The dispersion of defective endogenous murine retroviral elements suggests retrotransposition-mediated amplification.

The dispersion of defective endogenous murine retroviral elements suggests retrotransposition-mediated amplification.
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有缺陷的内源性鼠逆转录病毒元件的分散表明逆转录转座介导的扩增。

DOI:
10.1089/dna.1991.10.713
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发表时间:
1991
影响因子:
3.1
通讯作者:
Wilson,MC
Wilson,MC
中科院分区:
生物学4区
文献类型:
--
作者:
Fredholm,M;Policastro,PF;Wilson,MC

文献摘要

被引文献

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在13个小鼠近交系和亚系中,研究了最初在129个品系小鼠中检测到的4种复制缺陷型内源性前病毒的分散情况,这些前病毒表现出gag、pol和denv基因区域的广泛缺失。使用探针的序列侧翼的整合位点在129只小鼠,独特的genomicEcoRI片段被分配到每一个的四个内源性前病毒元件。分析显示,这些前病毒元件中的某些存在于与菌株129密切相关的菌株中(即,菌株101和LP/J)和更远的相关菌株(即,菌株BALB/cJ、A/J和C3 H/HeJ)。在缺乏前病毒整合在特定位点的小鼠品系中,相应EcoRI基因组片段的大小和特征性Kpn I位点的缺失表明缺乏残留的孤立长末端重复。区分这些元素内存在的特定缺失的寡核苷酸探针的杂交在所有研究的菌株中的许多不同位点鉴定了额外的类似前病毒整合。这些数据表明,在近交系中发现的这些前病毒元件的多样化是通过新拷贝的整合产生的,而不是通过同源重组切除。此外,该结果与提供包装缺陷病毒RNA所必需的反式作用蛋白的其他内源性逆转录病毒一致。
The dispersion of four replication-defective endogenous proviruses, originally detected in 129 strain mice and shown to have extensive deletions ofgag, pol,andenvgene regions, was investigated in 13 inbred strains and substrains of mice. Using probes to sequences flanking the integration sites in 129 mice, unique genomicEcoRI fragments were assigned to each of the four endogenous proviral elements. Analyses revealed that certain of these proviral elements are present both in strains closely related to strain 129 (i.e.,strains 101 and LP/J) and in more distantly related strains (i.e.,strains BALB/cJ, A/J, and C3H/HeJ). In mouse strains lacking proviral integration at a particular locus, the size of the correspondingEcoRI genomic fragment and absence of a characteristicKpnI site indicated the lack of a residual solitary long terminal repeat. Hybridization of oligonucleotide probes that distinguish the specific deletions present within these elements identified additional analogous proviral integrations at many different sites in all strains investigated. These data indicate that the diversification of these proviral elements found in inbred strains is generated by integration of new copies, rather than excision through homologous recombination. Moreover, the results are consistent with other endogenous retroviruses providing thetrans-acting proteins necessary to package the defective viral RNA.