Regulating colicin synthesis to cope with stress and lethality of colicin production

2012 ◽  
Vol 40 (6) ◽  
pp. 1507-1511 ◽  
Author(s):  
Darja Žgur-Bertok
Keyword(s):  
Escherichia Coli ◽  
Genetic Diversity ◽  
Related Species ◽  
Sos Response ◽  
Translational Efficiency ◽  
Closely Related Species ◽  
E Coli ◽  
Lexa Protein ◽  
Transcription Regulators ◽  
Fine Tune

Colicins are plasmid-encoded bacteriocins active against Escherichia coli and closely related species of Enterobacteriaceae. They promote microbial diversity and genetic diversity in E. coli populations. Colicin synthesis is characteristically repressed by the LexA protein, the key regulator of the SOS response. As colicins are released by cell lysis, generally two LexA dimers binding to two overlapping SOS boxes control untimely expression. Nevertheless, genetic organization of the colicin clusters, additional transcription regulators as well as post-transcriptional mechanisms involving translational efficiency of the lysis and activity genes fine-tune colicin expression and protect against lethality of colicin production.

scholarly journals Quorum Sensing Is a Global Regulatory Mechanism in Enterohemorrhagic Escherichia coli O157:H7

2001 ◽  
Vol 183 (17) ◽  
pp. 5187-5197 ◽  
Author(s):  
Vanessa Sperandio ◽  
Alfredo G. Torres ◽  
Jorge A. Girón ◽  
James B. Kaper
Keyword(s):  
Escherichia Coli ◽  
Quorum Sensing ◽  
Type Strain ◽  
Wild Type Strain ◽  
Regulatory Mechanism ◽  
Sos Response ◽  
Enterohemorrhagic Escherichia Coli ◽  
Trna Genes ◽  
Wild Type ◽  
E Coli

ABSTRACT Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is responsible for outbreaks of bloody diarrhea and hemolytic-uremic syndrome in many countries. EHEC virulence mechanisms include the production of Shiga toxins (Stx) and formation of attaching and effacing (AE) lesions on intestinal epithelial cells. We recently reported that genes involved in the formation of the AE lesion were regulated by quorum sensing through autoinducer-2, which is synthesized by the product of the luxS gene. In this study we hybridized an E. coli gene array with cDNA synthesized from RNA that was extracted from EHEC strain 86-24 and its isogenicluxS mutant. We observed that 404 genes were regulated by luxS at least fivefold, which comprises approximately 10% of the array genes; 235 of these genes were up-regulated and 169 were down-regulated in the wild-type strain compared to in theluxS mutant. Down-regulated genes included several involved in cell division, as well as ribosomal and tRNA genes. Consistent with this pattern of gene expression, theluxS mutant grows faster than the wild-type strain (generation times of 37.5 and 60 min, respectively, in Dulbecco modified Eagle medium). Up-regulated genes included several involved in the expression and assembly of flagella, motility, and chemotaxis. Using operon::lacZ fusions to class I, II, and III flagellar genes, we were able to confirm this transcriptional regulation. We also observed fewer flagella by Western blotting and electron microscopy and decreased motility halos in semisolid agar in the luxS mutant. The average swimming speeds for the wild-type strain and the luxS mutant are 12.5 and 6.6 μm/s, respectively. We also observed an increase in the production of Stx due to quorum sensing. Genes encoding Stx, which are transcribed along with λ-like phage genes, are induced by an SOS response, and genes involved in the SOS response were also regulated by quorum sensing. These results indicate that quorum sensing is a global regulatory mechanism for basic physiological functions of E. coli as well as for virulence factors.

Mutagenesis and More: umuDC and the Escherichia coli SOS Response

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1599-1610 ◽  
Author(s):  
Bradley T Smith ◽  
Graham C Walker
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Cellular Response ◽  
Sos Response ◽  
Posttranslational Regulation ◽  
E Coli ◽  
Sos Mutagenesis ◽  
Induced Mutagenesis ◽  
Mechanistic Basis ◽  
Increase Cell Survival

