《生命科学》 2010, 22(3): 237-239
摘 要：
摘 要：真核生物在漫长的进化繁衍过程中，一直处在抵御转座元件对基因组侵害的“斗争”中。在过去的十多年中，越来越多的证据指明，小分子RNA扮演了这样一个抵御转座子侵袭的角色。尽管这种抵御侵害的策略对于不同物种各具特点，但它们都呈现出惊人相似的共同特征。基本上，所有的机制都包含三个组成部分：首先，转座元件促使产生小分子RNA，在某些物种中主要是Piwi-interacting RNAs，而在其他物种中主要是small interfering RNAs；第二，作用于活跃转座子的小分子RNA通过RNA依赖性RNA聚合酶或切割机制进行扩增；第三，这些小分子RNA与含有Argonaute蛋白或Piwi蛋白的效应复合物相结合，从而作用于目标转座子的转录本，实现转录后沉默，或作用于目标转座子DNA，抑制染色质修饰和DNA甲基化。这些属性特征构成了一个限制由转座元件活动所造成的严重后果的系统，从而防止转座子侵袭所带来的突变积累，基因表达谱的改变，以及生殖腺发育不良和不育。
关键词：piRNAs；转座子抵御；染色体修饰；DNA甲基化
Abstract:
Abstract: 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 posttranscriptional 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.
Key words: small RNA; piRNAs; transposon defense; chromatin modificatin; DNA methylation
