RNase III, Ribosome Biogenesis and Beyond

Lejars, Maxence; Kobayashi, Asaki; Hajnsdorf, Eliane

doi:10.3390/microorganisms9122608

Cited by 3 publications

(4 citation statements)

References 166 publications

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“…The observed changes regarding the translation-relevant factors could be a consequence of defects in rRNA processing associated with the loss of RNase III. It is well known that RNase III initiates maturation of the ribosomal RNAs encoded on the pre-rRNA transcript by an initial series of processing events, which are subsequently cleaved and trimmed by other ribonucleases [78–81][82]. In RNase III-deficient bacteria 30 S rRNA precursors (including 16S, 23S, 5S rRNA, and tRNA sequences) are produced [78–81][83].…”

Section: Discussionmentioning

confidence: 99%

“…The 30 S rRNA can be processed by alternative maturation pathways. However, this involves the formation and incorporation of not fully matured rRNAs (prRNAs) into the ribosomes, which alter their overall activity [84][82,85,86]. The RNase III-deficient bacteria may indirectly compensate for these alterations by the upregulation of translation factors.…”

Section: Discussionmentioning

confidence: 99%

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RNase-mediated reprogramming ofYersiniavirulence

Meyer,

Volk,

Salto

et al. 2024

Preprint

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RNA degradation is an essential process that allows bacteria to regulate gene expression and has emerged as an important mechanism for controlling virulence. However, the individual contributions of RNases in this process are mostly unknown. Here, we report that of 11 tested potential RNases of the intestinal pathogenYersinia pseudotuberculosis, two, the endoribonuclease RNase III and the exoribonuclease PNPase, repress the synthesis of the master virulence regulator LcrF. LcrF activates the expression of virulence plasmid genes encoding the type III secretion system (Ysc-T3SS) and its substrates (Yop proteins), that are employed to inhibit immune cell functions during infection. Loss of both RNases led to an increase inlcrFmRNA levels and stability. Our work indicates that PNPase exerts its influence via YopD, known to acceleratelcrFmRNA degradation. Loss of RNase III results in the downregulation of the CsrB and CsrC RNAs, leading to increased availability of active CsrA, which has previously been shown to enhancelcrFmRNA translation and stability. Other factors that influence the translation process and were found to be differentially expressed in the RNase III-deficient mutant could support this process.Transcriptomic profiling further revealed that Ysc-T3SS-mediated Yop secretion leads to global reprogramming of theYersiniatranscriptome with a massive shift of the expression from chromosomal towards virulence plasmid-encoded genes. A similar extensive transcriptional reprogramming was also observed in the RNase III-deficient mutant under non-secretion conditions. This illustrates that RNase III enables immediate coordination of virulence traits, such as Ysc-T3SS/Yops, with other functions required for host-pathogen interactions and survival in the host.Author SummaryBacterial pathogens need to quickly adapt the expression of virulence- and fitness-relevant traits in response to host defenses. PathogenicYersiniaspecies rapidly upregulate a type III secretion system (T3SS) to inject antiphagocytic and cell toxic effector proteins, namedYersiniaouter proteins (Yops), into attacking immune cells. For this purpose, they display complex and resilient regulatory mechanisms. At the post-transcriptional level, this is mediated by different RNA-binding regulators including YopD and CsrA, while the fate of mRNAs is balanced by ribonucleases. Here, we demonstrate that out of 11 tested putative RNases ofYersinia, two major RNases, the endoribonuclease RNase III, and the exonuclease and degradosome component PNPase play a crucial role in the activation of the Ysc-T3SS/Yop machinery. We show that they promote the decay of thelcrFmRNA encoding the common transcriptional activator LcrF of the Ysc-T3SS/Yop components. PNPase seems to act through the control of the effector YopD, known to promote the decay of thelcrFtranscript. In contrast, RNase III triggers processes that reducelcrFmRNA translation and stability, and involve CsrA.A transcriptome analysis further revealed that RNase III controls a series of events that include rapid and massive genetic reprogramming from mainly chromosomal-encoded genes to virulence-plasmid-encodedysc-T3SS/yopgenes. This control process does not only ensure immediate counter-measures during an immune attack, it also helps to overcome accompanying energetic and stress burdens and allows to rapidly readjust the genetic program after a successful defense.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

RNase-mediated reprogramming ofYersiniavirulence

Meyer,

Volk,

Salto

et al. 2024

Preprint

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“…However, we want to stress that two contra-indicatory points should be considered: first RNase III inhibition in E. coli increases the sensitivity to temperature and oxidative stress but also increases resistance to osmotic choc and favors biofilm formation, which may lead to adverse outcomes that could preclude clinical uses. Second, targeting RNase III will be difficult to limit to a single species and will affect a whole range of species due to the strong conservation of RNase III in bacteria (reviewed in [5]). Thus, the use of RNase III modulators would have to be carefully assessed in a clinical setting.…”

Section: Rnase III Is a General Stress Response Regulator And A Poten...mentioning

confidence: 99%

“…The endoribonuclease III (RNase III) domain, widely conserved in bacteria and eukaryotes, provides the specificity for double-stranded RNA (dsRNA) cleavage (reviewed in [5][6][7]). RNase III enzymes are involved in different processes, such as the repression and also activation of gene expression and maturation of stable and regulatory RNAs.…”

Section: Introductionmentioning

confidence: 99%

RNase III Participates in the Adaptation to Temperature Shock and Oxidative Stress in Escherichia coli

Lejars

Hajnsdorf

2022

Microorganisms

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Bacteria thrive in ever-changing environments by quickly remodeling their transcriptome and proteome via complex regulatory circuits. Regulation occurs at multiple steps, from the transcription of genes to the post-translational modification of proteins, via both protein and RNA regulators. At the post-transcriptional level, the RNA fate is balanced through the binding of ribosomes, chaperones and ribonucleases. We aim to decipher the role of the double-stranded-RNA-specific endoribonuclease RNase III and to evaluate its biological importance in the adaptation to modifications of the environment. The inactivation of RNase III affects a large number of genes and leads to several phenotypical defects, such as reduced thermotolerance in Escherichia coli. In this study, we reveal that RNase III inactivation leads to an increased sensitivity to temperature shock and oxidative stress. We further show that RNase III is important for the induction of the heat shock sigma factor RpoH and for the expression of the superoxide dismutase SodA.

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Bacterial RNase III: Targets and physiology

Lejars

Hajnsdorf

2024

Biochimie

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RNase III, Ribosome Biogenesis and Beyond

Cited by 3 publications

References 166 publications

RNase-mediated reprogramming ofYersiniavirulence

RNase-mediated reprogramming ofYersiniavirulence

RNase III Participates in the Adaptation to Temperature Shock and Oxidative Stress in Escherichia coli

Bacterial RNase III: Targets and physiology

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