Dear Mohammed,

The following publications cover the answer to your question:

1-MBio. 2015 May 5;6(3):e00285-15. doi: 10.1128/mBio.00285-15.

New players in the toxin field: polymorphic toxin systems in bacteria.

Jamet A1, Nassif X.

Author information

Abstract

Bacteria have evolved numerous strategies to increase their competitiveness and fight against each other. Indeed, a large arsenal of antibacterial weapons is available in order to inhibit the proliferation of competitor cells. Polymorphic toxin systems (PTS), recently identified by bioinformatics in all major bacterial lineages, correspond to such a system primarily involved in conflict between related bacterial strains. They are typically composed of a secreted multidomain toxin, a protective immunity protein, and multiple cassettes encoding alternative toxic domains. The C-terminal domains of polymorphic toxins carry the toxic activity, whereas the N-terminal domains are related to the trafficking mode. In silico analysis of PTS identified over 150 distinct toxin domains, including putative nuclease, deaminase, or peptidase domains. Immunity genes found immediately downstream of the toxin genes encode small proteins that protect bacteria against their own toxins or against toxins secreted by neighboring cells. PTS encompass well-known colicins and pyocins, contact-dependent growth inhibition systems which include CdiA and Rhs toxins and some effectors of type VI secretion systems. We have recently characterized the MafB toxins, a new family of PTS deployed by pathogenic Neisseria spp. Many other putative PTS have been identified by in silico predictions but have yet to be characterized experimentally. However, the high number of these systems suggests that PTS have a fundamental role in bacterial biology that is likely to extend beyond interbacterial competition.

http://www.ncbi.nlm.nih.gov/pubmed/25944858

2-Trends Microbiol. 2013 May;21(5):230-7. doi: 10.1016/j.tim.2013.02.003. Epub 2013 Mar 7.

Bacterial contact-dependent growth inhibition.

Ruhe ZC1, Low DA, Hayes CS.

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Abstract

Bacteria cooperate to form multicellular communities and compete against one another for environmental resources. Here, we review recent advances in the understanding of bacterial competition mediated by contact-dependent growth inhibition (CDI) systems. Different CDI+ bacteria deploy a variety of toxins to inhibit neighboring cells and protect themselves from autoinhibition by producing specific immunity proteins. The genes encoding CDI toxin-immunity protein pairs appear to be exchanged between cdi loci and are often associated with other toxin-delivery systems in diverse bacterial species. CDI also appears to facilitate cooperative behavior between kin, suggesting that these systems may have other roles beyond competition.

http://www.ncbi.nlm.nih.gov/pubmed/23473845

3- The role of contact-dependent growth inhibition toxin systems in bacterial competition and biofilm development

 King, Andrew D (2015) The role of contact-dependent growth inhibition toxin systems in bacterial competition and biofilm development. PhD thesis, University of York.

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PhDThesisAndrewDKing.pdf

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Abstract

Contact-dependent growth inhibition (CDI) toxins are a recently identified family of polymorphic toxins, initially found in Escherichia coli. CDI toxins are found widely spread in Gram-negative bacterial species, including pathogenic strains, and have been shown to possess a wide range of toxin types which are effective against other bacteria. This research shows that the E. coli EC93 CDI system confers a competitive advantage on bacteria growing in multi strain biofilms with susceptible bacteria. This advantage is due to two factors, firstly the EC93 CDI toxin was shown to be capable of inhibiting the growth of susceptible bacteria in a biofilm and secondly the conserved region of the EC93 CdiA protein was found to increase the rate of biofilm formation. Analysis of the effects of the EC93 and EC869o11 CDI toxins at the single cell level showed that different classes of CDI toxins can act at different rates and with varying degrees of reversibility. Understanding the variable impact of CDI toxins, in concert with CDI’s role in enhancing biofilm formation, aids our understanding of bacterial competition in the natural environment.

http://etheses.whiterose.ac.uk/10571/

4-Bacterial Warfare

UCSB researchers demonstrate how gram-negative bacteria deliver toxins to kill neighboring bacteria

By Jim Logan

- See more at: http://www.news.ucsb.edu/2015/015838/bacterial-warfare#sthash.QmGc2Y9G.dpuf

It’s bacteria against bacteria, and one of them is going down.

