Posttranscriptional mechanisms are responsible for accumulation of truncated c- myc RNAs in murine plasma cell tumors
c-myc messenger RNAs are known to be extremely unstable (t 1 2 = 10 min) in normal and tumor cells, suggesting that degradation could play an important role in regulating their steady state level in the cytoplasm. We have investigated the stabilities of c- myc mRNAs in three murine plasmacytomas, wh...
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Veröffentlicht in: | Cell 1985-09, Vol.42 (2), p.589-597 |
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creator | Piechaczyk, Marc Yang, Jian-Qing Blanchard, Jean-Marie Jeanteur, Philippe Marcu, Kenneth B. |
description | c-myc messenger RNAs are known to be extremely unstable (t
1
2
= 10 min) in normal and tumor cells, suggesting that degradation could play an important role in regulating their steady state level in the cytoplasm. We have investigated the stabilities of c-
myc mRNAs in three murine plasmacytomas, where the c-
myc gene either remains intact (ABPC20) or exists in a truncated form (MPC-11 and J558L) subsequent to 6;15 or 12;15 chromosome translocations respectively, and in an A-MuLV-induced pre-B lymphoma line (18–81.5) that lacks chromosome translocations and contains both c-
myc genes in their normal context. The truncated
myc genes in J558L and MPC-11 lack the promoters of the normal gene but are transcribed from cryptic promoters within the first c-
myc intron. We found that posttranscriptional processes are largely responsible for the higher steady state accumulations of truncated c-
myc transcripts, while broken and intact c-
myc genes are transcribed at comparable rates. |
doi_str_mv | 10.1016/0092-8674(85)90116-3 |
format | Article |
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1
2
= 10 min) in normal and tumor cells, suggesting that degradation could play an important role in regulating their steady state level in the cytoplasm. We have investigated the stabilities of c-
myc mRNAs in three murine plasmacytomas, where the c-
myc gene either remains intact (ABPC20) or exists in a truncated form (MPC-11 and J558L) subsequent to 6;15 or 12;15 chromosome translocations respectively, and in an A-MuLV-induced pre-B lymphoma line (18–81.5) that lacks chromosome translocations and contains both c-
myc genes in their normal context. The truncated
myc genes in J558L and MPC-11 lack the promoters of the normal gene but are transcribed from cryptic promoters within the first c-
myc intron. We found that posttranscriptional processes are largely responsible for the higher steady state accumulations of truncated c-
myc transcripts, while broken and intact c-
myc genes are transcribed at comparable rates.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/0092-8674(85)90116-3</identifier><identifier>PMID: 2411425</identifier><identifier>CODEN: CELLB5</identifier><language>eng</language><publisher>Cambridge, MA: Elsevier Inc</publisher><subject>Animals ; B-Lymphocytes ; Base Sequence ; Biological and medical sciences ; Cell Line ; Cytoplasm - metabolism ; Dactinomycin - pharmacology ; Fundamental and applied biological sciences. Psychology ; Half-Life ; Lymphoma - genetics ; Mice ; Molecular and cellular biology ; Molecular genetics ; Nucleic Acid Hybridization ; Oncogenes ; Plasmacytoma - genetics ; Promoter Regions, Genetic ; RNA Processing, Post-Transcriptional ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Neoplasm - genetics ; RNA, Neoplasm - metabolism ; Transcription, Genetic ; Transcription. Transcription factor. Splicing. Rna processing ; Translocation, Genetic</subject><ispartof>Cell, 1985-09, Vol.42 (2), p.589-597</ispartof><rights>1985</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-d95ca4abf1007566f5c2179c48223dd3a1b746ddc2b996cb2e19a150b05b4e4d3</citedby><cites>FETCH-LOGICAL-c483t-d95ca4abf1007566f5c2179c48223dd3a1b746ddc2b996cb2e19a150b05b4e4d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0092-8674(85)90116-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8529092$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2411425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Piechaczyk, Marc</creatorcontrib><creatorcontrib>Yang, Jian-Qing</creatorcontrib><creatorcontrib>Blanchard, Jean-Marie</creatorcontrib><creatorcontrib>Jeanteur, Philippe</creatorcontrib><creatorcontrib>Marcu, Kenneth B.</creatorcontrib><title>Posttranscriptional mechanisms are responsible for accumulation of truncated c- myc RNAs in murine plasma cell tumors</title><title>Cell</title><addtitle>Cell</addtitle><description>c-myc messenger RNAs are known to be extremely unstable (t
1
2
= 10 min) in normal and tumor cells, suggesting that degradation could play an important role in regulating their steady state level in the cytoplasm. We have investigated the stabilities of c-
myc mRNAs in three murine plasmacytomas, where the c-
myc gene either remains intact (ABPC20) or exists in a truncated form (MPC-11 and J558L) subsequent to 6;15 or 12;15 chromosome translocations respectively, and in an A-MuLV-induced pre-B lymphoma line (18–81.5) that lacks chromosome translocations and contains both c-
myc genes in their normal context. The truncated
myc genes in J558L and MPC-11 lack the promoters of the normal gene but are transcribed from cryptic promoters within the first c-
myc intron. We found that posttranscriptional processes are largely responsible for the higher steady state accumulations of truncated c-
myc transcripts, while broken and intact c-
