INTRAGENOMIC SEQUENCE TRANSPOSITION IN MONKEYPOX VIRUS
INTRAGENOMIC SEQUENCE TRANSPOSITION IN MONKEYPOX VIRUS
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DOI：
10.1016/0042-6822(81)90495-5
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发表时间：
1981-01-01
期刊：
影响因子：
3.7
通讯作者：
OBIJESKI, JF
中科院分区：
文献类型：
--
作者：
ESPOSITO, JJ;CABRADILLA, CD;OBIJESKI, JF
构建出袋猴痘病毒哥本哈根株（COPE）的限制性内切DNA图谱（采用HindIII、SacI和SmaI）；从感染了cope的CAM（鸡绒毛膜尿囊膜）中随机抽取CpCR病毒1个出血性麻袋子代，两次麻袋纯化；2种白痘病毒，CpCW-N1和CpCW-N2，是从分离的cpcr感染的CAM中纯化出来的。COPE病毒和CpCR病毒的末端区DNA限制性片段摩尔浓度差异和DNA-DNA片段交叉杂交表明，COPE在CAM上复制时发生了DNA的自发转位，从而产生了CpCR病毒。COPE和CpCR的图谱是相同的，除了CpCR中的COPE 5兆道尔顿右端反向重复区由于从原5-Md左端重复区邻近的DNA中复制了8兆道尔顿（Md）的DNA片段而在CpCR中被放大。因此，在CpCR中，每个反向末端重复区为13 Md。COPE和CpCR在主基因组体和各自的右端重复区交界处的序列差异很明显。COPE病毒的DNA长度为125 Md， CpCR和CpCW-N1病毒的DNA长度均为133 Md，且与上述酶具有相同的限制性内切图谱。对CpCw-N2 DNA图谱（119 Md）的检查表明，CpCR右端倒置末端重复序列附近的14 Md序列被删除以产生该变体。
Restriction DNA maps were constructed (using HindIII, SacI and SmaI) for hemorrhagic-pock monkey poxvirus, Copenhagen strain (COPE); 1 hemorrhagic-pock progeny, CpCR virus, randomly selected from a COPE-infected CAM (chick chorioallantoic membrane) and twice pock purified; and 2 white-pock variants, CpCW-N1 and CpCW-N2 viruses, that were pock purified from separate CpCR-infected CAM. Terminal region DNA restriction fragment molarity differences and DNA-DNA fragment cross-hybridizations between COPE and CpCR viruses suggested that a spontaneous transposition of DNA occurred during COPE replication on CAM to produce CpCR virus. The maps of COPE and CpCR were identical except that the COPE 5 megadalton right-end inverted repeat region appeared enlarged in CpCR by the inverted insertion of a DNA segment of 8 megadaltons (Md) copied from DNA adjacent to the original 5-Md left-end repeat region. Thus, in CpCR each inverted terminal repeat region was 13 Md. Sequence differences between COPE and CpCR were apparent at the junction of the main genome body and the respective right-end repeat region of each. The DNA of COPE was 125 Md. The DNA of CpCR and CpCW-N1 viruses were each 133 Md and each had identical restriction maps with the enzymes above. Inspection of the map of CpCw-N2 DNA (119 Md) suggested that 14 Md of sequences adjacent to the CpCR right-end inverted terminal repeat were deleted to produce this variant.