scholarly journals Bacterial respiration during stationary phase induces intracellular damage that leads to dormancy

2020 ◽  
Author(s):  
Spencer Cesar ◽  
Lisa Willis ◽  
Kerwyn Casey Huang
Keyword(s):  
Stationary Phase ◽  
Learning Algorithm ◽  
Damage Control ◽  
Quantitative Agreement ◽  
Small Population ◽  
Phase Cell ◽  
Phase Image ◽  
Bacterial Respiration ◽  
Polar Phase ◽  
Dormant Cells

AbstractMost bacteria frequently encounter nutrient-depleted conditions, necessitating regulatory mechanisms that alter cellular physiology and allow for survival of starvation. Here, we show that regrowth of Escherichia coli from prolonged stationary phase upon encountering fresh nutrients is heterogeneous, with one subpopulation suddenly regrowing after a delay (dormancy) and another of nongrowing cells that represented an increasing fraction as the culture aged. Moreover, a sizeable fraction of cells rejuvenated immediately, even when the inoculum was from very old cultures. The size of the dormant and nongrowing subpopulations depended on the time cells had endured stationary phase, as opposed to time-dependent changes to the medium. Regrowth of dormant cells was correlated with the dissolution of polar phase-bright foci that likely represent aggregates of damage, and a deep-learning algorithm was able to distinguish cellular fates based on a single stationary-phase image. Growth restarted in dormant cells after the upregulation of chaperones and DNA repair enzymes, and deletion of the chaperone DnaK resulted in compromised stationary-phase cell morphology and higher incidence of non-growing cells. A mathematical model of damage accumulation and division-mediated partitioning was in quantitative agreement with experimental data, including the small population of cells capable of immediate regrowth even in old cultures. Cells that endured stationary-phase without the ability to respire all immediately and homogeneously regrew in fresh nutrients, indicating that respiration in stationary phase is the driver of dormancy. These findings establish the importance of intracellular damage control when nutrients are sparse, and repair when nutrients are plentiful.

GROWTH STUDIES ON ARTHROBACTER GLOBIFORMIS: II. CHANGES IN MACROMOLECULAR LEVELS DURING GROWTH

1962 ◽  
Vol 8 (5) ◽  
pp. 655-661 ◽  
Author(s):  
I. L. Stevenson
Keyword(s):  
Stationary Phase ◽  
Fold Increase ◽  
Growth Cycle ◽  
Phase Cell ◽  
Lag Phase ◽  
Differential Rate ◽  
Protein Ratio ◽  
Stationary Phase Culture ◽  
Protein Levels ◽  
Dna And Protein Synthesis

Changes in macromolecular levels (RNA, DNA, protein) have been followed during the growth cycle of A. globiformis. When a stationary phase culture is transferred to fresh medium a 12-fold increase in RNA level and 6-fold increases in DNA and protein levels are observed during the predivisional lag phase. Initially RNA synthesis precedes DNA and protein synthesis but all reach the same differential rate 2 to 3 hours prior to division. During the predivisional lag period the RNA/protein ratio per cell expands from 0.19 to 0.36. Once division occurs, cells of A. globiformis remain in the enlarged pleomorphic form until the medium becomes limiting; at this time synthesis of macromolecules ceases and the continued division (three to four generations) results in progressively smaller cells until the coccoid stationary phase cell-type is reached.

scholarly journals Control of Acid Resistance inEscherichia coli

1999 ◽  
Vol 181 (11) ◽  
pp. 3525-3535 ◽  
Author(s):  
Marie-Pierre Castanie-Cornet ◽  
Thomas A. Penfound ◽  
Dean Smith ◽  
John F. Elliott ◽  
John W. Foster
Keyword(s):  
Stationary Phase ◽  
Sigma Factor ◽  
Glutamate Decarboxylase ◽  
Glucose Repression ◽  
Acid Resistance ◽  
Receptor Protein ◽  
Phase Cell ◽  
Alternative Sigma Factor ◽  
E Coli ◽  
Acid Challenge