Two UC Santa Barbara graduate students have demonstrated how certain microbes exploit proteins in nearby bacteria to deliver toxins and kill them. The mechanisms behind this bacterial warfare, the researchers suggest, could be harnessed to target pathogenic bacteria. Their findings appear in the Proceedings of the National Academy of Sciences.

Lead authors Julia L.E. Willett and Grant C. Gucinski have detailed how gram-negative bacteria use contact-dependent growth inhibition (CDI) systems to infiltrate and deliver protein toxins into neighboring cells. By studying the bacteria Escherichia coli (E. coli), they were able to document how CDI “translocation domains” can use multiple pathways to transfer those toxins into a cell. By understanding that mechanism, Willett said, it could be possible to use it as a model for pinpoint targeting of bacteria.

“The long-term, real-world potential is that if we know bacteria can deliver their own proteins into other cells, we might be able to use this as a delivery system for antibiotics and other therapeutics,” said Willett, a doctoral student in UCSB’s Department of Molecular, Cellular and Developmental Biology (MCDB). She and Gucinski conducted the work under the direction of faculty adviser and MCDB professor Chris Hayes. Hayes is the second author on the paper.

“If we know the detailed mechanisms of delivery maybe we can target specific groups of bacteria,” Willett continued. “Instead of taking an antibiotic that targets all bacteria, we might be able to deliver one that could specifically target one group of bad bacteria that leaves the good bacteria in your gut alone.”

Gucinski, a graduate student researcher in UCSB’s Biomolecular Science and Engineering Program, began studying E. coli as an undergraduate. Although it has a reputation as a nasty pathogen, that group of bacteria is generic enough to make an ideal research subject.

“E. coli is the easiest system to work with and very representative of the majority of other bacteria,” Gucinski said. “The kind of CDI systems that we study are also found in a lot of different kinds of bacteria. This is the tip of the iceberg in our understanding of what we’ll find in other CDI systems in other bacteria.”

CDI were first described by David Low, professor of MCDB, in 2005. Low, a co-author of the current PNAS paper, reported how a bacterial cell would touch a neighboring cell — one that was competing for resources in the environment — and inject it with a toxin. Willett and Gucinski’s research builds on Low’s work by identifying the multiple ways CDI toxins exploit target cells. The key was in understanding the genetics of those targeted bacteria.

“We know that the cells would have these CDI systems; we know the genetics that are required to make this toxin system, but we were interested in the genetics on the other side, the genetics that are required in the cell that’s being inhibited or the cell that’s receiving this toxin,” Willett explained. “What specifically in that cell is required for the toxin to go from outside the cell to inside the cell?”

Willett and Gucinski found that mutations in the target cells allowed CDI to exploit those cells and inject them with toxins.

“What these CDI systems have done is they’ve actually hijacked machinery that the cells already have,” Willett said. “And so cells when they’re growing need to take in nutrients, and the CDI systems hijack those pre-existing systems to deliver these toxins. It’s not really tricking the target cells, but it’s basically hijacking what’s already there for the inhibitor cell’s own benefit.”

Looking ahead, Willett and Gucinski say potential therapeutic applications are tantalizing but years away. “We’re still trying to understand the routes that we can get different CDI toxins into the cell,” Gucinski said. “One interesting direction would be what other cargo we can deliver with E. coli, how we can manipulate and control the system to target the pathogens.”

Given the rise of drug-resistant bacteria and a dearth of research into new antibiotics, Willett and Gucinski’s research has the potential to open a new front in the fight against pathogenic bacteria.

“We hear on the news that a lot of pathogens are becoming resistant or people can no longer take certain antibiotics,” Willett said. “And so this might be a new way to get around that. Instead of treating everything on a broad spectrum, if we could learn how a natural antibacterial system delivers things that kill other bacteria we might be able to more learn how we can deliver things like specific proteins or specific antibiotics to kill other bacteria.”

Also contributing to the research was UCSB undergraduate Jackson P. Fatheree. The study was supported by a grant from the National Institutes of Health and a National Science Foundation Graduate Research Fellowship.

http://www.news.ucsb.edu/2015/015838/bacterial-warfare

Hoping this will be helpful,

Rafik

Thank you Dr. Rafik 

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