scholarly journals Glucose confers protection to Escherichia coli against contact killing by Vibrio cholerae

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cristian V. Crisan ◽  
Holly L. Nichols ◽  
Sophia Wiesenfeld ◽  
Gabi Steinbach ◽  
Peter J. Yunker ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Vibrio Cholerae ◽  
Effector Proteins ◽  
Microbial Interactions ◽  
Receptor Protein ◽  
Target Cells ◽  
Type Vi Secretion System ◽  
Arms Races ◽  
Defensive Strategies ◽  
Camp Receptor

AbstractEvolutionary arms races are broadly prevalent among organisms including bacteria, which have evolved defensive strategies against various attackers. A common microbial aggression mechanism is the type VI secretion system (T6SS), a contact-dependent bacterial weapon used to deliver toxic effector proteins into adjacent target cells. Sibling cells constitutively express immunity proteins that neutralize effectors. However, less is known about factors that protect non-sibling bacteria from T6SS attacks independently of cognate immunity proteins. In this study, we observe that human Escherichia coli commensal strains sensitive to T6SS attacks from Vibrio cholerae are protected when co-cultured with glucose. We confirm that glucose does not impair V. cholerae T6SS activity. Instead, we find that cells lacking the cAMP receptor protein (CRP), which regulates expression of hundreds of genes in response to glucose, survive significantly better against V. cholerae T6SS attacks even in the absence of glucose. Finally, we show that the glucose-mediated T6SS protection varies with different targets and killers. Our findings highlight the first example of an extracellular small molecule modulating a genetically controlled response for protection against T6SS attacks. This discovery may have major implications for microbial interactions during pathogen-host colonization and survival of bacteria in environmental communities.

scholarly journals Glucose promotes resistance of human commensal Escherichia coli against contact-killing by pandemic Vibrio cholerae

2020 ◽  
Author(s):  
Cristian V Crisan ◽  
Holly Nichols ◽  
Sophia Wiesenfeld ◽  
Gabi Steinbach ◽  
Peter J Yunker ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Vibrio Cholerae ◽  
Defense Mechanism ◽  
Metabolic Response ◽  
Microbial Community Composition ◽  
Microbial Interactions ◽  
Receptor Protein ◽  
Target Cells ◽  
Type Vi Secretion System ◽  
E Coli

ABSTRACTEvolutionary arms races among organisms are broadly prevalent and bacteria have evolved defensive strategies against various attackers. A common microbial aggression mechanism is the Type VI Secretion System (T6SS), a contact-dependent bacterial weapon used to deliver toxic effector proteins into adjacent target cells. Sibling cells constitutively express immunity proteins that neutralize effectors. However, less is known about mechanisms that allow non-sibling bacteria to respond to external cues and survive T6SS attacks independently of immunity proteins. In this study, we show that resistance to T6SS attacks is promoted by a genetically controlled response to exogenous glucose. We observe that multiple human Escherichia coli commensal strains lacking immunity proteins are sensitive to T6SS attacks from pandemic Vibrio cholerae on nutrient-rich media. By contrast, E. coli cells become resistant to attacks when co-cultured on the same media with glucose. We confirm that glucose does not impair V. cholerae T6SS activity. Instead, we find that cAMP receptor protein (CRP), which alters expression of hundreds of genes in response to glucose, controls resistance to T6SS attacks in E. coli cells. Consistent with the observed resistance on media with glucose, an E. coli crp disruption mutant survives significantly better against V. cholerae T6SS attacks even in the absence of glucose. Finally, we also show that resistance to T6SS attacks depends on the pH of the medium and varies based on the target and killer strains.IMPORTANCEMany Gram-negative bacteria, including important pathogens, encode T6SS genes to deliver toxic effectors and eliminate competitors. Our results uncover a novel defense mechanism against T6SS attacks that is triggered by an external stimulus and mediated by a metabolic response in non-kin target cells. In microbiomes such as those in gastrointestinal tracts where T6SS activity is known to occur, signaling by metabolites like glucose may affect the efficacy of T6SS attacks and alter microbial community composition. Our findings could have vast implications for microbial interactions during pathogen colonization of hosts and survival of bacterial cells in environmental communities. Furthermore, the glucose-mediated resistance observed here might provide a novel example of an evolutionary arms race between killer T6SS cells and target bacteria.

scholarly journals Interactions between the Escherichia coli cAMP receptor protein and the C-terminal domain of the α subunit of RNA polymerase at Class I promoters

1999 ◽  
Vol 337 (3) ◽  
pp. 415-423 ◽  
Author(s):  
Emma C. LAW ◽  
Nigel J. SAVERY ◽  
Stephen J. W. BUSBY
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Transcription Initiation ◽  
Class I ◽  
Receptor Protein ◽  
Camp Receptor Protein ◽  
Α Subunit ◽  
Terminal Domain ◽  
Up Elements ◽  
Camp Receptor

The Escherichia coli cAMP receptor protein (CRP) is a factor that activates transcription at over 100 target promoters. At Class I CRP-dependent promoters, CRP binds immediately upstream of RNA polymerase and activates transcription by making direct contacts with the C-terminal domain of the RNA polymerase α subunit (αCTD). Since αCTD is also known to interact with DNA sequence elements (known as UP elements), we have constructed a series of semi-synthetic Class I CRP-dependent promoters, carrying both a consensus DNA-binding site for CRP and a UP element at different positions. We previously showed that, at these promoters, the CRP–αCTD interaction and the CRP–UP element interaction contribute independently and additively to transcription initiation. In this study, we show that the two halves of the UP element can function independently, and that, in the presence of the UP element, the best location for the DNA site for CRP is position -69.5. This suggests that, at Class I CRP-dependent promoters where the DNA site for CRP is located at position -61.5, the two αCTDs of RNA polymerase are not optimally positioned. Two experiments to test this hypothesis are presented.

