scholarly journals Impact of bacterial sRNAs in stress responses

2017 ◽  
Vol 45 (6) ◽  
pp. 1203-1212 ◽  
Author(s):  
Erik Holmqvist ◽  
E. Gerhart H. Wagner
Keyword(s):  
Dna Damage ◽  
Stress Response ◽  
Stress Responses ◽  
Transcriptional Control ◽  
Iron Homeostasis ◽  
Stress Relief ◽  
Regulatory Circuits ◽  
Envelope Stress ◽  
Key Players ◽  
Non Coding Rnas

Bacterial life is harsh and involves numerous environmental and internal challenges that are perceived as stresses. Consequently, adequate responses to survive, cope with, and counteract stress conditions have evolved. In the last few decades, a class of small, non-coding RNAs (sRNAs) has been shown to be involved as key players in stress responses. This review will discuss — primarily from an enterobacterial perspective — selected stress response pathways that involve antisense-type sRNAs. These include themes of how bacteria deal with severe envelope stress, threats of DNA damage, problems with poisoning due to toxic sugar intermediates, issues of iron homeostasis, and nutrient limitation/starvation. The examples discussed highlight how stress relief can be achieved, and how sRNAs act mechanistically in regulatory circuits. For some cases, we will propose scenarios that may suggest why contributions from post-transcriptional control by sRNAs, rather than transcriptional control alone, appear to be a beneficial and universally selected feature.

scholarly journals The Rcs System in Enterobacteriaceae: Envelope Stress Responses and Virulence Regulation

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiao Meng ◽  
Glenn Young ◽  
Jingyu Chen
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Bacterial Infections ◽  
Pathogenic Bacteria ◽  
Cell Envelope ◽  
Regulatory System ◽  
Virulence Regulation ◽  
Bacterial Interaction ◽  
Envelope Stress

The bacterial cell envelope is a protective barrier at the frontline of bacterial interaction with the environment, and its integrity is regulated by various stress response systems. The Rcs (regulator of capsule synthesis) system, a non-orthodox two-component regulatory system (TCS) found in many members of the Enterobacteriaceae family, is one of the envelope stress response pathways. The Rcs system can sense envelope damage or defects and regulate the transcriptome to counteract stress, which is particularly important for the survival and virulence of pathogenic bacteria. In this review, we summarize the roles of the Rcs system in envelope stress responses (ESRs) and virulence regulation. We discuss the environmental and intrinsic sources of envelope stress that cause activation of the Rcs system with an emphasis on the role of RcsF in detection of envelope stress and signal transduction. Finally, the different regulation mechanisms governing the Rcs system’s control of virulence in several common pathogens are introduced. This review highlights the important role of the Rcs system in the environmental adaptation of bacteria and provides a theoretical basis for the development of new strategies for control, prevention, and treatment of bacterial infections.

scholarly journals A Suppressor Mutation That Creates a Faster and More Robust σE Envelope Stress Response

2016 ◽  
Vol 198 (17) ◽  
pp. 2345-2351 ◽  
Author(s):  
Anna Konovalova ◽  
Jaclyn A. Schwalm ◽  
Thomas J. Silhavy
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Novel Mutation ◽  
Signal Transduction Pathway ◽  
Normal Growth ◽  
Internal Stresses ◽  
Content Type ◽  
Envelope Stress ◽  
Genetic Perturbations ◽  
Periplasmic Stress

