scholarly journals A Novel Fur- and Iron-Regulated Small RNA, NrrF, Is Required for Indirect Fur-Mediated Regulation of the sdhA and sdhC Genes in Neisseria meningitidis

2007 ◽  
Vol 189 (10) ◽  
pp. 3686-3694 ◽  
Author(s):  
J. R. Mellin ◽  
Sulip Goswami ◽  
Susan Grogan ◽  
Brian Tjaden ◽  
Caroline A. Genco
Keyword(s):  
Neisseria Meningitidis ◽  
Gene Transcription ◽  
Small Rna ◽  
Iron Homeostasis ◽  
A Priori ◽  
Regulatory Rna ◽  
Rna Molecules ◽  
Small Regulatory Rna ◽  
Regulator Protein ◽  
Microarray Studies

ABSTRACT Iron is both essential for bacterial growth and toxic at higher concentrations; thus, iron homeostasis is tightly regulated. In Neisseria meningitidis the majority of iron-responsive gene regulation is mediated by the ferric uptake regulator protein (Fur), a protein classically defined as a transcriptional repressor. Recently, however, microarray studies have identified a number of genes in N. meningitidis that are iron and Fur activated, demonstrating a new role for Fur as a transcriptional activator. Since Fur has been shown to indirectly activate gene transcription through the repression of small regulatory RNA molecules in other organisms, we hypothesized that a similar mechanism could account for Fur-dependent, iron-activated gene transcription in N. meningitidis. In this study, we used a bioinformatics approach to screen for the presence of Fur-regulated small RNA molecules in N. meningitidis MC58. This screen identified one small RNA, herein named NrrF (for neisserial regulatory RNA responsive to iron [Fe]), which was demonstrated to be both iron responsive and Fur regulated and which has a well-conserved orthologue in N. gonorrhoeae. In addition, this screen identified a number of other likely, novel small RNA transcripts. Lastly, we utilized a new bioinformatics approach to predict regulatory targets of the NrrF small RNA. This analysis led to the identification of the sdhA and sdhC genes, which were subsequently demonstrated to be under NrrF regulation in an nrrF mutant. This study is the first report of small RNAs in N. meningitidis and the first to use a bioinformatics approach to identify, a priori, regulatory targets of a small RNA.

scholarly journals A Versatile Method to Design Stem-Loop Primer-Based Quantitative PCR Assays for Detecting Small Regulatory RNA Molecules

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e55168 ◽  
Author(s):  
Zsolt Czimmerer ◽  
Julianna Hulvely ◽  
Zoltan Simandi ◽  
Eva Varallyay ◽  
Zoltan Havelda ◽  
...  
Keyword(s):  
Quantitative Pcr ◽  
Regulatory Rna ◽  
Stem Loop ◽  
Rna Molecules ◽  
Loop Primer ◽  
Small Regulatory Rna ◽  
Pcr Assays

scholarly journals Elucidating the Small Regulatory RNA Repertoire of the Sea Anemone Anemonia viridis Based on Whole Genome and Small RNA Sequencing

2018 ◽  
Vol 10 (2) ◽  
pp. 410-426 ◽  
Author(s):  
Ilona Urbarova ◽  
Hardip Patel ◽  
Sylvain Forêt ◽  
Bård Ove Karlsen ◽  
Tor Erik Jørgensen ◽  
...  
Keyword(s):  
Rna Sequencing ◽  
Small Rna ◽  
Sea Anemone ◽  
Small Rna Sequencing ◽  
Whole Genome ◽  
Regulatory Rna ◽  
Small Regulatory Rna ◽  
Anemonia Viridis

scholarly journals Recognition of the small regulatory RNA RydC by the bacterial Hfq protein

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Daniela Dimastrogiovanni ◽  
Kathrin S Fröhlich ◽  
Katarzyna J Bandyra ◽  
Heather A Bruce ◽  
Susann Hohensee ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Small Rna ◽  
Small Rnas ◽  
Regulatory Networks ◽  
Target Recognition ◽  
Seed Region ◽  
Regulatory Rna ◽  
E Coli ◽  
Small Regulatory Rna ◽  
Rna Complex

