Riboswitches are thought generally to function by modulating transcription elongation or translation initiation. In rare instances, ligand binding to a riboswitch has been found to alter the rate of RNA degradation by directly stimulating or inhibiting nearby cleavage. Here, we show that guanidine-induced pseudoknot formation by the aptamer domain of a guanidine III riboswitch from Legionella pneumophila has a different effect, stabilizing mRNA by protecting distal cleavage sites en masse from ribonuclease attack. It does so by creating a coaxially base-paired obstacle that impedes scanning from a monophosphorylated 5′ end to those sites by the regulatory endonuclease RNase E. Ligand binding by other riboswitch aptamers peripheral to the path traveled by RNase E does not inhibit distal cleavage. These findings reveal that a riboswitch aptamer can function independently of any overlapping expression platform to regulate gene expression by acting directly to prolong mRNA longevity in response to ligand binding.

核糖开关通常被认为通过调节转录延伸或翻译起始来发挥作用。在极少数情况下，已发现与核糖开关结合的配体通过直接刺激或抑制附近的切割来改变 RNA 降解的速率。这里，我们显示通过从胍III核糖开关的适体结构域胍诱导的假结形成嗜肺军团杆菌具有不同的效果，通过保护远侧切割位点的mRNA稳定集体从核糖核酸酶攻击。它通过创建一个同轴碱基配对障碍物来阻止调节性核酸内切酶 RNase E 从单磷酸化的 5' 端扫描到这些位点。配体与 RNase E 行进路径外围的其他核糖开关适体结合不会抑制远端切割。这些发现表明，核糖开关适体可以独立于任何重叠表达平台发挥作用，通过直接作用于响应配体结合而延长 mRNA 寿命来调节基因表达。