ABSTRACTThe σE envelope stress response is an essential signal transduction pathway which detects and removes mistargeted outer membrane (OM) β-barrel proteins (OMPs) in the periplasm ofEscherichia coli. It relies on σE, an alternative sigma factor encoded by therpoEgene. Here we report a novel mutation, a nucleotide change of C to A in the third base of the second codon, which increases levels of σE (rpoE_S2R). TherpoE_S2Rmutation does not lead to the induction of the stress response during normal growth but instead changes the dynamics of induction upon periplasmic stress, resulting in a faster and more robust response. This allows cells to adapt faster to the periplasmic stress, avoiding lethal accumulation of unfolded OMPs in the periplasm caused by severe defects in the OMP assembly pathway.IMPORTANCESurvival of bacteria under conditions of external or internal stresses depends on timely induction of stress response signaling pathways to regulate expression of appropriate genes that function to maintain cellular homeostasis. Previous studies have shown that strong preinduction of envelope stress responses can allow bacteria to survive a number of lethal genetic perturbations. In our paper, we describe a unique mutation that enhances kinetics of the σE envelope stress response pathway rather than preinducing the response. This allows bacteria to quickly adapt to sudden and severe periplasmic stress.

scholarly journals Cpx Signal Transduction Is Influenced by a Conserved N-Terminal Domain in the Novel Inhibitor CpxP and the Periplasmic Protease DegP

2005 ◽  
Vol 187 (19) ◽  
pp. 6622-6630 ◽  
Author(s):  
Daelynn R. Buelow ◽  
Tracy L. Raivio
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Feedback Inhibition ◽  
Functional Domain ◽  
The Novel ◽  
Loss Of Function ◽  
Terminal Domain ◽  
Envelope Stress ◽  
Cpx Pathway ◽  
Α Helix

ABSTRACT In Escherichia coli, envelope stress can be overcome by three different envelope stress responses: the σE stress response and the Bae and Cpx two-component systems. The Cpx envelope stress response is controlled by the sensor kinase CpxA, the response regulator CpxR, and the novel periplasmic protein CpxP. CpxP mediates feedback inhibition of the Cpx pathway through a hypothetical interaction with the sensing domain of CpxA. No informative homologues of CpxP are known, and thus it is unclear how CpxP exerts this inhibition. Here, we identified six cpxP loss-of-function mutations using a CpxP-β-lactamase (CpxP′-′Bla) translational fusion construct. These loss-of-function mutations identified a highly conserved, predicted α-helix in the N-terminal domain of CpxP that affects both the function and the stability of the protein. In the course of this study, we also found that CpxP′-′Bla stability is differentially controlled by the periplasmic protease DegP in response to inducing cues and that mutation of degP diminishes Cpx pathway activity. We propose that the N-terminal α-helix is an important functional domain for inhibition of the Cpx pathway and that CpxP is subject to DegP-dependent proteolysis.

scholarly journals Riboregulation in Nitrogen-Fixing Endosymbiotic Bacteria

2020 ◽  
Vol 8 (3) ◽  
pp. 384 ◽  
Author(s):  
Marta Robledo ◽  
Natalia I. García-Tomsig ◽  
José I. Jiménez-Zurdo
Keyword(s):  
Stress Responses ◽  
Regulatory Networks ◽  
Transcriptional Control ◽  
Genetic Regulation ◽  
Regulation Of Gene Expression ◽  
Nodule Development ◽  
Nitrogen Fixing ◽  
Endosymbiotic Bacteria ◽  
Non Coding Rnas ◽  
Post Transcriptional Regulation

Small non-coding RNAs (sRNAs) are ubiquitous components of bacterial adaptive regulatory networks underlying stress responses and chronic intracellular infection of eukaryotic hosts. Thus, sRNA-mediated regulation of gene expression is expected to play a major role in the establishment of mutualistic root nodule endosymbiosis between nitrogen-fixing rhizobia and legume plants. However, knowledge about this level of genetic regulation in this group of plant-interacting bacteria is still rather scarce. Here, we review insights into the rhizobial non-coding transcriptome and sRNA-mediated post-transcriptional regulation of symbiotic relevant traits such as nutrient uptake, cell cycle, quorum sensing, or nodule development. We provide details about the transcriptional control and protein-assisted activity mechanisms of the functionally characterized sRNAs involved in these processes. Finally, we discuss the forthcoming research on riboregulation in legume symbionts.

scholarly journals Plant Non-Coding RNAs: Origin, Biogenesis, Mode of Action and Their Roles in Abiotic Stress