scholarly journals Fur-Dam Regulatory Interplay at an Internal Promoter of the Enteroaggregative Escherichia coli Type VI Secretion sci1 Gene Cluster

2020 ◽  
Vol 202 (10) ◽  
Author(s):  
Yannick R. Brunet ◽  
Christophe S. Bernard ◽  
Eric Cascales
Keyword(s):  
Escherichia Coli ◽  
Gene Cluster ◽  
Gene Clusters ◽  
Secretion System ◽  
Target Cells ◽  
Type Vi Secretion System ◽  
Content Type ◽  
Internal Promoter ◽  
E Coli ◽  
Type Vi Secretion

ABSTRACT The type VI secretion system (T6SS) is a weapon for delivering effectors into target cells that is widespread in Gram-negative bacteria. The T6SS is a highly versatile machine, as it can target both eukaryotic and prokaryotic cells, and it has been proposed that T6SSs are adapted to the specific needs of each bacterium. The expression of T6SS gene clusters and the activation of the secretion apparatus are therefore tightly controlled. In enteroaggregative Escherichia coli (EAEC), the sci1 T6SS gene cluster is subject to a complex regulation involving both the ferric uptake regulator (Fur) and DNA adenine methylase (Dam)-dependent DNA methylation. In this study, an additional, internal, promoter was identified within the sci1 gene cluster using +1 transcriptional mapping. Further analyses demonstrated that this internal promoter is controlled by a mechanism strictly identical to that of the main promoter. The Fur binding box overlaps the −10 transcriptional element and a Dam methylation site, GATC-32. Hence, the expression of the distal sci1 genes is repressed and the GATC-32 site is protected from methylation in iron-rich conditions. The Fur-dependent protection of GATC-32 was confirmed by an in vitro methylation assay. In addition, the methylation of GATC-32 negatively impacted Fur binding. The expression of the sci1 internal promoter is therefore controlled by iron availability through Fur regulation, whereas Dam-dependent methylation maintains a stable ON expression in iron-limited conditions. IMPORTANCE Bacteria use weapons to deliver effectors into target cells. One of these weapons, the type VI secretion system (T6SS), assembles a contractile tail acting as a spring to propel a toxin-loaded needle. Its expression and activation therefore need to be tightly regulated. Here, we identified an internal promoter within the sci1 T6SS gene cluster in enteroaggregative E. coli. We show that this internal promoter is controlled by Fur and Dam-dependent methylation. We further demonstrate that Fur and Dam compete at the −10 transcriptional element to finely tune the expression of T6SS genes. We propose that this elegant regulatory mechanism allows the optimum production of the T6SS in conditions where enteroaggregative E. coli encounters competing species.

scholarly journals The cyclic AMP (cAMP)-cAMP receptor protein complex functions both as an activator and as a corepressor at the tsx-p2 promoter of Escherichia coli K-12.

1991 ◽  
Vol 173 (17) ◽  
pp. 5419-5430 ◽  
Author(s):  
P Gerlach ◽  
L Søgaard-Andersen ◽  
H Pedersen ◽  
J Martinussen ◽  
P Valentin-Hansen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cyclic Amp ◽  
Protein Complex ◽  
Receptor Protein ◽  
Camp Receptor Protein ◽  
Complex Functions ◽  
P2 Promoter ◽  
Camp Receptor ◽  
K 12

scholarly journals Structural Energy Landscapes and Plasticity of the Microstates of Apo Escherichia coli cAMP Receptor Protein

Biochemistry ◽  
2019 ◽  
Vol 59 (4) ◽  
pp. 460-470 ◽  
Author(s):  
Rati Chkheidze ◽  
Wilfredo Evangelista ◽  
Mark A. White ◽  
Y. Whitney Yin ◽  
J. Ching Lee
Keyword(s):  
Escherichia Coli ◽  
Receptor Protein ◽  
Energy Landscapes ◽  
Camp Receptor Protein ◽  
Camp Receptor

Determination of the rates of synthesis and degradation of adenosine 3′,5′-cyclic monophosphate in Escherichia coli CRP− and CRP+ strains

1978 ◽  
Vol 56 (9) ◽  
pp. 849-852 ◽  
Author(s):  
Ann D. E. Fraser ◽  
Hiroshi Yamazaki
Keyword(s):  
Escherichia Coli ◽  
Receptor Protein ◽  
Camp Receptor Protein ◽  
Balanced Growth ◽  
E Coli ◽  
Cyclic Monophosphate ◽  
Camp Receptor ◽  
Extracellular Camp ◽  
Synthesis And Degradation

We have developed a method for estimating the rates of synthesis and degradation of adenosine 3′,5′-cyclic monophosphate (cAMP) in Escherichia coli during balanced growth. Applying this method, we have found that an E. coli CRP− mutant 5333 (deficient for cAMP receptor protein) synthesizes cAMP about 25 times faster than does its CRP+ parent 1100. This accounts for the abnormally high intracellular and extracellular cAMP accumulation in 5333.

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