Desmarais Erick, Belkhir Khalid, Garza John Carlos, Bonhomme François
Laboratoire Génome, Populations, Interactions, Adaptation, UMR5171 CNRS-IFREMER, Université Montpellier II, CC-G3 Montpellier Place E. Bataillon 34095, France.
J Mol Evol. 2006 Nov;63(5):662-75. doi: 10.1007/s00239-005-0301-2. Epub 2006 Oct 29.
Solitary LTR loci are the predominant form of LTR retrotransposons in most eukaryotic genomes. They originate from recombination between the two LTRs of an ancestral retrovirus and are therefore incapable of transposition. Despite this inactivity, they appear to have a substantial impact on the host genome. Here we use the murine RMER10 LTR family as an example to describe how such elements can reshape regions of the genome through multiple mutations on an evolutionary time scale. Specifically, we use phylogenetic analysis of multiple copies of RMER10 in rodent species, as well as comparisons of orthologous pairs in mouse and rat, to argue that insertions of members of this family have locally induced the emergence of tandem repeat loci as well as many indels. Analysis of structural aspects of these sequences (secondary structures and transcription factors signals) may explain why RMER10 can become endogenous "mutagenic" factors through induction of replication fork blockages and/or error-prone repair of aberrant DNA structures. This hypothesis is also consistent with features of other interspersed repeated elements.
在大多数真核生物基因组中，孤立的长末端重复序列（LTR）位点是LTR逆转录转座子的主要形式。它们起源于祖先逆转录病毒两个LTR之间的重组，因此不能进行转座。尽管不具有活性，但它们似乎对宿主基因组有重大影响。在这里，我们以小鼠RMER10 LTR家族为例，描述这类元件如何在进化时间尺度上通过多次突变重塑基因组区域。具体而言，我们对啮齿动物物种中多个RMER10拷贝进行系统发育分析，以及对小鼠和大鼠的直系同源对进行比较，以证明该家族成员的插入在局部诱导了串联重复序列位点以及许多插入缺失的出现。对这些序列结构方面（二级结构和转录因子信号）的分析可能解释了为什么RMER10可以通过诱导复制叉阻滞和/或对异常DNA结构进行易错修复而成为内源性“诱变”因子。这一假设也与其他散在重复元件的特征一致。
