Contact-Dependent Inhibition of Growth in
            <i>Escherichia coli</i>

Aoki, Stephanie K.; Pamma, Rupinderjit; Hernday, Aaron D.; Bickham, Jessica E.; Braaten, Bruce A.; Low, David A.

doi:10.1126/science.1115109

Cited by 366 publications

(527 citation statements)

References 16 publications

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“…1A). This result suggested that CFT073 could prevent MG1655 FЈ biofilm formation, either by direct contact or secretion of an inhibitory molecule (14,15). To distinguish between these two possibilities, we conducted in vitro adhesion assays in poly(vinyl chloride) microtiter plates and microfermentors, containing filtersterilized CFT073 supernatant of a stationary phase culture.…”

Section: Cft073mentioning

confidence: 99%

Broad-spectrum biofilm inhibition by a secreted bacterial polysaccharide

Valle

Henry

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

236

208

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The development of surface-attached biofilm bacterial communities is considered an important source of nosocomial infections. Recently, bacterial interference via signaling molecules and surface active compounds was shown to antagonize biofilm formation, suggesting that nonantibiotic molecules produced during competitive interactions between bacteria could be used for biofilm reduction. Hence, a better understanding of commensal͞pathogen interactions within bacterial community could lead to an improved control of exogenous pathogens. To reveal adhesion or growthrelated bacterial interference, we investigated interactions between uropathogenic and commensal Escherichia coli in mixed in vitro biofilms. We demonstrate here that the uropathogenic strain CFT073 and all E. coli expressing group II capsules release into their environment a soluble polysaccharide that induces physicochemical surface alterations, which prevent biofilm formation by a wide range of Gram-positive and Gram-negative bacteria. We show that the treatment of abiotic surfaces with group II capsular polysaccharides drastically reduces both initial adhesion and biofilm development by important nosocomial pathogens. These findings identify capsular polymers as antiadhesion bacterial interference molecules, which may prove to be of significance in the design of new strategies to limit biofilm formation on medical in dwelling devices.bacterial interference ͉ Escherichia coli ͉ group II capsule ͉ extraintestinal

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Section: Cft073mentioning

confidence: 99%

Broad-spectrum biofilm inhibition by a secreted bacterial polysaccharide

Valle

Henry

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

236

208

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“…PAI I-III and V contain genes that either are absent in strain CFT073 [e.g., several adhesin gene clusters and the cdiAB genes required for contact-dependent growth inhibition of other bacteria (22)] or which are located in similar islands located elsewhere in the CFT073 genome. PAI IV is very similar in both UPEC strains.…”

Section: E Coli 536 Genome Sequence Determination and Comparative Anal-mentioning

confidence: 99%

How to become a uropathogen: Comparative genomic analysis of extraintestinal pathogenic Escherichia coli strains

Brzuszkiewicz

Brüggemann

Liesegang

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

327

275

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Uropathogenic Escherichia coli (UPEC) strain 536 (O6:K15:H31) is one of the model organisms of extraintestinal pathogenic E. coli (ExPEC). To analyze this strain's genetic basis of urovirulence, we sequenced the entire genome and compared the data with the genome sequence of UPEC strain CFT073 (O6:K2:H1) and to the available genomes of nonpathogenic E. coli strain MG1655 (K-12) and enterohemorrhagic E. coli. The genome of strain 536 is Ϸ292 kb smaller than that of strain CFT073. Genomic differences between both UPEC are mainly restricted to large pathogenicity islands, parts of which are unique to strain 536 or CFT073. Genome comparison underlines that repeated insertions and deletions in certain parts of the genome contribute to genome evolution. Furthermore, 427 and 432 genes are only present in strain 536 or in both UPEC, respectively. The majority of the latter genes is encoded within smaller horizontally acquired DNA regions scattered all over the genome. Several of these genes are involved in increasing the pathogens' fitness and adaptability. Analysis of virulence-associated traits expressed in the two UPEC O6 strains, together with genome comparison, demonstrate the marked genetic and phenotypic variability among UPEC. The ability to accumulate and express a variety of virulence-associated genes distinguishes ExPEC from many commensals and forms the basis for the individual virulence potential of ExPEC. Accordingly, instead of a common virulence mechanism, different ways exist among ExPEC to cause disease.fitness ͉ genome comparison ͉ uropathogenic Escherichia coli

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“…The underlying mechanisms by which cells are inhibited in the SCDI reported here and the CDI reported by Aoki et al (2005) have not yet been elucidated. However, it is clear that these two inhibitory processes are functionally and genetically distinct.…”

Section: Discussionmentioning

confidence: 87%

“…How important the CDI reported by Aoki et al (2005) and that observed in this study are to the ecology of bacteria is unclear at this time but is certainly intriguing and worthy of further investigation. If in natural populations CDI and SCDI have effects of the magnitude observed in these laboratory studies, they could have a profound effect on the structure of bacterial communities.…”

Section: Discussionmentioning

confidence: 95%

See 1 more Smart Citation

The evolution of contact-dependent inhibition in non-growing populations ofEscherichia coli

et al. 2007

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In the course of liquid culture, serial passage experiments with Escherichia coli K-12 bearing a mutator gene deletion (DmutS) we observed the evolution of strains that appeared to kill or inhibit the growth of the bacteria from where they were derived, their ancestors. We demonstrate that this inhibition occurs after the cells stop growing and requires physical contact between the evolved and ancestral bacteria. Thereby, it is referred to as stationary phase contact-dependent inhibition (SCDI ). The evolution of this antagonistic relationship is not anticipated from existing theory and experiments of competition in mass (liquid) culture. Nevertheless, it occurred in the same way (parallel evolution) in the eight independent serial transfer cultures, through different single base substitutions in a gene in the glycogen synthesis pathway, glgC. We demonstrate that the observed mutations in glgC, which codes for ADP-glucose pyrophosphorylase, are responsible for both the ability of the evolved bacteria to inhibit or kill their ancestors and their immunity to that inhibition or killing. We present evidence that without additional evolution, mutator genes, or known mutations in glgC, other strains of E. coli K-12 are also capable of SCDI or sensitive to this inhibition. We interpret this, in part, as support for the generality of SCDI and also as suggesting that the glgC mutations responsible for the SCDI, which evolved in our experiments, may suppress the action of one or more genes responsible for the sensitivity of E. coli to SCDI. Using numerical solutions to a mathematical model and in vitro experiments, we explore the population dynamics of SCDI and postulate the conditions responsible for its evolution in mass culture. We conclude with a brief discussion of the potential ecological significance of SCDI and its possible utility for the development of antimicrobial agents, which unlike existing antibiotics, can kill or inhibit the growth of bacteria that are not growing.

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Contact-Dependent Inhibition of Growth in Escherichia coli

Cited by 366 publications

References 16 publications

Broad-spectrum biofilm inhibition by a secreted bacterial polysaccharide

Broad-spectrum biofilm inhibition by a secreted bacterial polysaccharide

How to become a uropathogen: Comparative genomic analysis of extraintestinal pathogenic Escherichia coli strains

The evolution of contact-dependent inhibition in non-growing populations ofEscherichia coli

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