从序列比较推断螺旋体基因组变异与spv1样病毒DNA相关的机制

U Melcher, Y Sha, F Ye, J Fletcher
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引用次数: 24

摘要

柑橘螺旋体病毒株的基因组在其进化过程中经常重排,部分原因是螺旋体病毒的多个整合序列。为了更好地理解病毒序列在基因组进化中的作用,我们检测了柑橘染色体中可用的病毒样元件的核苷酸序列。螺旋体病毒SpV1-C74 DNA的整合与非整合序列的比较表明,它是属于插入序列(IS3)家族成员的环状转位中间体的封装形式。一个SpV1-C74病毒DNA片段被鉴定为中断DNA腺嘌呤修饰甲基化酶基因的残余。病毒DNA插入SpV1-R8A2 B DNA具有被位点特异性重组系统内部删除的特征。同源重组可能导致病毒DNA中的一些缺失。同源重组事件之间的部分病毒DNA插入和类似的染色体序列推断。来自spv1样C4开放阅读框(orf)的分散序列被确定参与了复杂的缺失-反转事件。因此,spv1样序列可能通过插入活性基因,破坏其功能,为位点特异性重组提供靶标,介导其整合位点附近序列的缺失,以及为同源重组提供靶标,从而改变螺原体基因组,从而导致倒位。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanisms of spiroplasma genome variation associated with SpV1-like viral DNA inferred from sequence comparisons.

Genomes of Spiroplasma citri strains have rearranged frequently during their evolution, partly due to multiple integrated sequences of spiroplasma viruses. To understand better the role of viral sequences in genome evolution, we examined available nucleotide sequences of viruslike elements in the S. citri chromosome. Comparison of integrated and nonintegrated sequences of spiroplasma virus SpV1-C74 DNA suggested that it is an encapsidated form of the circular transposition intermediate belonging to an insertion sequence (IS3) family member. One SpV1-C74 viral DNA fragment was identified as interrupting the remains of a DNA adenine modification methylase gene. A viral DNA insertion of SpV1-R8A2 B DNA had hallmarks of having suffered an internal deletion by a site-specific recombination system. Homologous recombination likely was responsible for several deletions within viral DNA. A homologous recombination event was inferred between part of a viral DNA insertion and a similar chromosomal sequence. Dispersed sequences from SpV1-like C4 open reading frames (ORFs) were identified as involved in a complex deletion-inversion event. Thus, SpV1-like sequences likely have altered spiroplasma genomes by inserting within active genes, destroying their function, by providing targets for site-specific recombination, by mediating deletions of sequences adjacent to their integration sites, and by providing targets for homologous recombination, leading to inversions.

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