Moloney murine leukemia virus-induced tumors: recombinant proviruses in active chromatin regions
The DNase I sensitivity of chromosomal DNA regions carrying integrated proviral genomes of Moloney (M-MuLV) and AKR Murine Leukemia Virus (AKR-MuLV), and the cellular homologue of the mos-gene (c-mos) of Moloney Sarcoma Virus (MSV) were studied in tumor tissues of leukemic mice. The genetically tran...
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Veröffentlicht in: | Nucleic acids research 1982-01, Vol.10 (2), p.577-592 |
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description | The DNase I sensitivity of chromosomal DNA regions carrying integrated proviral genomes of Moloney (M-MuLV) and AKR Murine Leukemia Virus (AKR-MuLV), and the cellular homologue of the mos-gene (c-mos) of Moloney Sarcoma Virus (MSV) were studied in tumor tissues of leukemic mice. The genetically transmitted sequences of M-MuLV, AKR-MuLV and the c-mos gene are all in DNase I resistant chromatin conformations in M-MuLV-induced tumors. Each M-MuLV-induced tumor contained at least one somatically acquired integrated recombinant MuLV genome that displayed two main characteristic features of active chromatin: a) a configuration hypersensitive to DNase I, and b) extensive hypomethylation. DNase I hypersensitive sites were mapped at the junction of cellular sequences and the 5′-viral large terminal repeat (LTR). Expression of a recombinant MuLV seems therefore to be a necessary feature to maintain the transformed state. |
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The genetically transmitted sequences of M-MuLV, AKR-MuLV and the c-mos gene are all in DNase I resistant chromatin conformations in M-MuLV-induced tumors. Each M-MuLV-induced tumor contained at least one somatically acquired integrated recombinant MuLV genome that displayed two main characteristic features of active chromatin: a) a configuration hypersensitive to DNase I, and b) extensive hypomethylation. DNase I hypersensitive sites were mapped at the junction of cellular sequences and the 5′-viral large terminal repeat (LTR). 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The genetically transmitted sequences of M-MuLV, AKR-MuLV and the c-mos gene are all in DNase I resistant chromatin conformations in M-MuLV-induced tumors. Each M-MuLV-induced tumor contained at least one somatically acquired integrated recombinant MuLV genome that displayed two main characteristic features of active chromatin: a) a configuration hypersensitive to DNase I, and b) extensive hypomethylation. DNase I hypersensitive sites were mapped at the junction of cellular sequences and the 5′-viral large terminal repeat (LTR). Expression of a recombinant MuLV seems therefore to be a necessary feature to maintain the transformed state.</description><subject>Akr murine leukemia virus</subject><subject>AKR murine leukemia virus - genetics</subject><subject>Animals</subject><subject>Cell Line</subject><subject>Cell Nucleus - physiology</subject><subject>Cell Transformation, Neoplastic</subject><subject>Chromatin - physiology</subject><subject>Deoxyribonuclease I</subject><subject>Deoxyribonucleases</subject><subject>DNA Restriction Enzymes</subject><subject>DNA, Recombinant - analysis</subject><subject>Endonucleases</subject><subject>Leukemia, Experimental - microbiology</subject><subject>Methylation</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Moloney murine leukemia virus - genetics</subject><subject>Murine leukemia virus</subject><issn>0305-1048</issn><issn>1362-4962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1982</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS0EKkvhxhUpJ06k9Uf8hcQBltIiLXABgXoxjjNpTRN7sZNV-9_jZVcrOPU0T_N-M7LnIfSc4BOCNTsNNp0WTU-4lA_QgjBB60YL-hAtMMO8JrhRj9GTnH9hTBrCmyN0JKhUDaUL9PNTHGKAu2qckw9QDTDfwOhttfFpzrUP3eygq6Z5jCm_rhK4OLY-2DBV6xT_QpArHyrrJr-Byl2nONqpNBJc-RjyU_Sot0OGZ_t6jL59OPu6vKhXX84_Lt-uatdINdWMiI5TLq0mFpPOitY62-ueAZcge6watVWKWKd7S1TXtw6kVq2gPSddy47Rm93e9dyO0DkIU7KDWSc_2nRnovXmfyf4a3MVN4ZRQbgu8y_38yn-niFPZvTZwTDYAHHORjItdUPFvSApp-dM4_tBzpRUkhXw1Q50KeacoD-8mmCzjdiUiLeamhJxwV_8-9MDvM-0-PXO93mC24Nt040RkkluLn5cmverd_r75_NLs2R_AE7ZtYQ</recordid><startdate>19820122</startdate><enddate>19820122</enddate><creator>van der Putten, Herman</creator><creator>Quint, Wim</creator><creator>Verma, Inder M.</creator><creator>Berns, Anton</creator><general>Oxford University Press</general><scope>BSCLL</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>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7T5</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19820122</creationdate><title>Moloney murine leukemia virus-induced tumors: recombinant proviruses in active chromatin regions</title><author>van der Putten, Herman ; 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The genetically transmitted sequences of M-MuLV, AKR-MuLV and the c-mos gene are all in DNase I resistant chromatin conformations in M-MuLV-induced tumors. Each M-MuLV-induced tumor contained at least one somatically acquired integrated recombinant MuLV genome that displayed two main characteristic features of active chromatin: a) a configuration hypersensitive to DNase I, and b) extensive hypomethylation. DNase I hypersensitive sites were mapped at the junction of cellular sequences and the 5′-viral large terminal repeat (LTR). Expression of a recombinant MuLV seems therefore to be a necessary feature to maintain the transformed state.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>6278422</pmid><doi>10.1093/nar/10.2.577</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Akr murine leukemia virus AKR murine leukemia virus - genetics Animals Cell Line Cell Nucleus - physiology Cell Transformation, Neoplastic Chromatin - physiology Deoxyribonuclease I Deoxyribonucleases DNA Restriction Enzymes DNA, Recombinant - analysis Endonucleases Leukemia, Experimental - microbiology Methylation Mice Mice, Inbred BALB C Moloney murine leukemia virus - genetics Murine leukemia virus |
title | Moloney murine leukemia virus-induced tumors: recombinant proviruses in active chromatin regions |
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