Depletion of the Signal Recognition Particle Receptor Inactivates Ribosomes in Escherichia coli
Depletion of the Signal Recognition Particle Receptor Inactivates Ribosomes in Escherichia coli
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DOI：
10.1128/jb.00208-09
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发表时间：
2009-11-15
影响因子：
3.2
通讯作者：
Koch, Hans-Georg
中科院分区：
文献类型：
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作者：
Buerk, Jonas;Weiche, Benjamin;Koch, Hans-Georg
信号识别颗粒（SignalRecognitionParticle，SRP）依赖的蛋白质共翻译靶向细菌细胞质膜或真核生物内质网膜是大多数生物体的重要过程。真核细胞已显示通过（i）抑制核糖体生物合成，导致蛋白质合成减少，和（ii）通过增加蛋白质质量控制机制（如伴侣蛋白和蛋白酶）的表达来响应SRP途径的损伤。在目前的研究中，我们分析了大肠杆菌等细菌如何对细菌SRP受体FtsY的逐渐耗尽做出反应。我们使用无细胞转录/翻译系统的分析表明，FtsY耗竭抑制SRP依赖性和SRP非依赖性蛋白的翻译。这种合成缺陷是多方面反应的结果，包括核糖体失活蛋白核糖体调节因子（RMF）的上调。尽管E.大肠杆菌中的一些作用与真核细胞中观察到的一些作用非常相似，一个显著的区别是，大肠杆菌显然不会通过下调核糖体生物合成来降低蛋白质合成速率。相反，RMF的上调导致直接和可逆的翻译抑制。
The signal recognition particle (SRP)-dependent cotranslational targeting of proteins to the cytoplasmic membrane in bacteria or the endoplasmic reticulum membrane in eukaryotes is an essential process in most living organisms. Eukaryotic cells have been shown to respond to an impairment of the SRP pathway by (i) repressing ribosome biogenesis, resulting in decreased protein synthesis, and (ii) by increasing the expression of protein quality control mechanisms, such as chaperones and proteases. In the current study, we have analyzed how bacteria like Escherichia coli respond to a gradual depletion of FtsY, the bacterial SRP receptor. Our analyses using cell-free transcription/translation systems showed that FtsY depletion inhibits the translation of both SRP-dependent and SRP-independent proteins. This synthesis defect is the result of a multifaceted response that includes the upregulation of the ribosome-inactivating protein ribosome modulation factor (RMF). Although the consequences of these responses in E. coli are very similar to some of the effects also observed in eukaryotic cells, one striking difference is that E. coli obviously does not reduce the rate of protein synthesis by downregulating ribosome biogenesis. Instead, the upregulation of RMF leads to a direct and reversible inhibition of translation.