2020 ◽  
Vol 21 (21) ◽  
pp. 8401
Author(s):  
Joram Kiriga Waititu ◽  
Chunyi Zhang ◽  
Jun Liu ◽  
Huan Wang
Keyword(s):  
Abiotic Stress ◽  
Stress Response ◽  
Stress Responses ◽  
Current Knowledge ◽  
Fine Tuning ◽  
Abiotic Stress Response ◽  
Underlying Basis ◽  
Substantial Progress ◽  
Non Coding Rnas ◽  
Sequencing And Expression

As sessile species, plants have to deal with the rapidly changing environment. In response to these environmental conditions, plants employ a plethora of response mechanisms that provide broad phenotypic plasticity to allow the fine-tuning of the external cues related reactions. Molecular biology has been transformed by the major breakthroughs in high-throughput transcriptome sequencing and expression analysis using next-generation sequencing (NGS) technologies. These innovations have provided substantial progress in the identification of genomic regions as well as underlying basis influencing transcriptional and post-transcriptional regulation of abiotic stress response. Non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs), short interfering RNAs (siRNAs), and long non-coding RNAs (lncRNAs), have emerged as essential regulators of plants abiotic stress response. However, shared traits in the biogenesis of ncRNAs and the coordinated cross-talk among ncRNAs mechanisms contribute to the complexity of these molecules and might play an essential part in regulating stress responses. Herein, we highlight the current knowledge of plant microRNAs, siRNAs, and lncRNAs, focusing on their origin, biogenesis, modes of action, and fundamental roles in plant response to abiotic stresses.

scholarly journals Specific microRNAs Regulate Heat Stress Responses in Caenorhabditis elegans

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Camilla Nehammer ◽  
Agnieszka Podolska ◽  
Sebastian D. Mackowiak ◽  
Konstantinos Kagias ◽  
Roger Pocock
Keyword(s):  
Heat Stress ◽  
Caenorhabditis Elegans ◽  
Stress Response ◽  
Stress Responses ◽  
Posttranscriptional Regulation ◽  
Transcriptional Control ◽  
Heat Stress Response ◽  
C Elegans ◽  
Additional Layer ◽  
Sense And Respond

Abstract The ability of animals to sense and respond to elevated temperature is essential for survival. Transcriptional control of the heat stress response has been much studied, whereas its posttranscriptional regulation by microRNAs (miRNAs) is not well understood. Here we analyzed the miRNA response to heat stress in Caenorhabditis elegans and show that a discrete subset of miRNAs is thermoregulated. Using in-depth phenotypic analyses of miRNA deletion mutant strains we reveal multiple developmental and post-developmental survival and behavioral functions for specific miRNAs during heat stress. We have identified additional functions for already known players (mir-71 and mir-239) as well as identifying mir-80 and the mir-229 mir-64-66 cluster as important regulators of the heat stress response in C. elegans. These findings uncover an additional layer of complexity to the regulation of stress signaling that enables animals to robustly respond to the changing environment.

scholarly journals 1726. Candida albicans Virulence Genes Induced During Intra-abdominal Candidiasis (IAC) in the Absence of Antifungal Exposure Mediate Echinocandin Resistance

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S633-S633 ◽  
Author(s):  
Cornelius J Clancy ◽  
Palash Samanta ◽  
Shaoji Cheng ◽  
Kevin Squires ◽  
Minh-Hong Nguyen
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Iron Homeostasis ◽  
Drug Exposure ◽  
Glyoxylate Cycle ◽  
Transcriptional Profiling ◽  
Hyphal Growth ◽  
Illumina Miseq ◽  
Core Gene ◽  
Echinocandin Resistance

