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1
Distinct segments within the enhancer region collaborate to specify the type of leukemia induced by nondefective Friend and Moloney viruses.增强子区域内不同的片段协同作用,以确定由无缺陷的Friend病毒和莫洛尼病毒诱导的白血病类型。
J Virol. 1989 Jan;63(1):328-37. doi: 10.1128/JVI.63.1.328-337.1989.
2
Disease specificity of nondefective Friend and Moloney murine leukemia viruses is controlled by a small number of nucleotides.无缺陷型Friend和莫洛尼鼠白血病病毒的疾病特异性由少数核苷酸控制。
J Virol. 1987 Mar;61(3):693-700. doi: 10.1128/JVI.61.3.693-700.1987.
3
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J Virol. 1989 Oct;63(10):4210-23. doi: 10.1128/JVI.63.10.4210-4223.1989.
4
Sequences responsible for erythroid and lymphoid leukemia in the long terminal repeats of Friend-mink cell focus-forming and Moloney murine leukemia viruses.弗瑞德-貂细胞集落形成病毒和莫洛尼鼠白血病病毒长末端重复序列中负责红系和淋巴系白血病的序列。
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6
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7
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Role for the 3' end of the genome in determining disease specificity of Friend and Moloney murine leukemia viruses.基因组3'端在决定弗瑞德和莫洛尼鼠白血病病毒疾病特异性中的作用。
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A DNA element responsible for the different tissue specificities of Friend and Moloney retroviral enhancers.一种负责Friend和莫洛尼逆转录病毒增强子不同组织特异性的DNA元件。
J Virol. 1988 Feb;62(2):614-8. doi: 10.1128/JVI.62.2.614-618.1988.
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Mutation of the core or adjacent LVb elements of the Moloney murine leukemia virus enhancer alters disease specificity.莫洛尼鼠白血病病毒增强子核心或相邻的LVb元件发生突变会改变疾病特异性。
Genes Dev. 1990 Feb;4(2):233-42. doi: 10.1101/gad.4.2.233.

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本文引用的文献

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Recombinant genomes which express chloramphenicol acetyltransferase in mammalian cells.在哺乳动物细胞中表达氯霉素乙酰转移酶的重组基因组。
Mol Cell Biol. 1982 Sep;2(9):1044-51. doi: 10.1128/mcb.2.9.1044-1051.1982.
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Characterization of enhancer elements in the long terminal repeat of Moloney murine sarcoma virus.莫洛尼鼠肉瘤病毒长末端重复序列中增强子元件的特性分析。
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Structure of a cloned circular Moloney murine leukemia virus DNA molecule containing an inverted segment: implications for retrovirus integration.含有反向片段的克隆环状莫洛尼鼠白血病病毒DNA分子的结构:对逆转录病毒整合的影响
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Cell-specific expression controlled by the 5'-flanking region of insulin and chymotrypsin genes.由胰岛素基因和胰凝乳蛋白酶基因的5'侧翼区域控制的细胞特异性表达。
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Molecular analysis of the envelope gene and long terminal repeat of Friend mink cell focus-inducing virus: implications for the functions of these sequences.弗氏貂细胞灶性诱导病毒包膜基因和长末端重复序列的分子分析:这些序列功能的启示
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Role for the 3' end of the genome in determining disease specificity of Friend and Moloney murine leukemia viruses.基因组3'端在决定弗瑞德和莫洛尼鼠白血病病毒疾病特异性中的作用。
Proc Natl Acad Sci U S A. 1983 Jul;80(14):4408-11. doi: 10.1073/pnas.80.14.4408.
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Thymotropism of murine leukemia virus is conferred by its long terminal repeat.鼠白血病病毒的亲胸腺性由其长末端重复序列赋予。
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增强子区域内不同的片段协同作用,以确定由无缺陷的Friend病毒和莫洛尼病毒诱导的白血病类型。

Distinct segments within the enhancer region collaborate to specify the type of leukemia induced by nondefective Friend and Moloney viruses.

作者信息

Golemis E, Li Y, Fredrickson T N, Hartley J W, Hopkins N

机构信息

Biology Department, Massachusetts Institute of Technology, Cambridge 02139.

出版信息

J Virol. 1989 Jan;63(1):328-37. doi: 10.1128/JVI.63.1.328-337.1989.

