Role of the general stress response during strong overexpression of a heterologous gene in Escherichia coli

2002 ◽  
Vol 58 (3) ◽  
pp. 330-337 ◽  
Author(s):  
T. Schweder, H. Lin, B. Jürgen
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Heterologous Gene ◽  
General Stress Response ◽  
General Stress

scholarly journals Role of Sphingomonas sp. Strain Fr1 PhyR-NepR- EcfG Cascade in General Stress Response and Identification of a Negative Regulator of PhyR

2011 ◽  
Vol 193 (23) ◽  
pp. 6629-6638 ◽  
Author(s):  
A. Kaczmarczyk ◽  
S. Campagne ◽  
F. Danza ◽  
L. C. Metzger ◽  
J. A. Vorholt ◽  
...  
Keyword(s):  
Stress Response ◽  
Negative Regulator ◽  
General Stress Response ◽  
General Stress

scholarly journals A Mutant RNA Polymerase Activates the General Stress Response, Enabling Escherichia coli Adaptation to Late Prolonged Stationary Phase

mSphere ◽  
2020 ◽  
Vol 5 (2) ◽  
Author(s):  
Pabitra Nandy ◽  
Savita Chib ◽  
Aswin Seshasayee
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Stationary Phase ◽  
Sigma Factor ◽  
Slow Growth ◽  
Content Type ◽  
General Stress Response ◽  
E Coli ◽  
General Stress ◽  
Small Colony

ABSTRACT Escherichia coli populations undergo repeated replacement of parental genotypes with fitter variants deep in stationary phase. We isolated one such variant, which emerged after 3 weeks of maintaining an E. coli K-12 population in stationary phase. This variant displayed a small colony phenotype and slow growth and was able to outcompete its ancestor over a narrow time window in stationary phase. The variant also shows tolerance to beta-lactam antibiotics, though not previously exposed to the antibiotic. We show that an RpoC(A494V) mutation confers the slow growth and small colony phenotype on this variant. The ability of this mutation to confer a growth advantage in stationary phase depends on the availability of the stationary-phase sigma factor σS. The RpoC(A494V) mutation upregulates the σS regulon. As shown over 20 years ago, early in prolonged stationary phase, σS attenuation, but not complete loss of activity, confers a fitness advantage. Our study shows that later mutations enhance σS activity, either by mutating the gene for σS directly or via mutations such as RpoC(A494V). The balance between the activities of the housekeeping major sigma factor and σS sets up a trade-off between growth and stress tolerance, which is tuned repeatedly during prolonged stationary phase. IMPORTANCE An important general mechanism of a bacterium’s adaptation to its environment involves adjusting the balance between growing fast and tolerating stresses. One paradigm where this plays out is in prolonged stationary phase: early studies showed that attenuation, but not complete elimination, of the general stress response enables early adaptation of the bacterium E. coli to the conditions established about 10 days into stationary phase. We show here that this balance is not static and that it is tilted back in favor of the general stress response about 2 weeks later. This can be established by direct mutations in the master regulator of the general stress response or by mutations in the core RNA polymerase enzyme itself. These conditions can support the development of antibiotic tolerance although the bacterium is not exposed to the antibiotic. Further exploration of the growth-stress balance over the course of stationary phase will necessarily require a deeper understanding of the events in the extracellular milieu.

scholarly journals Role of the PFXFATG[G/Y] Motif in the Activation of SdrG, a Response Regulator Involved in the Alphaproteobacterial General Stress Response

Structure ◽  
2016 ◽  
Vol 24 (8) ◽  
pp. 1237-1247 ◽  
Author(s):  
Sébastien Campagne ◽  
Sebastian Dintner ◽  
Lisa Gottschlich ◽  
Maxence Thibault ◽  
Miriam Bortfeld-Miller ◽  
...  
Keyword(s):  
Stress Response ◽  
Response Regulator ◽  
General Stress Response ◽  
General Stress

Mitophagy, mitochondrial dynamics and the general stress response in yeast

2011 ◽  
Vol 39 (5) ◽  
pp. 1514-1519 ◽  
Author(s):  
Matthias Müller ◽  
Andreas S. Reichert
Keyword(s):  
Quality Control ◽  
Stress Response ◽  
Neurodegenerative Disorders ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Nutrient Sensing ◽  
Control Mechanisms ◽  
General Stress Response ◽  
General Stress

Autophagy is a fundamental cellular process promoting survival under various environmental stress conditions. Selective types of autophagy have gained much interest recently as they are involved in specific quality control mechanisms removing, for example, aggregated proteins or dysfunctional mitochondria. This is considered to counteract the development of a number of neurodegenerative disorders and aging. Here we review the role of mitophagy and mitochondrial dynamics in ensuring quality control of mitochondria. In particular, we provide possible explanations why mitophagy in yeast, in contrast with the situation in mammals, was found to be independent of mitochondrial fission. We further discuss recent findings linking these processes to nutrient sensing pathways and the general stress response in yeast. In particular, we propose a model for how the stress response protein Whi2 and the Ras/PKA (protein kinase A) signalling pathway are possibly linked and thereby regulate mitophagy.

