Girard Angélique, Hannon Gregory J
Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.
Trends Cell Biol. 2008 Mar;18(3):136-48. doi: 10.1016/j.tcb.2008.01.004. Epub 2008 Feb 20.
Eukaryotes are engaged in a constant struggle against transposable elements, which have invaded and profoundly shaped their genomes. Over the past decade, a growing body of evidence has pointed to a role for small RNAs in transposon defense. Although the strategies used in different organisms vary in their details, they have strikingly similar general properties. Basically, all mechanisms consist of three components. First, transposon detection prompts the production of small RNAs, which are Piwi-interacting RNAs in some organisms and small interfering RNAs in others. Second, the population of small RNAs targeting active transposons is amplified through an RNA-dependent RNA polymerase-based or Slicer-based mechanism. Third, small RNAs are incorporated into Argonaute- or Piwi-containing effector complexes, which target transposon transcripts for post-transcriptional silencing and/or target transposon DNA for repressive chromatin modification and DNA methylation. These properties produce robust systems that limit the catastrophic consequences of transposon mobilization, which can result in the accumulation of deleterious mutations, changes in gene expression patterns, and conditions such as gonadal hypotrophy and sterility.
真核生物一直在与转座元件进行持续斗争,转座元件已经侵入并深刻塑造了它们的基因组。在过去十年中,越来越多的证据表明小RNA在转座子防御中发挥作用。尽管不同生物体中使用的策略在细节上有所不同,但它们具有惊人相似的一般特性。基本上,所有机制都由三个部分组成。首先,转座子检测促使小RNA的产生,在某些生物体中是Piwi相互作用RNA,在其他生物体中是小干扰RNA。其次,靶向活跃转座子的小RNA群体通过基于RNA依赖的RNA聚合酶或基于核酸酶的机制进行扩增。第三,小RNA被整合到含有Argonaute或Piwi的效应复合物中,这些复合物靶向转座子转录本进行转录后沉默和/或靶向转座子DNA进行抑制性染色质修饰和DNA甲基化。这些特性产生了强大的系统,限制了转座子移动的灾难性后果,转座子移动可能导致有害突变的积累、基因表达模式的改变以及诸如性腺发育不全和不育等情况。