TnpB nucleases represent the evolutionary precursors to CRISPR-Cas12 and are widespread in all domains of life. IS605-family TnpB homologs function as programmable RNA-guided homing endonucleases in bacteria, driving transposon maintenance through DNA double-strand break–stimulated homologous recombination. In this work, we uncovered molecular mechanisms of the transposition life cycle of IS607-family elements that, notably, also encode group I introns. We identified specific features for a candidate “IStron” from Clostridium botulinum that allow the element to carefully control the relative levels of spliced products versus functional guide RNAs. Our results suggest that IStron transcripts evolved an ability to balance competing and mutually exclusive activities that promote selfish transposon spread while limiting adverse fitness costs on the host. Collectively, this work highlights molecular innovation in the multifunctional utility of transposon-encoded noncoding RNAs.

中文翻译：

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转座子编码的内含子和引导RNA之间的拮抗冲突


TnpB 核酸酶代表了 CRISPR-Cas12 的进化前身，广泛存在于生命的各个领域。 IS605 家族 TnpB 同源物在细菌中充当可编程 RNA 引导的归巢核酸内切酶，通过 DNA 双链断裂刺激的同源重组驱动转座子维持。在这项工作中，我们揭示了 IS607 家族元件转座生命周期的分子机制，值得注意的是，这些元件也编码 I 组内含子。我们确定了候选“IStron”的具体特征肉毒杆菌允许该元件仔细控制剪接产物与功能指导RNA的相对水平。我们的结果表明，IStron 转录本进化出了一种平衡竞争和相互排斥活动的能力，这些活动促进自私的转座子传播，同时限制宿主的不利健康成本。总的来说，这项工作突出了转座子编码的非编码 RNA 多功能用途的分子创新。