scholarly journals RNase III-mediated processing of a trans-acting bacterial sRNA and its cis-encoded antagonist

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Sarah Lauren Svensson ◽  
Cynthia Mira Sharma

Bacterial small RNAs (sRNAs) are important post-transcriptional regulators in stress responses and virulence. They can be derived from an expanding list of genomic contexts, such as processing from parental transcripts by RNase E. The role of RNase III in sRNA biogenesis is less well understood despite its well-known roles in rRNA processing, RNA decay, and cleavage of sRNA-mRNA duplexes. Here, we show that RNase III processes a pair of cis-encoded sRNAs (CJnc190 and CJnc180) of the foodborne pathogen Campylobacter jejuni. While CJnc180 processing by RNase III requires CJnc190, In contrast, RNase III processes CJnc190 independent of CJnc180 via cleavage of an intramolecular duplex. We also show that CJnc190 directly represses translation of the colonization factor PtmG by targeting a G-rich ribosome binding site, and uncover that CJnc180 is a cis-acting antagonist of CJnc190, indirectly affecting ptmG regulation. Our study highlights a role for RNase III in sRNA biogenesis and adds cis-encoded RNAs to the expanding diversity of transcripts that antagonize bacterial sRNAs.

2021 ◽  
Author(s):  
Sarah L Svensson ◽  
Cynthia M. Sharma

Small RNAs (sRNAs) are emerging as important and diverse post-transcriptional gene expression regulators in bacterial stress responses and virulence. While originally identified mainly in intergenic regions, genome-wide approaches have revealed sRNAs encoded in diverse contexts, such as processed from parental transcripts by RNase E. Despite its well-known roles in rRNA processing, RNA decay, cleavage of sRNA-mRNA duplexes, the role of RNase III in sRNA biogenesis is less well understood. Here, we show that a pair of cis-encoded sRNAs (CJnc190 and CJnc180) are processed by RNase III in the foodborne pathogen Campylobacter jejuni. While CJnc180 processing requires CJnc190, RNase III cleaves an intramolecular duplex in CJnc190, independent of CJnc180. Moreover, we demonstrate that CJnc190 directly represses translation of the colonization factor PtmG by binding its G-rich ribosome binding site, and show that CJnc180 is a cis-acting antagonist of CJnc190, thereby indirectly affecting ptmG regulation. Our results expand the diversity of known genomic locations of bacterial sRNA sponges and highlight a role for bacterial RNase III that parallels miRNA processing by related eukaryotic Dicer and Drosha.


Plant Gene ◽  
2017 ◽  
Vol 11 ◽  
pp. 180-189 ◽  
Author(s):  
Sagar Banerjee ◽  
Anil Sirohi ◽  
Abid A. Ansari ◽  
Sarvajeet Singh Gill

2010 ◽  
Vol 192 (21) ◽  
pp. 5559-5571 ◽  
Author(s):  
Colleen A. McCullen ◽  
Jihane N. Benhammou ◽  
Nadim Majdalani ◽  
Susan Gottesman

ABSTRACT Small noncoding RNAs (sRNAs) regulate gene expression in Escherichia coli by base pairing with mRNAs and modulating translation and mRNA stability. The sRNAs DsrA and RprA stimulate the translation of the stress response transcription factor RpoS by base pairing with the 5′ untranslated region of the rpoS mRNA. In the present study, we found that the rpoS mRNA was unstable in the absence of DsrA and RprA and that expression of these sRNAs increased both the accumulation and the half-life of the rpoS mRNA. Mutations in dsrA, rprA, or rpoS that disrupt the predicted pairing sequences and reduce translation of RpoS also destabilize the rpoS mRNA. We found that the rpoS mRNA accumulates in an RNase E mutant strain in the absence of sRNA expression and, therefore, is degraded by an RNase E-mediated mechanism. DsrA expression is required, however, for maximal translation even when rpoS mRNA is abundant. This suggests that DsrA protects rpoS mRNA from degradation by RNase E and that DsrA has a further activity in stimulating RpoS protein synthesis. rpoS mRNA is subject to degradation by an additional pathway, mediated by RNase III, which, in contrast to the RNase E-mediated pathway, occurs in the presence and absence of DsrA or RprA. rpoS mRNA and RpoS protein levels are increased in an RNase III mutant strain with or without the sRNAs, suggesting that the role of RNase III in this context is to reduce the translation of RpoS even when the sRNAs are acting to stimulate translation.


mSphere ◽  
2021 ◽  
Vol 6 (4) ◽  
Author(s):  
Gyles Ifill ◽  
Travis Blimkie ◽  
Amy Huei-Yi Lee ◽  
George A. Mackie ◽  
Qing Chen ◽  
...  

Noncoding, regulatory RNAs in bacterial pathogens are critical components required for rapid changes in gene expression profiles. However, little is known about the role of regulatory RNAs in the growth and pathogenesis of Bordetella pertussis .