Bacterial small RNAs (sRNAs) are key elements of regulatory networks that modulate gene expression. The sRNA RydC of Salmonella sp. and Escherichia coli is an example of this class of riboregulators. Like many other sRNAs, RydC bears a ‘seed’ region that recognises specific transcripts through base-pairing, and its activities are facilitated by the RNA chaperone Hfq. The crystal structure of RydC in complex with E. coli Hfq at a 3.48 Å resolution illuminates how the protein interacts with and presents the sRNA for target recognition. Consolidating the protein–RNA complex is a host of distributed interactions mediated by the natively unstructured termini of Hfq. Based on the structure and other data, we propose a model for a dynamic effector complex comprising Hfq, small RNA, and the cognate mRNA target.

scholarly journals A small RNA controls bacterial resistance to gentamicin during iron starvation

2018 ◽  
Author(s):  
Sylvia Chareyre ◽  
Frédéric Barras ◽  
Pierre Mandin
Keyword(s):  
Escherichia Coli ◽  
Iron Homeostasis ◽  
Bacterial Resistance ◽  
Proton Motive Force ◽  
Motive Force ◽  
Regulatory Rna ◽  
Iron Starvation ◽  
Phenotypic Resistance ◽  
Respiratory Complexes ◽  
Small Regulatory Rna

ABSTRACTPhenotypic resistance describes a bacterial population that becomes transiently resistant to an antibiotic without requiring a genetic change. We here investigated the role of the small regulatory RNA (sRNA) RyhB, a key contributor to iron homeostasis, in the phenotypic resistance ofEscherichia colito various classes of antibiotics. We found that RyhB induces resistance to gentamicin, an aminoglycoside that targets the ribosome, when iron is scarce. RyhB induced resistance is due to the inhibition of respiratory complexes Nuo and Sdh activities. These complexes, which contain numerous Fe-S clusters, are crucial for generating a proton motive force (pmf) that allows gentamicin uptake. RyhB directly represses the expression ofnuoandsdhoperons by binding to their mRNAs, thereby inhibiting their translation. Indirectly, RyhB also inhibits the maturation of Nuo and Sdh by repressing synthesis of the Isc Fe-S biogenesis machinery. Notably, our study identifiesnuoas a new direct RyhB target and shows that respiratory complexes activity levels are predictive of the bacterial sensitivity to gentamicin. Altogether, these results unveil a new role for RyhB in the adaptation to antibiotic stress, an unprecedented consequences of its role in iron starvation stress response.AUTHOR’S SUMMARYUnderstanding the mechanisms at work behind bacterial antibiotic resistance has become a major health issue in the face of the antibiotics crisis. Here, we show that RyhB, a bacterial small regulatory RNA, induces resistance ofEscherichia colito the antibiotic gentamicin when iron is scarce, an environmental situation prevalent during host-pathogen interactions. This resistance is due to RyhB repression of the synthesis and post-translational maturation of the respiratory complexes Nuo and Sdh. These complexes are crucial in producing the proton motive force that allows uptake of the antibiotics in the cell. Altogether, these data point out to a major role for RyhB in escaping antibacterial action.

Small Regulatory Molecules Acting Big in Cancer: Potential Role of Mito-miRs in Cancer

2019 ◽  
Vol 19 (9) ◽  
pp. 621-631 ◽  
Author(s):  
Praveen Sharma ◽  
Bharat ◽  
Nilambra Dogra ◽  
Sandeep Singh
Keyword(s):  
Gene Expression ◽  
Mitochondrial Genome ◽  
Potential Role ◽  
Regulatory Rna ◽  
Rna Molecules ◽  
Small Regulatory Rna ◽  
Physiological Processes ◽  
Current Review ◽  
Posttranscriptional Level