Abstract The cellular response to DNA damage that has been most extensively studied is the SOS response of Escherichia coli. Analyses of the SOS response have led to new insights into the transcriptional and posttranslational regulation of processes that increase cell survival after DNA damage as well as insights into DNA-damage-induced mutagenesis, i.e., SOS mutagenesis. SOS mutagenesis requires the recA and umuDC gene products and has as its mechanistic basis the alteration of DNA polymerase III such that it becomes capable of replicating DNA containing miscoding and noncoding lesions. Ongoing investigations of the mechanisms underlying SOS mutagenesis, as well as recent observations suggesting that the umuDC operon may have a role in the regulation of the E. coli cell cycle after DNA damage has occurred, are discussed.

scholarly journals A newly identified prophage-encoded gene, ymfM, causes SOS-inducible filamentation in Escherichia coli

2021 ◽  
Author(s):  
Shirin Ansari ◽  
James C. Walsh ◽  
Amy L. Bottomley ◽  
Iain G. Duggin ◽  
Catherine Burke ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Division ◽  
Pathogenic Bacteria ◽  
Bacterial Resistance ◽  
Sos Response ◽  
E Coli ◽  
Ring Assembly ◽  
Multiple Alternative ◽  
Z Ring ◽  
Cell Division Inhibitor

Rod-shaped bacteria such as Escherichia coli can regulate cell division in response to stress, leading to filamentation, a process where cell growth and DNA replication continues in the absence of division, resulting in elongated cells. The classic example of stress is DNA damage which results in the activation of the SOS response. While the inhibition of cell division during SOS has traditionally been attributed to SulA in E. coli, a previous report suggests that the e14 prophage may also encode an SOS-inducible cell division inhibitor, previously named SfiC. However, the exact gene responsible for this division inhibition has remained unknown for over 35 years. A recent high-throughput over-expression screen in E. coli identified the e14 prophage gene, ymfM, as a potential cell division inhibitor. In this study, we show that the inducible expression of ymfM from a plasmid causes filamentation. We show that this expression of ymfM results in the inhibition of Z ring formation and is independent of the well characterised inhibitors of FtsZ ring assembly in E. coli, SulA, SlmA and MinC. We confirm that ymfM is the gene responsible for the SfiC phenotype as it contributes to the filamentation observed during the SOS response. This function is independent of SulA, highlighting that multiple alternative division inhibition pathways exist during the SOS response. Our data also highlight that our current understanding of cell division regulation during the SOS response is incomplete and raises many questions regarding how many inhibitors there actually are and their purpose for the survival of the organism. Importance: Filamentation is an important biological mechanism which aids in the survival, pathogenesis and antibiotic resistance of bacteria within different environments, including pathogenic bacteria such as uropathogenic Escherichia coli. Here we have identified a bacteriophage-encoded cell division inhibitor which contributes to the filamentation that occurs during the SOS response. Our work highlights that there are multiple pathways that inhibit cell division during stress. Identifying and characterising these pathways is a critical step in understanding survival tactics of bacteria which become important when combating the development of bacterial resistance to antibiotics and their pathogenicity.

Contribution of SOS Genes to H2O2-induced Apoptosis-like Death in Escherichia Coli

2021 ◽  
Author(s):  
Heesu Kim ◽  
Dong Gun Lee
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Treatment Strategies ◽  
Sos Response ◽  
Bacterial Dna ◽  
E Coli ◽  
New Treatment ◽  
Induced Apoptosis ◽  
And Function ◽  
The Relationship

Abstract Hydrogen peroxide (H2O2) is a debriding agent that damages the microbial structure and function by generating various reactive oxygen species (ROS). H2O2-produced hydroxyl radical (OH∙) also exert oxidative stress on microorganisms. The spread of antibiotic resistance in bacteria is a serious issue worldwide, and greater efforts are needed to identify and characterize novel antibacterial mechanisms to develop new treatment strategies. Therefore, this study aimed to clarify the relationship between H2O2 and Escherichia coli and to elucidate a novel antibacterial mechanism(s) of H2O2. Following H2O2 exposure, increased levels of 8-hydroxyldeoxyguanosine and malondialdehyde indicated that H2O2 accelerates oxidation of bacterial DNA and lipids in E. coli. As oxidative damage worsened, the SOS response was triggered. Cell division arrest and resulting filamentation were identified in cells, indicating that LexA was involved in DNA replication. It was also verified that RecA, a representative SOS gene, helps self-cleavage of LexA and acts as a bacterial caspase-like protein. Our findings also showed that dinF is essential to preserve E. coli from H2O2-induced ROS, and furthermore, demonstrated that H2O2-induced SOS response and SOS genes participate differently in guarding E. coli from oxidative stress. As an extreme SOS response is considered apoptosis-like death (ALD) in bacteria, additional experiments were performed to examine the characteristics of ALD. DNA fragmentation and membrane depolarization appeared in H2O2-treated cells, suggesting that H2O2 causes ALD in E. coli. In conclusion, our investigations revealed that ALD is a novel antibacterial mode of action(s) of H2O2 with important contributions from SOS genes.

