scholarly journals Slower growth of Escherichia coli leads to longer survival in carbon starvation due to a decrease in the maintenance rate

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Elena Biselli ◽  
Severin Josef Schink ◽  
Ulrich Gerland
Keyword(s):  
Escherichia Coli ◽  
Carbon Starvation ◽  
Maintenance Rate

Reduction of a Kinetic Model of the Carbon Starvation Response in Escherichia coli

2009 ◽  
Vol 42 (10) ◽  
pp. 27-32
Author(s):  
Delphine Ropers ◽  
Valentina Baldazzi ◽  
Hidde de Jong
Keyword(s):  
Escherichia Coli ◽  
Kinetic Model ◽  
Carbon Starvation ◽  
Starvation Response

scholarly journals Mass spectrometry-based profiling of the carbon starved Escherichia coli proteome reveals upregulation of stress-inducible pathways implicated in biofilm formation and antibiotic resistance

2015 ◽  
Author(s):  
Rakhan Aimbetov ◽  
Vasily Ogryzko
Keyword(s):  
Escherichia Coli ◽  
Gene Ontology ◽  
Antibiotic Resistance ◽  
Nutrient Deficiency ◽  
Carbon Starvation ◽  
Label Free ◽  
Ontology Term ◽  
Complex Adaptive ◽  
Proteome Level ◽  
Proteomic Investigation

Starvation is a complex adaptive response to insufficiency of nutrients that has been known to implicate a number of stress networks, and modulate pathogenicity and antibiotic resistance in bacteria. However, naturally occurring abrupt elimination of nutrients and prolonged periods of their complete absence, e.g. when bacteria are placed in natural or artificial water reservoirs, are qualitatively different from in-culture late stationary phase energy source diminution. Despite the obvious importance of proteomic investigation of bacteria exposed to nutrient deficiency, no comprehensive study on the subject has been published. In order to address the said shortage of knowledge, we decided to quantitatively look into the proteome-level alterations elicited by the complete lack of nutrients that constitute a viable source of carbon, i.e. carbon starvation, in the Escherichia coli HT115-derived SLE1 strain cells using the combination of label-free and SILAC-based proteomics. As a result, we obtained protein ratios for 1,757 and 1,241 protein groups for each technique respectively, 2D-annotated the quantifiable proteins present in both datasets, identified over- and underrepresented Gene Ontology terms, and isolated protein groups ≥2-fold up- and downregulated in response to carbon starvation (44 and 36 protein groups respectively). We observed upregulation of proteins implicated in various stress-related networks, most notably those that constitute the Gene Ontology term 'Biological adhesion', as well as various terms related to stress. Additionally, we identified several uncharacterized proteins, and our report is the first to ascribe them to a stress-induced proteome. Our data are available via ProteomeXchange with identifier PXD003255 and DOI:10.6019/PXD003255.

Qualitative simulation of the carbon starvation response in Escherichia coli

Biosystems ◽  
2006 ◽  
Vol 84 (2) ◽  
pp. 124-152 ◽  
Author(s):  
Delphine Ropers ◽  
Hidde de Jong ◽  
Michel Page ◽  
Dominique Schneider ◽  
Johannes Geiselmann
Keyword(s):  
Escherichia Coli ◽  
Carbon Starvation ◽  
Starvation Response ◽  
Qualitative Simulation

scholarly journals Expression of Different-Size Transcripts from theclpP-clpX Operon of Escherichia coli during Carbon Deprivation

2000 ◽  
Vol 182 (23) ◽  
pp. 6630-6637 ◽  
Author(s):  
Chin Li ◽  
Yi Ping Tao ◽  
Lee D. Simon
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Type Strain ◽  
Wild Type Strain ◽  
Transcription Termination ◽  
Carbon Starvation ◽  
Lower Percentage ◽  
Wild Type ◽  
Lower Efficiency ◽  
E Coli

ABSTRACT Transcription of the clpP-clpX operon ofEscherichia coli leads to the production of two different sizes of transcripts. In log phase, the level of the longer transcript is higher than the level of the shorter transcript. Soon after the onset of carbon starvation, the level of the shorter transcript increases significantly, and the level of the longer transcript decreases. The longer transcript consists of the entireclpP-clpX operon, whereas the shorter transcript contains the entire clpP gene but none of the clpXcoding sequence. The RpoH protein is required for the increase in the level of the shorter transcript during carbon starvation. Primer extension experiments suggest that there is increased usage of the ς32-dependent promoter of the clpP-clpXoperon within 15 min after the start of carbon starvation. Expression of the clpP-clpX operon from the promoters upstream of theclpP gene decreases to a very low level by 20 min after the onset of carbon starvation. Various pieces of evidence suggest, though they do not conclusively prove, that production of the shorter transcript may involve premature termination of the longer transcript. The half-life of the shorter transcript is much less than that of the longer transcript during carbon starvation. E. coli rpoBmutations that affect transcription termination efficiency alter the ratio of the shorter clpP-clpX transcript to the longer transcript. The E. coli rpoB3595 mutant, with an RNA polymerase that terminates transcription with lower efficiency than the wild type, accumulates a lower percentage of the shorter transcript during carbon starvation than does the isogenic wild-type strain. In contrast, the rpoB8 mutant, with an RNA polymerase that terminates transcription with higher efficiency than the wild type, produces a higher percentage of the shorter clpP-clpXtranscript when E. coli is in log phase. These and other data are consistent with the hypothesis that the shorter transcript results from premature transcription termination during production of the longer transcript.