MicroRNAs [miRNAs] are short, non-coding, single stranded RNA molecules regulating gene expression of their targets at the posttranscriptional level by either degrading mRNA or by inhibiting translation. Previously, miRNAs have been reported to be present inside the mitochondria and these miRNAs have been termed as mito-miRs. Origin of these mito-miRs may either be from mitochondrial genome or import from nucleus. The second class of mito-miRs makes it important to unravel the involvement of miRNAs in crosstalk between nucleus and mitochondria. Since miRNAs are involved in various physiological processes, their deregulation is often associated with disease progression, including cancer. The current review focuses on the involvement of miRNAs in different mitochondrial mediated processes. It also highlights the importance of exploring the interaction of miRNAs with mitochondrial genome, which may lead to the development of small regulatory RNA based therapeutic options.

scholarly journals Farnesylated heat shock protein 40 is a component of membrane-bound RISC in Arabidopsis

2018 ◽  
Vol 293 (43) ◽  
pp. 16608-16622 ◽  
Author(s):  
Lars Sjögren ◽  
Maïna Floris ◽  
Andrea Barghetti ◽  
Franziska Völlmy ◽  
Rune Linding ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Small Rna ◽  
Transcriptional Gene Silencing ◽  
Regulatory Rna ◽  
Farnesyl Transferase ◽  
Small Regulatory Rna ◽  
Post Transcriptional Gene Silencing ◽  
Membrane Bound ◽  
Interfering Rna

ARGONAUTE1 (AGO1) binds directly to small regulatory RNA and is a key effector protein of post-transcriptional gene silencing mediated by microRNA (miRNA) and small interfering RNA (siRNA) in Arabidopsis. The formation of an RNA-induced silencing complex (RISC) of AGO1 and small RNA requires the function of the heat shock protein 70/90 chaperone system. Some functions of AGO1 occur in association with endomembranes, in particular the rough endoplasmic reticulum (RER), but proteins interacting with AGO1 in membrane fractions remain unidentified. In this study, we show that the farnesylated heat shock protein 40 homologs, J2 and J3, associate with AGO1 in membrane fractions in a manner that involves protein farnesylation. We also show that three changes in AGO1 function are detectable in mutants in protein farnesylation and J2/J3. First, perturbations of the HSP40/70/90 pathway by mutation of J3, HSP90, and farnesyl transferase affect the amounts of AGO1 associated with membranes. Second, miRNA association with membrane-bound polysomes is increased in farnesyl transferase and farnesylation-deficient J2/J3 mutants. Third, silencing by noncell autonomously acting short interfering RNAs is impaired. These observations highlight the involvement of farnesylated J2/J3 in small RNA-mediated gene regulation, and suggest that the importance of chaperone-AGO1 interaction is not limited to the RISC assembly process.

scholarly journals The Hfq-Dependent Small Noncoding RNA NrrF Directly Mediates Fur-Dependent Positive Regulation of Succinate Dehydrogenase in Neisseria meningitidis

2008 ◽  
Vol 191 (4) ◽  
pp. 1330-1342 ◽  
Author(s):  
Matteo M. E. Metruccio ◽  
Laura Fantappiè ◽  
Davide Serruto ◽  
Alessandro Muzzi ◽  
Davide Roncarati ◽  
...  
Keyword(s):  
Succinate Dehydrogenase ◽  
Noncoding Rna ◽  
Iron Homeostasis ◽  
Transcriptional Analysis ◽  
Positive Regulation ◽  
Small Noncoding Rna ◽  
Small Regulatory Rna ◽  
Microarray Studies