scholarly journals Genomewide Mutational Diversity in Escherichia coli Population Evolving in Prolonged Stationary Phase

mSphere ◽  
2017 ◽  
Vol 2 (3) ◽  
Author(s):  
Savita Chib ◽  
Farhan Ali ◽  
Aswin Sai Narain Seshasayee
Keyword(s):  
Escherichia Coli ◽  
Genetic Diversity ◽  
Stationary Phase ◽  
Phenotypic Diversity ◽  
Model System ◽  
Content Type ◽  
Neutral Drift ◽  
E Coli ◽  
Evolution By Natural Selection ◽  
Over Time

ABSTRACT Prolonged stationary phase in bacteria, contrary to its name, is highly dynamic, with extreme nutrient limitation as a predominant stress. Stationary-phase cultures adapt by rapidly selecting a mutation(s) that confers a growth advantage in stationary phase (GASP). The phenotypic diversity of starving E. coli populations has been studied in detail; however, only a few mutations that accumulate in prolonged stationary phase have been described. This study documented the spectrum of mutations appearing in Escherichia coli during 28 days of prolonged starvation. The genetic diversity of the population increases over time in stationary phase to an extent that cannot be explained by random, neutral drift. This suggests that prolonged stationary phase offers a great model system to study adaptive evolution by natural selection. Prolonged stationary phase is an approximation of natural environments presenting a range of stresses. Survival in prolonged stationary phase requires alternative metabolic pathways for survival. This study describes the repertoire of mutations accumulating in starving Escherichia coli populations in lysogeny broth. A wide range of mutations accumulates over the course of 1 month in stationary phase. Single nucleotide polymorphisms (SNPs) constitute 64% of all mutations. A majority of these mutations are nonsynonymous and are located at conserved loci. There is an increase in genetic diversity in the evolving populations over time. Computer simulations of evolution in stationary phase suggest that the maximum frequency of mutations observed in our experimental populations cannot be explained by neutral drift. Moreover, there is frequent genetic parallelism across populations, suggesting that these mutations are under positive selection. Finally, functional analysis of mutations suggests that regulatory mutations are frequent targets of selection. IMPORTANCE Prolonged stationary phase in bacteria, contrary to its name, is highly dynamic, with extreme nutrient limitation as a predominant stress. Stationary-phase cultures adapt by rapidly selecting a mutation(s) that confers a growth advantage in stationary phase (GASP). The phenotypic diversity of starving E. coli populations has been studied in detail; however, only a few mutations that accumulate in prolonged stationary phase have been described. This study documented the spectrum of mutations appearing in Escherichia coli during 28 days of prolonged starvation. The genetic diversity of the population increases over time in stationary phase to an extent that cannot be explained by random, neutral drift. This suggests that prolonged stationary phase offers a great model system to study adaptive evolution by natural selection.

scholarly journals Genetic diversity of Escherichia coli recovered from the oral cavity of beef cattle and their relatedness to faecal E. coli

2004 ◽  
Vol 39 (6) ◽  
pp. 523-527 ◽  
Author(s):  
M. Aslam ◽  
G.G. Greer ◽  
F.M. Nattress ◽  
C.O. Gill ◽  
L.M. McMullen
Keyword(s):  
Escherichia Coli ◽  
Genetic Diversity ◽  
Oral Cavity ◽  
Beef Cattle ◽  
E Coli

scholarly journals Origin of Contamination and Genetic Diversity of Escherichia coli in Beef Cattle

2003 ◽  
Vol 69 (5) ◽  
pp. 2794-2799 ◽  
Author(s):  
Mueen Aslam ◽  
Frances Nattress ◽  
Gordon Greer ◽  
Chris Yost ◽  
Colin Gill ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Genetic Diversity ◽  
Beef Cattle ◽  
Ground Beef ◽  
Rflp Analysis ◽  
E Coli ◽  
Cattle Feces ◽  
Genetic Subtypes ◽  
Random Amplification ◽  
Pcr Rflp