Abstract Background We developed and validated a mouse model of C. albicans IAC that mimics peritonitis and abscesses (IAA) in humans, and that is amenable to temporal–spatial transcriptional profiling and virulence studies. Methods We measured C. albicans SC5314 gene expression by RNA-Seq (RiboPure extraction; Illumina MiSeq) in triplicate during early peritonitis (within 30 minutes of infection), late peritonitis (24 hours) and IAA (48 hours). Differential expression was defined by ≥2-fold differences at false discovery rate ≤0.01. Results ≥7 million C. albicans reads were detected in each experiment. 67% of C. albicans reads mapped to coding sequences, covering 93% of open reading frames. The 50 C. albicans genes most highly expressed during early peritonitis were associated with pH (including RIM101 and PHR1) and oxidative stress responses, and adhesion/hyphal growth (e.g., ALS3, HWP1, ECM331, SAP6). The corresponding 50 C. albicans late peritonitis genes were associated with neutrophil/macrophage responses and nutrient acquisition (glyoxylate cycle, fatty acid β-oxidation, iron homeostasis). Responses within IAA included DNA damage and iron metabolism, reflecting stress response and nutrient/metal limitation. The top 50 core gene responses for all stages were associated with adhesion, stress response, and glucose transport. Among the most up-regulated genes in late peritonitis and IAA compared with early peritonitis were those involved antifungal drug resistance (CDR family, MDR1, FLU1, and ERG family), although mice were not exposed to antifungals. Null and reconstitution mutants for genes involved in adhesion (ALS3), copper transport (CCC2), DNA (DDI1) and cell wall damage responses (DAP1 homologs), and glycerol biosynthesis (RHR2) were attenuated for virulence in temporal-spatial fashion during peritonitis and IAA, and/or hyper-susceptible to phagocytosis and echinocandins (table). Conclusion C. albicans relies upon diverse biologic processes to cause peritonitis and IAA. Multiple genes induced in response to stress during IAC mediate virulence, phagocyte, and echinocandin resistance. Therefore, pathogenic strategies used by C. albicans during IAC may lessen responses to echinocandin treatment, even in the absence of drug exposure or FKS mutations. Disclosures All authors: No reported disclosures.

scholarly journals Fine-Tuning of σEActivation Suppresses Multiple Assembly-Defective Mutations inEscherichia coli

2019 ◽  
Vol 201 (11) ◽  
Author(s):  
Elizabeth M. Hart ◽  
Aileen O’Connell ◽  
Kimberly Tang ◽  
Joseph S. Wzorek ◽  
Marcin Grabowicz ◽  
...  
Keyword(s):  
Stress Response ◽  
Cell Viability ◽  
Outer Membrane ◽  
Stress Responses ◽  
Expression Profiles ◽  
Outer Membrane Proteins ◽  
Fine Tuning ◽  
Permeability Barrier ◽  
Gram Negative ◽  
Envelope Stress

ABSTRACTThe Gram-negative outer membrane (OM) is a selectively permeable asymmetric bilayer that allows vital nutrients to diffuse into the cell but prevents toxins and hydrophobic molecules from entering. Functionally and structurally diverse β-barrel outer membrane proteins (OMPs) build and maintain the permeability barrier, making the assembly of OMPs crucial for cell viability. In this work, we characterize an assembly-defective mutant of the maltoporin LamB, LamBG439D. We show that the folding defect of LamBG439Dresults in an accumulation of unfolded substrate that is toxic to the cell when the periplasmic protease DegP is removed. Selection for suppressors of this toxicity identified the novel mutantdegSA323Eallele. The mutant DegSA323Eprotein contains an amino acid substitution at the PDZ/protease domain interface that results in a partially activated conformation of this protein. This activation increases basal levels of downstream σEstress response signaling. Furthermore, the enhanced σEactivity of DegSA323Esuppresses a number of other assembly-defective conditions without exhibiting the toxicity associated with high levels of σEactivity. We propose that the increased basal levels of σEsignaling primes the cell to respond to envelope stress before OMP assembly defects threaten cell viability. This finding addresses the importance of envelope stress responses in monitoring the OMP assembly process and underpins the critical balance between envelope defects and stress response activation.IMPORTANCEGram-negative bacteria, such asEscherichia coli, inhabit a natural environment that is prone to flux. In order to cope with shifting growth conditions and the changing availability of nutrients, cells must be capable of quickly responding to stress. Stress response pathways allow cells to rapidly shift gene expression profiles to ensure survival in this unpredictable environment. Here we describe a mutant that partially activates the σEstress response pathway. The elevated basal level of this stress response allows the cell to quickly respond to overwhelming stress to ensure cell survival.