scholarly journals CsrA Regulates Translation of the Escherichia coli Carbon Starvation Gene, cstA, by Blocking Ribosome Access to the cstA Transcript

2003 ◽  
Vol 185 (15) ◽  
pp. 4450-4460 ◽  
Author(s):  
Ashok K. Dubey ◽  
Carol S. Baker ◽  
Kazushi Suzuki ◽  
A. Daniel Jones ◽  
Pallavi Pandit ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Genomic Sequence ◽  
Carbon Starvation ◽  
Receptor Protein ◽  
Peptide Transporter ◽  
Wild Type ◽  
Mobility Shift ◽  
Ribosome Binding ◽  
Mutant Strains ◽  
Shine Dalgarno Sequence

ABSTRACT CsrA is a global regulator that binds to two sites in the glgCAP leader transcript, thereby blocking ribosome access to the glgC Shine-Dalgarno sequence. The upstream CsrA binding site (GCACACGGAU) was used to search the Escherichia coli genomic sequence for other genes that might be regulated by CsrA. cstA contained an exact match that overlapped its Shine-Dalgarno sequence. cstA was previously shown to be induced by carbon starvation and to encode a peptide transporter. Expression of a cstA′-′lacZ translational fusion in wild-type and csrA mutant strains was examined. Expression levels in the csrA mutant were approximately twofold higher when cells were grown in Luria broth (LB) and 5- to 10-fold higher when LB was supplemented with glucose. It was previously shown that cstA is regulated by the cyclic AMP (cAMP)-cAMP receptor protein complex and transcribed by Εσ70. We investigated the influence of σS on cstA expression and found that a σS deficiency resulted in a threefold increase in cstA expression in wild-type and csrA mutant strains; however, CsrA-dependent regulation was retained. The mechanism of CsrA-mediated cstA regulation was also examined in vitro. Cross-linking studies demonstrated that CsrA is a homodimer. Gel mobility shift results showed that CsrA binds specifically to cstA RNA, while coupled-transcription-translation and toeprint studies demonstrated that CsrA regulates CstA synthesis by inhibiting ribosome binding to cstA transcripts. RNA footprint and boundary analyses revealed three or four CsrA binding sites, one of which overlaps the cstA Shine-Dalgarno sequence, as predicted. These results establish that CsrA regulates translation of cstA by sterically interfering with ribosome binding.

scholarly journals Mutations Enhancing Amino Acid Catabolism Confer a Growth Advantage in Stationary Phase

1999 ◽  
Vol 181 (18) ◽  
pp. 5800-5807 ◽  
Author(s):  
Erik R. Zinser ◽  
Roberto Kolter
Keyword(s):  
Escherichia Coli ◽  
Amino Acids ◽  
Amino Acid ◽  
Stationary Phase ◽  
Carbon Starvation ◽  
Amino Acid Catabolism ◽  
Rich Media ◽  
Dying Cells

ABSTRACT Starved cultures of Escherichia coli undergo successive rounds of population takeovers by mutants of increasing fitness. These mutants express the growth advantage in stationary phase (GASP) phenotype. Previous work identified the rpoS819 allele as a GASP mutation allowing cells to take over stationary-phase cultures after growth in rich media (M. M. Zambrano, D. A. Siegele, M. A. Almirón, A. Tormo, and R. Kolter, Science 259:1757–1760, 1993). Here we have identified three new GASP loci from an aged rpoS819 strain: sgaA, sgaB, and sgaC. Each locus is capable of conferring GASP on therpoS819 parent, and they can provide successively higher fitnesses for the bacteria in the starved cultures. All four GASP mutations isolated thus far allow for faster growth on both individual and mixtures of amino acids. Each mutation confers a growth advantage on a different subset of amino acids, and these mutations act in concert to increase the overall catabolic capacity of the cell. We present a model whereby this enhanced ability to catabolize amino acids is responsible for the fitness gain during carbon starvation, as it may allow GASP mutants to outcompete the parental cells when growing on the amino acids released by dying cells.

scholarly journals Multiple Regulators Control Expression of the Entner-Doudoroff Aldolase (Eda) of Escherichia coli

2005 ◽  
Vol 187 (3) ◽  
pp. 991-1000 ◽  
Author(s):  
Elizabeth L. Murray ◽  
Tyrrell Conway
Keyword(s):  
Escherichia Coli ◽  
Phosphate Starvation ◽  
Growth Conditions ◽  
Carbon Starvation ◽  
Expression Level ◽  
Phosphate Limitation ◽  
Induced Stress ◽  
Indirect Mechanism ◽  
Complex Regulation

ABSTRACT The Escherichia coli eda gene, which encodes the Entner-Doudoroff aldolase, is central to the catabolism of several sugar acids. Here, we show that Eda synthesis is induced by growth on gluconate, glucuronate, or methyl-β-d-glucuronide; phosphate limitation; and carbon starvation. Transcription of eda initiates from three promoters, designated P1, P2, and P4, each of which is responsible for induction under different growth conditions. P1 controls eda induction on gluconate and is regulated by GntR. P2 controls eda induction on glucuronate and galacturonate and is regulated by KdgR. P4 is active under conditions of phosphate starvation and is directly controlled by PhoB. In addition, CsrA activates Eda synthesis, apparently by an indirect mechanism that may be involved in the modest changes in expression level that are associated with carbon starvation. The complex regulation of eda is discussed with respect to its several physiological roles, which apparently accommodate not only sugar acid catabolism but also detoxification of metabolites that could accumulate during starvation-induced stress.

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