ABSTRACT The possible origin of beef contamination and genetic diversity of Escherichia coli populations in beef cattle, on carcasses and ground beef, was examined by using random amplification of polymorphic DNA (RAPD) and PCR-restriction fragment length polymorphism (PCR-RFLP) analysis of the fliC gene. E. coli was recovered from the feces of 10 beef cattle during pasture grazing and feedlot finishing and from hides, carcasses, and ground beef after slaughter. The 1,403 E. coli isolates (855 fecal, 320 hide, 153 carcass, and 75 ground beef) were grouped into 121 genetic subtypes by using the RAPD method. Some of the genetic subtypes in cattle feces were also recovered from hides, prechilled carcasses, chilled carcasses, and ground beef. E. coli genetic subtypes were shared among cattle at all sample times, but a number of transient types were unique to individual animals. The genetic diversity of the E. coli population changed over time within individual animals grazing on pasture and in the feedlot. Isolates from one animal (59 fecal, 30 hide, 19 carcass, and 12 ground beef) were characterized by the PCR-RFLP analysis of the fliC gene and were grouped into eight genotypes. There was good agreement between the results obtained with the RAPD and PCR-RFLP techniques. In conclusion, the E. coli contaminating meat can originate from cattle feces, and the E. coli population in beef cattle was highly diverse. Also, genetic subtypes can be shared among animals or can be unique to an animal, and they are constantly changing.

scholarly journals Transmission of IncN Plasmids Carrying blaCTX-M-1 between Commensal Escherichia coli in Pigs and Farm Workers

2009 ◽  
Vol 53 (4) ◽  
pp. 1709-1711 ◽  
Author(s):  
Arshnee Moodley ◽  
Luca Guardabassi
Keyword(s):  
Escherichia Coli ◽  
Genetic Diversity ◽  
Farm Workers ◽  
High Genetic Diversity ◽  
Air Samples ◽  
E Coli ◽  
Pig Farms ◽  
Cephalosporin Resistance ◽  
Human Animal

ABSTRACT CTX-M-1-producing Escherichia coli were isolated from 56 pigs, three farm personnel, two manure samples, and two air samples from two Danish pig farms where an association between prophylactic ceftiofur use and the occurrence of cephalosporin resistance was previously demonstrated. Human, animal, and environmental strains displayed high genetic diversity but harbored indistinguishable or closely related IncN plasmids carrying bla CTX-M-1, indicating that IncN plasmids mediating cephalosporin resistance were transmitted between pigs and farm workers across multiple E. coli lineages.

scholarly journals Emergence of antibiotic resistance from multinucleated bacterial filaments

2014 ◽  
Vol 112 (1) ◽  
pp. 178-183 ◽  
Author(s):  
Julia Bos ◽  
Qiucen Zhang ◽  
Saurabh Vyawahare ◽  
Elizabeth Rogers ◽  
Susan M. Rosenberg ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Antibiotic Resistance ◽  
Sos Response ◽  
Single Cell Level ◽  
Environmental Niche ◽  
Cell Level ◽  
E Coli ◽  
Enhanced Resistance ◽  
New Alleles

Bacteria can rapidly evolve resistance to antibiotics via the SOS response, a state of high-activity DNA repair and mutagenesis. We explore here the first steps of this evolution in the bacteriumEscherichia coli. Induction of the SOS response by the genotoxic antibiotic ciprofloxacin changes theE. colirod shape into multichromosome-containing filaments. We show that at subminimal inhibitory concentrations of ciprofloxacin the bacterial filament divides asymmetrically repeatedly at the tip. Chromosome-containing buds are made that, if resistant, propagate nonfilamenting progeny with enhanced resistance to ciprofloxacin as the parent filament dies. We propose that the multinucleated filament creates an environmental niche where evolution can proceed via generation of improved mutant chromosomes due to the mutagenic SOS response and possible recombination of the new alleles between chromosomes. Our data provide a better understanding of the processes underlying the origin of resistance at the single-cell level and suggest an analogous role to the eukaryotic aneuploidy condition in cancer.

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