General Stress Response Regulator RpoS in Adaptive Mutation and Amplification in Escherichia coli

Genetics ◽  
2004 ◽  
Vol 166 (2) ◽  
pp. 669-680 ◽  
Author(s):  
Mary-Jane Lombardo ◽  
Ildiko Aponyi ◽  
Susan M Rosenberg
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Stationary Phase ◽  
Point Mutation ◽  
Stress Responses ◽  
Genome Rearrangement ◽  
Adaptive Mutation ◽  
Induced Mutations ◽  
General Stress Response ◽  
General Stress

Abstract Microbial cells under growth-limiting stress can generate mutations by mechanisms distinct from those in rapidly growing cells. These mechanisms might be specific stress responses that increase mutation rates, potentially altering rates of evolution, or might reflect non-stress-specific processes in rare growing cells. In an Escherichia coli model system, both frameshift reversion mutations and gene amplifications occur as apparent starvation-induced mutations. Whereas frameshift reversion (“point mutation”) requires recombination proteins, the SOS response, and error-prone DNA polymerase IV (DinB), amplification requires neither SOS nor pol IV. We report that both point mutation and amplification require the stationary-phase and general stress response transcription factor RpoS (σS). Growth-dependent mutation does not. Alternative interpretations are excluded. The results imply, first, that point mutation and amplification are stress responses that occur in differentiated stationary-phase (not rare growing) cells and, second, that transient genetic instability, producing both point mutation and genome rearrangement, may be a previously unrecognized component of the RpoS-dependent general stress response.

scholarly journals Genome-Wide Analysis of the General Stress Response Network in Escherichia coli: σS-Dependent Genes, Promoters, and Sigma Factor Selectivity

2005 ◽  
Vol 187 (5) ◽  
pp. 1591-1603 ◽  
Author(s):  
Harald Weber ◽  
Tino Polen ◽  
Johanna Heuveling ◽  
Volker F. Wendisch ◽  
Regine Hengge
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Rna Polymerase ◽  
Sigma Factor ◽  
Regulatory Network ◽  
Cell Physiology ◽  
Data Set ◽  
General Stress Response ◽  
General Stress ◽  
Genome Wide

ABSTRACT The σS (or RpoS) subunit of RNA polymerase is the master regulator of the general stress response in Escherichia coli. While nearly absent in rapidly growing cells, σS is strongly induced during entry into stationary phase and/or many other stress conditions and is essential for the expression of multiple stress resistances. Genome-wide expression profiling data presented here indicate that up to 10% of the E. coli genes are under direct or indirect control of σS and that σS should be considered a second vegetative sigma factor with a major impact not only on stress tolerance but on the entire cell physiology under nonoptimal growth conditions. This large data set allowed us to unequivocally identify a σS consensus promoter in silico. Moreover, our results suggest that σS-dependent genes represent a regulatory network with complex internal control (as exemplified by the acid resistance genes). This network also exhibits extensive regulatory overlaps with other global regulons (e.g., the cyclic AMP receptor protein regulon). In addition, the global regulatory protein Lrp was found to affect σS and/or σ70 selectivity of many promoters. These observations indicate that certain modules of the σS-dependent general stress response can be temporarily recruited by stress-specific regulons, which are controlled by other stress-responsive regulators that act together with σ70 RNA polymerase. Thus, not only the expression of genes within a regulatory network but also the architecture of the network itself can be subject to regulation.

scholarly journals Loss of RpoS results in attenuated Escherichia coli colonization of human intestinal organoids and a competitive disadvantage within the germ-free mouse intestine

2020 ◽  
Author(s):  
Madeline R. Barron ◽  
Roberto J. Cieza ◽  
David R. Hill ◽  
Sha Huang ◽  
Veda K. Yadagiri ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
General Stress Response ◽  
E Coli ◽  
Germ Free ◽  
General Stress ◽  
Intestinal Organoids ◽  
Mouse Intestine

AbstractPluripotent stem-cell-derived human intestinal organoids (HIOs) are three-dimensional, multicellular structures that model a previously uncolonized, naïve intestinal epithelium in an in vitro system. We recently demonstrated that microinjection of the non-pathogenic Escherichia coli strain, ECOR2, into HIOs induced morphological and functional maturation of the HIO epithelium, including increased secretion of mucins and cationic antimicrobial peptides. In the current work, we use ECOR2 as a biological probe to investigate the bacterial response to colonization of the HIO lumen. In E. coli and other Gram-negative bacteria, adaptation to environmental stress is regulated by the general stress response sigma factor, RpoS. We generated an isogenic ∆rpoS ECOR2 mutant to compare challenges faced by a bacterium during colonization of the HIO lumen relative to the germ-free mouse intestine, which is currently the best available system for studying the initial establishment of bacterial populations within the gut. We demonstrate that loss of RpoS significantly decreases the ability of ECOR2 to colonize HIOs, though it does not prevent colonization of germ-free mice. Rather, the ∆rpoS ECOR2 exhibits a fitness defect in the germ-free mouse intestine only in the context of microbial competition. These results indicate that HIOs pose a differentially restrictive luminal environment to E. coli during colonization, thus increasing our understanding of the HIO model system as it pertains to studying the establishment of intestinal host-microbe symbioses.ImportanceTechnological advancements have and will continue to drive the adoption of organoid-based systems for investigating host-microbe interactions within the human intestinal ecosystem. Using E. coli deficient in the RpoS-mediated general stress response, we demonstrate that the type or severity of microbial stressors within the HIO lumen differ from those of the in vivo environment of the germ-free mouse gut. This study provides important insight into the nature of the HIO microenvironment from a microbiological standpoint.

Sign in / Sign up

Export Citation Format

Share Document