ABSTRACT Acid resistance (AR) in Escherichia coli is defined as the ability to withstand an acid challenge of pH 2.5 or less and is a trait generally restricted to stationary-phase cells. Earlier reports described three AR systems in E. coli. In the present study, the genetics and control of these three systems have been more clearly defined. Expression of the first AR system (designated the oxidative or glucose-repressed AR system) was previously shown to require the alternative sigma factor RpoS. Consistent with glucose repression, this system also proved to be dependent in many situations on the cyclic AMP receptor protein. The second AR system required the addition of arginine during pH 2.5 acid challenge, the structural gene for arginine decarboxylase (adiA), and the regulatorcysB, confirming earlier reports. The third AR system required glutamate for protection at pH 2.5, one of two genes encoding glutamate decarboxylase (gadA or gadB), and the gene encoding the putative glutamate:γ-aminobutyric acid antiporter (gadC). Only one of the two glutamate decarboxylases was needed for protection at pH 2.5. However, survival at pH 2 required both glutamate decarboxylase isozymes. Stationary phase and acid pH regulation of the gad genes proved separable. Stationary-phase induction of gadA and gadBrequired the alternative sigma factor ςS encoded byrpoS. However, acid induction of these enzymes, which was demonstrated to occur in exponential- and stationary-phase cells, proved to be ςS independent. Neither gad gene required the presence of volatile fatty acids for induction. The data also indicate that AR via the amino acid decarboxylase systems requires more than an inducible decarboxylase and antiporter. Another surprising finding was that the ςS-dependent oxidative system, originally thought to be acid induced, actually proved to be induced following entry into stationary phase regardless of the pH. However, an inhibitor produced at pH 8 somehow interferes with the activity of this system, giving the illusion of acid induction. The results also revealed that the AR system affording the most effective protection at pH 2 in complex medium (either Luria-Bertani broth or brain heart infusion broth plus 0.4% glucose) is the glutamate-dependent GAD system. Thus, E. coli possesses three overlapping acid survival systems whose various levels of control and differing requirements for activity ensure that at least one system will be available to protect the stationary-phase cell under naturally occurring acidic environments.

scholarly journals The LysR-type transcriptional regulator, CidR, regulates stationary phase cell death inStaphylococcus aureus

2016 ◽  
Vol 101 (6) ◽  
pp. 942-953 ◽  
Author(s):  
Sujata S. Chaudhari ◽  
Vinai C. Thomas ◽  
Marat R. Sadykov ◽  
Jeffrey L. Bose ◽  
Daniel J. Ahn ◽  
...  
Keyword(s):  
Cell Death ◽  
Stationary Phase ◽  
Transcriptional Regulator ◽  
Phase Cell ◽  
Stationary Phase Cell

scholarly journals Inhibition of stationary phase respiration impairs persister formation in E. coli

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Mehmet A. Orman ◽  
Mark P. Brynildsen
Keyword(s):  
Stationary Phase ◽  
Respiratory Activity ◽  
Redox Activity ◽  
Bacterial Respiration ◽  
Type I ◽  
E Coli ◽  
Improve Treatment ◽  
Endogenous Proteins ◽  
Prime Target

Abstract Bacterial persisters are rare phenotypic variants that temporarily tolerate high antibiotic concentrations. Persisters have been hypothesized to underlie the recalcitrance of biofilm infections, and strategies to eliminate these cells have the potential to improve treatment outcomes for many hospital-treated infections. Here we investigate the role of stationary phase metabolism in generation of type I persisters in Escherichia coli, which are those that are formed by passage through stationary phase. We find that persisters are unlikely to derive from bacteria with low redox activity, and that inhibition of respiration during stationary phase reduces persister levels by up to ∼1,000-fold. Loss of stationary phase respiratory activity prevents digestion of endogenous proteins and RNA, which yields bacteria that are more capable of translation, replication and concomitantly cell death when exposed to antibiotics. These findings establish bacterial respiration as a prime target for reducing the number of persisters formed in nutrient-depleted, non-growing populations.

scholarly journals The Stationary-Phase Cells of Saccharomyces cerevisiae Display Dynamic Actin Filaments Required for Processes Extending Chronological Life Span

2015 ◽  
Vol 35 (22) ◽  
pp. 3892-3908 ◽  
Author(s):  
Pavla Vasicova ◽  
Renata Lejskova ◽  
Ivana Malcova ◽  
Jiri Hasek
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Stationary Phase ◽  
Actin Filaments ◽  
Phase Cell ◽  
Content Type ◽  
Chronological Aging ◽  
Yeast Cultures ◽  
Actin Cables ◽  
Mitochondrial Networks

Stationary-growth-phaseSaccharomyces cerevisiaeyeast cultures consist of nondividing cells that undergo chronological aging. For their successful survival, the turnover of proteins and organelles, ensured by autophagy and the activation of mitochondria, is performed. Some of these processes are engaged in by the actin cytoskeleton. InS. cerevisiaestationary-phase cells, F actin has been shown to form static aggregates named actin bodies, subsequently cited to be markers of quiescence. Ourin vivoanalyses revealed that stationary-phase cultures contain cells with dynamic actin filaments, besides the cells with static actin bodies. The cells with dynamic actin displayed active endocytosis and autophagy and well-developed mitochondrial networks. Even more, stationary-phase cell cultures grown under calorie restriction predominantly contained cells with actin cables, confirming that the presence of actin cables is linked to successful adaptation to stationary phase. Cells with actin bodies were inactive in endocytosis and autophagy and displayed aberrations in mitochondrial networks. Notably, cells of the respiratory activity-deficientcox4Δ strain displayed the same mitochondrial aberrations and actin bodies only. Additionally, our results indicate that mitochondrial dysfunction precedes the formation of actin bodies and the appearance of actin bodies corresponds to decreased cell fitness. We conclude that the F-actin status reflects the extent of damage that arises from exponential growth.