2018 ◽  
Vol 28 (4) ◽  
pp. 179-182
Author(s):  
Tatsuaki  Kurata ◽  
Shinobu Nakanishi ◽  
Masayuki Hashimoto ◽  
Masato Taoka ◽  
Toshiaki Isobe ◽  
...  

<i>Escherichia coli</i> 16S, 23S, and 5S ribosomal RNAs (rRNAs) are transcribed as a single primary transcript, which is subsequently processed into mature rRNAs by several RNases. Three RNases (RNase III, RNase E, and RNase G) were reported to function in processing the 5′-leader of precursor 16S rRNA (pre-16S rRNA). Previously, we showed that a novel essential YqgF is involved in that processing. Here we investigated the ribosome subunits of the <i>yqgF</i><sup>ts</sup> mutant by LC-MS/MS. The mutant ribosome had decreased copy numbers of ribosome protein S1, suggesting that the <i>yqgF</i> gene enables incorporation of ribosomal protein S1 into ribosome by processing of the 5′-end of pre-16S rRNA. The ribosome protein S1 is essential for translation in <i>E. coli</i>; therefore, our results suggest that YqgF converts the inactive form of newly synthesized ribosome into the active form at the final step of ribosome assembly.


2018 ◽  
Author(s):  
Yusuke Himeoka ◽  
Namiko Mitarai

AbstractIn type-I toxin-antitoxin (TA) systems, the action of growth-inhibiting toxin proteins is counteracted by the antitoxin small RNAs (sRNAs) that prevent the translation of toxin messenger RNAs (mRNAs). When a TA module is encoded on a plasmid, the short lifetime of antitoxin sRNA compared to toxin mRNAs mediates post-segregational killing (PSK) that contribute the plasmid maintenance, while some of the chromosomal encoded TA loci have been reported to contribute to persister formation in response to a specific upstream signal. Some of the well studied type-I TA systems such ashok/sokare known to have a rather complex regulatory mechanism. Transcribed full-length toxin mRNAs fold such that the ribosome binding site is not accessible and hence cannot be translated. The mRNAs are slowly processed by RNases, and the truncated mRNAs can be either translated or bound by antitoxin sRNA to be quickly degraded. We analyze the role of this extra processing by a mathematical model. We first consider the PSK scenario, and demonstrate that the extra processing compatibly ensures the high toxin expression upon complete plasmid loss, without inducing toxin expression upon acquisition of a plasmid or decrease of plasmid number to a non-zero number. We further show that the extra processing help filtering the transcription noise, avoiding random activation of toxins in transcriptionally regulated TA systems as seen in chromosomal ones. The present model highlights impacts of the slow processing reaction, offering insights on why the slow processing reactions are commonly identified in multiple type-I TA systems.


Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1465 ◽  
Author(s):  
Christiaan J. Stavast ◽  
Stefan J. Erkeland

MicroRNAs (miRNAs) are critical regulators of gene expression. As miRNAs are frequently deregulated in many human diseases, including cancer and immunological disorders, it is important to understand their biological functions. Typically, miRNA-encoding genes are transcribed by RNA Polymerase II and generate primary transcripts that are processed by RNase III-endonucleases DROSHA and DICER into small RNAs of approximately 21 nucleotides. All miRNAs are loaded into Argonaute proteins in the RNA-induced silencing complex (RISC) and act as post-transcriptional regulators by binding to the 3′- untranslated region (UTR) of mRNAs. This seed-dependent miRNA binding inhibits the translation and/or promotes the degradation of mRNA targets. Surprisingly, recent data presents evidence for a target-mediated decay mechanism that controls the level of specific miRNAs. In addition, several non-canonical miRNA-containing genes have been recently described and unexpected functions of miRNAs have been identified. For instance, several miRNAs are located in the nucleus, where they are involved in the transcriptional activation or silencing of target genes. These epigenetic modifiers are recruited by RISC and guided by miRNAs to specific loci in the genome. Here, we will review non-canonical aspects of miRNA biology, including novel regulators of miRNA expression and functions of miRNAs in the nucleus.


Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 99
Author(s):  
Shweta Devi ◽  
Vijay Kumar ◽  
Sandeep Kumar Singh ◽  
Ashish Kant Dubey ◽  
Jong-Joo Kim

Neurodegenerative disorders, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), are the most concerning disorders due to the lack of effective therapy and dramatic rise in affected cases. Although these disorders have diverse clinical manifestations, they all share a common cellular stress response. These cellular stress responses including neuroinflammation, oxidative stress, proteotoxicity, and endoplasmic reticulum (ER)-stress, which combats with stress conditions. Environmental stress/toxicity weakened the cellular stress response which results in cell damage. Small molecules, such as flavonoids, could reduce cellular stress and have gained much attention in recent years. Evidence has shown the potential use of flavonoids in several ways, such as antioxidants, anti-inflammatory, and anti-apoptotic, yet their mechanism is still elusive. This review provides an insight into the potential role of flavonoids against cellular stress response that prevent the pathogenesis of neurodegenerative disorders.


Sign in / Sign up

Export Citation Format

Share Document