DOI:10.1128/JVI.63.1.328-337.1989
PMID:2783259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC247688/
Abstract

The nondefective Moloney and Friend murine leukemia viruses induce T-cell lymphomas and erythroleukemias, respectively, after being injected into newborn NFS mice. In previous studies, we showed that the distinct disease specificities of the two viruses could be switched by exchanging a small segment, about 200 nucleotides in length, encompassing their enhancer regions. This segment included the direct repeat sequence and an adjacent GC-rich region of about 20 nucleotides defined in studies of Moloney murine sarcoma virus enhancer-promoter function (L. A. Laimins, P. Gruss, R. Pozzatti, and G. Khoury, J. Virol. 49:183-189, 1984). The direct repeats of Friend and Moloney viruses are identical in a central core sequence of 32 nucleotides but have sequence differences on either side of this core as well as in their GC-rich segments. To determine whether disease specificity resides in part or in all of the direct repeat and GC-rich region, we constructed recombinants between Friend and Moloney viruses within this segment and tested them for their disease-inducing phenotypes. We found that disease specificity, in particular the ability of Friend virus sequence to confer erythroleukemogenicity on Moloney virus, is encoded throughout the region in at least three separable segments: the 5' and 3' halves of the direct repeat and the GC-rich segment. When just one of these segments (either both 5' halves of the direct repeat, both 3' halves, or just the GC-rich segment) from Friend virus was substituted into a Moloney virus genome, it conferred only a negligible or low incidence of erythroleukemia (less than or equal to 5% to between 10 and 15%). Any two segments together were considerably more potent (35 to 95% erythroleukemia), with the most effective pair being the two halves of the direct repeat. Individual segments and pairs of segments were considerably more potent determinants when they were matched with a genome of the same origin. Thus, although sequences outside the enhancer region are minor determinants of disease specificity when the enhancer is derived entirely from either Friend or Moloney virus, they can play a significant role when the enhancer is of mixed origin. Some recombinant enhancers conferred a long latent period of disease induction. This was particularly striking when the 5' halves of each copy of the direct repeat sequence were derived from Moloney virus and the 3' halves were derived from Friend virus.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

将无缺陷的莫洛尼氏和弗瑞德氏鼠白血病病毒注射到新生的NFS小鼠体内后,它们分别诱发T细胞淋巴瘤和红白血病。在先前的研究中,我们发现,通过交换一小段长度约为200个核苷酸、包含其增强子区域的片段,这两种病毒不同的疾病特异性可以相互转换。该片段包括直接重复序列以及在莫洛尼氏鼠肉瘤病毒增强子-启动子功能研究中确定的一个约20个核苷酸的相邻富含GC的区域(L. A. 莱明斯、P. 格鲁斯、R. 波扎蒂和G. 库里,《病毒学杂志》49:183 - 189, 1984)。弗瑞德氏和莫洛尼氏病毒的直接重复序列在一个32个核苷酸的中央核心序列中是相同的,但在该核心序列两侧以及它们富含GC的片段中存在序列差异。为了确定疾病特异性是部分还是全部存在于直接重复序列和富含GC的区域,我们在该片段内构建了弗瑞德氏和莫洛尼氏病毒之间的重组体,并测试它们的疾病诱导表型。我们发现,疾病特异性,特别是弗瑞德氏病毒序列赋予莫洛尼氏病毒致红白血病性的能力,在整个区域至少由三个可分离的片段编码:直接重复序列的5'和3'半段以及富含GC的片段。当将弗瑞德氏病毒的这些片段之一(直接重复序列的两个5'半段、两个3'半段或仅富含GC的片段)替换到莫洛尼氏病毒基因组中时,它仅导致可忽略不计或低发生率的红白血病(小于或等于5%至10%至15%之间)。任意两个片段组合在一起则效力显著更高(35%至95%的红白血病发生率),最有效的组合是直接重复序列的两个半段。当单个片段和片段组合与同源基因组匹配时,它们是效力显著更高的决定因素。因此,尽管当增强子完全源自弗瑞德氏或莫洛尼氏病毒时,增强子区域之外的序列是疾病特异性的次要决定因素,但当增强子是混合来源时,它们可以发挥重要作用。一些重组增强子导致疾病诱导的潜伏期延长。当直接重复序列每个拷贝的5'半段源自莫洛尼氏病毒而3'半段源自弗瑞德氏病毒时,这种情况尤为明显。(摘要截断于400字)