scholarly journals The BceABRS Four-Component System Regulates the Bacitracin-Induced Cell Envelope Stress Response in Streptococcus mutans

2010 ◽  
Vol 54 (9) ◽  
pp. 3895-3906 ◽  
Author(s):  
Jing Ouyang ◽  
Xiao-Lin Tian ◽  
Jennifer Versey ◽  
Alexander Wishart ◽  
Yung-Hua Li
Keyword(s):  
Stress Response ◽  
Streptococcus Mutans ◽  
Transcriptional Control ◽  
Cell Envelope ◽  
Genetic Locus ◽  
Binding Motif ◽  
Two Component System ◽  
Component System ◽  
Envelope Stress ◽  
Two Component

ABSTRACT Streptococcus mutans is known to be resistant to bacitracin, a cyclic polypeptide antibiotic produced by certain species of the genus Bacillus. This property is often exploited in the isolation of S. mutans strains from highly heterogeneous oral microflora. A genetic locus consisting of a four-gene operon, bceABRS (formerly mbrABCD), the component genes of which are homologous to Bacillus subtilis bceRS-bceAB (encoding a two-component system and an ABC transporter), is required for bacitracin resistance in S. mutans. Here we describe the identification of a DNA binding site for the BceR response regulator and its transcriptional control of the bceABRS operon in response to the presence of bacitracin. We provide evidence indicating that phosphorylated BceR binds directly to a conserved invert repeat located between bp −120 and −78 of the bceABRS promoter region and positively regulates expression of the bceABRS operon. We also demonstrate that sensing of bacitracin by the BceS histidine kinase requires the presence of an intact BceAB transporter, since deletion of either bceA or bceB abolishes BceRS-mediated bacitracin sensing. The results suggest that the BceAB transporter acts as a cosensor, together with the BceRS two-component system, for bacitracin perception in S. mutans. By searching the S. mutans genome databases, we have identified three additional genes that share the consensus BceR binding motif at their promoter regions. Our initial work has confirmed that expression of these genes is directly controlled by BceRS, indicating that the bceABRS operon, along with the three additional genes, forms the BceRS regulon in S. mutans. Taking these findings together, we conclude that BceABRS comprises a four-component system that plays an important role in stimulus sensing, signal transduction, the gene regulatory network, and substrate transport for the cell envelope stress response in S. mutans.

scholarly journals Mechanisms of Alcohol-Induced Endoplasmic Reticulum Stress and Organ Injuries

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Cheng Ji
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Er Stress ◽  
Stress Responses ◽  
Iron Homeostasis ◽  
Blood Stream ◽  
The Body ◽  
Excessive Alcohol Consumption ◽  
Er Stress Response ◽  
Therapeutic Benefits

Alcohol is readily distributed throughout the body in the blood stream and crosses biological membranes, which affect virtually all biological processes inside the cell. Excessive alcohol consumption induces numerous pathological stress responses, part of which is endoplasmic reticulum (ER) stress response. ER stress, a condition under which unfolded/misfolded protein accumulates in the ER, contributes to alcoholic disorders of major organs such as liver, pancreas, heart, and brain. Potential mechanisms that trigger the alcoholic ER stress response are directly or indirectly related to alcohol metabolism, which includes toxic acetaldehyde and homocysteine, oxidative stress, perturbations of calcium or iron homeostasis, alterations of S-adenosylmethionine to S-adenosylhomocysteine ratio, and abnormal epigenetic modifications. Interruption of the ER stress triggers is anticipated to have therapeutic benefits for alcoholic disorders.

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