstream from the mouse c-mos oncogene may function as a transcription termination signal</atitle><jtitle>DNA (New York, N.Y.)</jtitle><addtitle>DNA</addtitle><date>1986-08-01</date><risdate>1986</risdate><volume>5</volume><issue>4</issue><spage>289</spage><epage>298</epage><pages>289-298</pages><issn>0198-0238</issn><abstract>A region upstream from the mouse c-mos proto-oncogene, termed upstream mouse sequence (UMS), prevents expression of mos transforming activity. Previous studies suggested that the UMS prevented transcription readthrough. In this study, we constructed a recombinant DNA clone, pHTS3MS, with the UMS inserted downstream from both the mos gene and a truncated long terminal repeat containing only the U3 enhancer region. In this position UMS did not inhibit mos transforming activity. We examined cells transformed by pHTS3MS for RNA expression. S1 nuclease analysis showed that the UMS provides two polyadenylation signals to mos-containing RNA and nuclear run-on transcription showed that the primary transcripts terminate in UMS. In addition, using portions of the UMS, we found that a 360-bp fragment containing the UMS polyadenylation signals and sites inserted between the herpes simplex virus type 1 (HSV-1) thymidine kinase gene (tk) and its promoter inhibits tk transforming activity by 99% and prevents detectable expression of this construct in transient expression assays. Thus, the UMS must contain signals for polyadenylation and appears to function as a transcription terminator.</abstract><cop>United States</cop><pmid>3017657</pmid><doi>10.1089/dna.1986.5.289</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Base Sequence Cell Nucleus - physiology Cell Transformation, Viral Chromosome Mapping Cloning, Molecular Endonucleases Enhancer Elements, Genetic Gene Expression Regulation Genes, Regulator Mice Nucleic Acid Conformation Oncogenes Poly A - genetics Proto-Oncogene Proteins - genetics Single-Strand Specific DNA and RNA Endonucleases Terminator Regions, Genetic Thymidine Kinase - genetics Transcription, Genetic |
title | Sequences upstream from the mouse c-mos oncogene may function as a transcription termination signal |
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