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细菌 RNA 连接酶 RtcB 在释放抗生素压力后,加速了断裂 rRNA 的修复过程。

The bacterial RNA ligase RtcB accelerates the repair process of fragmented rRNA upon releasing the antibiotic stress.

机构信息

CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China.

University of Chinese Academy of Sciences, Beijing, 100190, China.

出版信息

Sci China Life Sci. 2020 Feb;63(2):251-258. doi: 10.1007/s11427-018-9405-y. Epub 2019 Jun 26.

Abstract

RtcB, a highly conserved RNA ligase, is found in all three domains of life, and demonstrated to be an essential tRNA splicing component in archaea and metazoans. However, the biological functions of RtcB in bacteria, where there is no splicing, remains to be clarified. We first performed bioinformatics analysis which revealed highly conserved structures and presumably conserved functions of RtcB in bacteria. However, its orthologs only occur in ∼ 0.5% of bacterial species across diverse phyla with significant signals of frequent horizontal transfer, highlighting its non-essential role in bacteria. Next, by constructing an rtcB-knockout strain, we find that the removal of antibiotic stress induces a significant impact on rtcB expression in wild-type strain, and furthermore the depletion of RtcB (ARtcB strain) delays the recovery process. Our transcriptomic analysis, comprising the 3'-end labeling of RNAs, highlights a significant increase in unmapped reads and cleaved rRNAs in the Δ RtcB strain, particularly during recovery. Our observations suggest that the conserved RNA ligase RtcB, repairs damaged rRNAs following stress, which potentially saves energy and accelerates recovery of its host. We propose that acquisition of RtcB by diverse bacterial taxa provides a competitive advantage under stressful conditions.

摘要

RtcB 是一种高度保守的 RNA 连接酶,存在于所有三个生命领域,并且被证明是古菌和后生动物中 tRNA 剪接的必需组成部分。然而,RtcB 在细菌中的生物学功能,即没有剪接,仍需阐明。我们首先进行了生物信息学分析,揭示了 RtcB 在细菌中高度保守的结构和可能保守的功能。然而,其同源物仅存在于不同门的细菌物种中约 0.5%,并且存在频繁水平转移的显著信号,突出了其在细菌中的非必需作用。接下来,通过构建 rtcB 敲除菌株,我们发现抗生素应激的消除对野生型菌株中 rtcB 表达有显著影响,并且 RtcB 的耗尽(ARtcB 菌株)会延迟恢复过程。我们的转录组分析,包括 RNA 的 3'-末端标记,突出显示在 Δ RtcB 菌株中未映射读数和切割 rRNA 的显著增加,特别是在恢复过程中。我们的观察表明,保守的 RNA 连接酶 RtcB 在应激后修复受损的 rRNA,这可能节省能量并加速其宿主的恢复。我们提出,不同细菌类群获得 RtcB 可以在应激条件下提供竞争优势。

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