ABSTRACT Previous microarray studies have suggested that an indirect mechanism of Fur regulation may be present in meningococcus at the posttranscriptional level through a small regulatory RNA (sRNA) system analogous to that of Escherichia coli and Pseudomonas aeruginosa. Recently, a Fur-regulated sRNA, NrrF, was identified that is involved in the iron regulation of the sdhA and sdhC succinate dehydrogenase genes. Here we report a detailed transcriptional analysis of the nrrF gene and show that NrrF is a Hfq-dependent sRNA. The Hfq protein mediates nrrF downregulation and Fur-dependent upregulation of the sdhCDAB operon, the major in vivo NrrF-regulated operon. NrrF forms a duplex in vitro with a region of complementarity overlapping the sdhDA mRNA junction. Furthermore, Hfq binds to NrrF in vitro and considerably enhances the efficiency of the interaction of the sRNA with the identified target. Our data suggest that Hfq-meditated binding of NrrF to the in vivo target in the sdhCDAB mRNA may cause the rapid degradation of the transcript, resulting in Fur-dependent positive regulation of succinate dehydrogenase. In addition, while the upregulation of sodB and fumB by Fur is dependent on the Hfq protein, it is unaffected in the nrrF knockout, which suggests that there is more than one sRNA regulator involved in iron homeostasis in meningococcus.

scholarly journals The Iron-Responsive Regulator Fur Is Transcriptionally Autoregulated and Not Essential in Neisseria meningitidis

2003 ◽  
Vol 185 (20) ◽  
pp. 6032-6041 ◽  
Author(s):  
Isabel Delany ◽  
Raffaele Ieva ◽  
Cristina Alaimo ◽  
Rino Rappuoli ◽  
Vincenzo Scarlato
Keyword(s):  
Neisseria Meningitidis ◽  
Gene Transcription ◽  
Binding Sites ◽  
Iron Homeostasis ◽  
Essential Gene ◽  
Iron Regulation ◽  
Coding Region ◽  
Protein Footprinting ◽  
Broad Array ◽  
Fine Tune

ABSTRACT Fur is a well-known iron-responsive repressor of gene transcription, which is used by many bacteria to respond to the low-iron environment that pathogens encounter during infection. The fur gene in Neisseria meningitidis has been described as an essential gene that may regulate a broad array of genes. We succeeded in obtaining an N. meningitidis mutant with the fur gene knocked out and used it to undertake studies of fur-mediated iron regulation. We show that expression of both Fur and the transferrin binding protein Tbp2 is iron regulated and demonstrate that this regulation is Fur mediated for the Tbp2 protein. Footprinting analysis revealed that Fur binds to two distinct sites upstream of its coding region with different affinities and that these binding sites overlap two promoters that differentially control transcription of the fur gene in response to iron. The presence of two independently regulated fur promoters may allow meningococcus to fine-tune expression of this regulator controlling iron homeostasis, possibly during infection.

Altered Yersinia pestis virulence is associated with the small regulatory RNA HmsA encoded on the plasmid pPCP1

2020 ◽  
Vol 15 (13) ◽  
pp. 1207-1215
Author(s):  
Xiaofang Gao ◽  
Min Wang ◽  
Zizhong Liu ◽  
Yujing Bi ◽  
Yajun Song ◽  
...  
Keyword(s):  
Yersinia Pestis ◽  
Iron Homeostasis ◽  
Regulatory Rna ◽  
Rna Seq ◽  
Competition Index ◽  
Wild Type ◽  
Expression Screening ◽  
Cellular Processes ◽  
Small Regulatory Rna ◽  
Upregulated Genes

Aim: The aim of this study was to access the effect of HmsA, a 65-nt small regulatory RNA encoded by the pPCP1 plasmid, on Yersinia pestis virulence. Materials & methods: Survival and the competition index were determined in mice infected with wild-type  Y. pestis and an hmsA deletion mutant. RNA-seq was used to identify HmsA-regulated genes. Results: HmsA deletion enhanced Y. pestis virulence. However, there was no overlap between 18 upregulated genes associated with pathogenicity and potential direct HmsA targets, based on gene expression screening after HmsA-pulse overexpression. Conclusion: HmsA inhibits Y. pestis virulence, but this effect may be mediated by indirect effects on pathogenesis, iron homeostasis and/or other cellular processes.

Sign in / Sign up

Export Citation Format

Share Document