scholarly journals Sigma S-Dependent Antioxidant Defense Protects Stationary-Phase Escherichia coli against the Bactericidal Antibiotic Gentamicin

2014 ◽  
Vol 58 (10) ◽  
pp. 5964-5975 ◽  
Author(s):  
Jing-Hung Wang ◽  
Rachna Singh ◽  
Michael Benoit ◽  
Mimi Keyhan ◽  
Matthew Sylvester ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Stationary Phase ◽  
Antioxidant Defense ◽  
Physiological State ◽  
Pentose Phosphate ◽  
Phase Cell ◽  
Content Type

ABSTRACTStationary-phase bacteria are important in disease. The σs-regulated general stress response helps them become resistant to disinfectants, but the role of σsin bacterial antibiotic resistance has not been elucidated. Loss of σsrendered stationary-phaseEscherichia colimore sensitive to the bactericidal antibiotic gentamicin (Gm), and proteomic analysis suggested involvement of a weakened antioxidant defense. Use of the psfiAgenetic reporter, 3′-(p-hydroxyphenyl) fluorescein (HPF) dye, and Amplex Red showed that Gm generated more reactive oxygen species (ROS) in the mutant. HPF measurements can be distorted by cell elongation, but Gm did not affect stationary-phase cell dimensions. Coadministration of the antioxidantN-acetyl cysteine (NAC) decreased drug lethality particularly in the mutant, as did Gm treatment under anaerobic conditions that prevent ROS formation. Greater oxidative stress, due to insufficient quenching of endogenous ROS and/or respiration-linked electron leakage, therefore contributed to the greater sensitivity of the mutant; infection by a uropathogenic strain in mice showed this to be the case alsoin vivo. Disruption of antioxidant defense by eliminating the quencher proteins, SodA/SodB and KatE/SodA, or the pentose phosphate pathway proteins, Zwf/Gnd and TalA, which provide NADPH for ROS decomposition, also generated greater oxidative stress and killing by Gm. Thus, besides its established mode of action, Gm also kills stationary-phase bacteria by generating oxidative stress, and targeting the antioxidant defense ofE. colican enhance its efficacy. Relevant aspects of the current controversy on the role of ROS in killing by bactericidal drugs of exponential-phase bacteria, which represent a different physiological state, are discussed.

Stationary phase and the cell cycle of Dictyostelium discoideum in liquid nutrient medium

1976 ◽  
Vol 20 (3) ◽  
pp. 513-523 ◽  
Author(s):  
D.R. Soll ◽  
J. Yarger ◽  
M. Mirick
Keyword(s):  
Cell Cycle ◽  
Stationary Phase ◽  
Dictyostelium Discoideum ◽  
Nutrient Medium ◽  
Nuclear Dna ◽  
Cell Concentration ◽  
Phase Cell ◽  
Cell Multiplication ◽  
Mean Cell Volume ◽  
Liquid Nutrient Medium

Cells of the axenic strain of the cellular slime mould Dictyostelium discoideum, AX-3, multiply in the liquid nutrient medium HL-5 with a doubling time of 12 h. When the cell concentration reaches approximately 1 X10(7) per ml the rate of cell multiplication begins decreasing and after 20–30 h reaches zero, at a stationary phase cell concentration of 2 to 2–5 X 10(7) cells per ml. The intercept of the extrapolated log phase and stationary phase plots has arbitrarily been considered the onset of the stationary phase. We have found that after cells have been in stationary phase for 24–32 h, mean cell volume increases by 25%, average dry weight by 37%, and average protein content by 24%. These values are close to the expected values for a cell population which is blocked at a point late in the cell cycle. Stationary phase cells also contain 25% more nuclear DNA than log phase cells, indicating that the population of cells at stationary phase is blocked after the DNA replication phase. Finally, when stationary phase cells are washed free of stationary phase medium and reinoculated into fresh medium, they reinitiate cell division synchronously. In the light of the demonstrated relationship between stationary phase and the cell cycle, a possible role for the growth inhibitor produced at stationary phase is considered.

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