myc genes are transcribed at comparable rates.</description><subject>Animals</subject><subject>B-Lymphocytes</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cytoplasm - metabolism</subject><subject>Dactinomycin - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Half-Life</subject><subject>Lymphoma - genetics</subject><subject>Mice</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Nucleic Acid Hybridization</subject><subject>Oncogenes</subject><subject>Plasmacytoma - genetics</subject><subject>Promoter Regions, Genetic</subject><subject>RNA Processing, Post-Transcriptional</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Neoplasm - genetics</subject><subject>RNA, Neoplasm - metabolism</subject><subject>Transcription, Genetic</subject><subject>Transcription. Transcription factor. Splicing. Rna processing</subject><subject>Translocation, Genetic</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2L1TAUxYMo43P0P1DIQkQX1SRN-rEZGAa_YFARXYf05hYjTVNzW2H-e1Pf4y11dRfndw6Xcxh7KsVrKWTzRoheVV3T6pededULKZuqvscOUvRtpWWr7rPDGXnIHhH9FEJ0xpgLdqG0lFqZA9u-JFrX7GaCHJY1pNlNPCL8cHOgSNxl5BlpSTOFYUI-pswdwBa3ye00TyNf8zaDW9FzqHi8A_710zXxMPO45TAjXyZH0XHAaeLrFlOmx-zB6CbCJ6d7yb6_e_vt5kN1-_n9x5vr2wp0V6-V7w047YZRCtGaphkNKNn2RVSq9r52cmh14z2ooe8bGBTK3kkjBmEGjdrXl-zFMXfJ6deGtNoYaP_DzZg2sm2jGq2k-i8odW1KX6KA-ghCTkQZR7vkEF2-s1LYfRa7d273zm1n7N9ZbF1sz0752xDRn02nHYr-_KQ7AjeNZRAIdMY6o_oSW7CrI4altN8BsyUIOAP6kBFW61P49x9_ALOEqlM</recordid><startdate>198509</startdate><enddate>198509</enddate><creator>Piechaczyk, Marc</creator><creator>Yang, Jian-Qing</creator><creator>Blanchard, Jean-Marie</creator><creator>Jeanteur, Philippe</creator><creator>Marcu, Kenneth B.</creator><general>Elsevier Inc</general><general>Cell Press</general><scope>IQODW</scope><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>198509</creationdate><title>Posttranscriptional mechanisms are responsible for accumulation of truncated c- myc RNAs in murine plasma cell tumors</title><author>Piechaczyk, Marc ; Yang, Jian-Qing ; Blanchard, Jean-Marie ; Jeanteur, Philippe ; Marcu, Kenneth B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-d95ca4abf1007566f5c2179c48223dd3a1b746ddc2b996cb2e19a150b05b4e4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Animals</topic><topic>B-Lymphocytes</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cytoplasm - metabolism</topic><topic>Dactinomycin - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Half-Life</topic><topic>Lymphoma - genetics</topic><topic>Mice</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Nucleic Acid Hybridization</topic><topic>Oncogenes</topic><topic>Plasmacytoma - genetics</topic><topic>Promoter Regions, Genetic</topic><topic>RNA Processing, Post-Transcriptional</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Neoplasm - genetics</topic><topic>RNA, Neoplasm - metabolism</topic><topic>Transcription, Genetic</topic><topic>Transcription. Transcription factor. Splicing. Rna processing</topic><topic>Translocation, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Piechaczyk, Marc</creatorcontrib><creatorcontrib>Yang, Jian-Qing</creatorcontrib><creatorcontrib>Blanchard, Jean-Marie</creatorcontrib><creatorcontrib>Jeanteur, Philippe</creatorcontrib><creatorcontrib>Marcu, Kenneth B.</creatorcontrib><collection>Pascal-Francis</collection><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>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Piechaczyk, Marc</au><au>Yang, Jian-Qing</au><au>Blanchard, Jean-Marie</au><au>Jeanteur, Philippe</au><au>Marcu, Kenneth B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Posttranscriptional mechanisms are responsible for accumulation of truncated c- myc RNAs in murine plasma cell tumors</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>1985-09</date><risdate>1985</risdate><volume>42</volume><issue>2</issue><spage>589</spage><epage>597</epage><pages>589-597</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><coden>CELLB5</coden><abstract>c-myc messenger RNAs are known to be extremely unstable (t
1
2
= 10 min) in normal and tumor cells, suggesting that degradation could play an important role in regulating their steady state level in the cytoplasm. We have investigated the stabilities of c-
myc mRNAs in three murine plasmacytomas, where the c-
myc gene either remains intact (ABPC20) or exists in a truncated form (MPC-11 and J558L) subsequent to 6;15 or 12;15 chromosome translocations respectively, and in an A-MuLV-induced pre-B lymphoma line (18–81.5) that lacks chromosome translocations and contains both c-
myc genes in their normal context. The truncated
myc genes in J558L and MPC-11 lack the promoters of the normal gene but are transcribed from cryptic promoters within the first c-
myc intron. We found that posttranscriptional processes are largely responsible for the higher steady state accumulations of truncated c-
myc transcripts, while broken and intact c-
myc genes are transcribed at comparable rates.</abstract><cop>Cambridge, MA</cop><pub>Elsevier Inc</pub><pmid>2411425</pmid><doi>10.1016/0092-8674(85)90116-3</doi><tpages>9</tpages></addata></record> |
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subjects | Animals B-Lymphocytes Base Sequence Biological and medical sciences Cell Line Cytoplasm - metabolism Dactinomycin - pharmacology Fundamental and applied biological sciences. Psychology Half-Life Lymphoma - genetics Mice Molecular and cellular biology Molecular genetics Nucleic Acid Hybridization Oncogenes Plasmacytoma - genetics Promoter Regions, Genetic RNA Processing, Post-Transcriptional RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Neoplasm - genetics RNA, Neoplasm - metabolism Transcription, Genetic Transcription. Transcription factor. Splicing. Rna processing Translocation, Genetic |
title | Posttranscriptional mechanisms are responsible for accumulation of truncated c- myc RNAs in murine plasma cell tumors |
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