Thursday, 22 January 2015

Hey Colin! Here's some more Vibrio for you. The use of the Type Six Secretion System to stab neighbouring bacteria and take their DNA

Horizontal gene transfer (HGT) occurs in bacteria and archaea through many different processes. Natural competence for transformation is a common mode of HGT and allows bacteria to take up free DNA from the environment. Vibrio cholerae is a mainly aquatic organism mostly found in marine habitats associating with plankton blooms as well as shellfish and is considered by the WHO to be the most important Vibrio sp. to humans. When growing on chitinous surfaces, V. cholerae can initiate natural competence through the production a regulatory protein, TfoX, due to the presence of chitin and its degradation products. The type VI secretion system (T6SS) is the most recently discovered mechanism for effector secretion that is now understood in gram-negative bacteria. Its structure and function resembles intracellular and membrane-attached phage tails and can pierce neighbouring bacterial and eukaryotic cells. A study by Borgeaud et. al. (2015) demonstrated the use of the T6SS by V. cholerae as part of the TfoX competence regulon and its expression when on chitinous surfaces.

V. cholerae was grown in the absence and presence of chitin-induced expression of TfoX. RNA-sequencing was then used to understand the extent of the competence regulon and enable an accurate assessment of the bacterial transcriptome. Two strains of V. cholerae were also used to simulate a predator-prey relationship to investigate whether competence induced T6SS-mediated killing affects transformation. Live-cell fluorescence microscopy imaging was used to visualise prey lysis and the transfer of genetic material.

Three T6SS encoding gene clusters were observed to be up-regulated upon the induction of TfoX, the major gene cluster and two auxiliary clusters. They concluded that the RNA-seq data suggests TfoX initiates the transcription of these clusters in the presence of a chitinous substrate and the T6SS genes were elevated after growth of V. cholerae on chitin flakes. The functionality of the T6SS was then assessed in an interspecies killing assay. V. cholerae strains with an inducible copy of TfoX were shown to have a significant killing behaviour toward Escherichia coli due to the activation of T6SS. They also found upon TfoX induction, in predator-prey relationship tests, natural transformants were readily obtained in predator cells and never or rarely found in T6SS-defective strains. In conclusion, upon competence induction V. cholerae induced the T6SS, this lead to the killing and lysis of non-immune neighbouring bacteria. This caused the release of DNA which transforms competent predatory cells. This technique resembles bacterial fractricide as described in Streptococcus pneumonia but, in contrast, V. cholerae seems to target strains with no compatible effector-immunity and is dependent on contact. Live-cell fluorescence microscopy showed high T6SS activity in predator cells followed by cell rounding and lysis of the prey. The close proximity observed of competent bacteria to lysed cells with the distinctive formation of certain proteins is indicative of DNA translocation into the predator cell. These gene transfer events were only observed in T6SS-positive strains.


These findings show the importance of the T6SS as a method of HGT in V. cholerae. Similar to S. pneumoniae and other bacteria, this uptake of DNA from the environment could lead to the emergence of multidrug resistant strains. This could have particular significance with antibiotics entering the water column, environmental V. cholerae could become resistant to these leading to cholera outbreaks which could be harder to fight and control. However, this papers findings could be used to develop new ways to fight V. cholerae; if a method could be found to interfere with the HGT pathways, similar to the effects of CRISPR on Staphylococcus epidermidis, then this may significantly reduce its evolution and thus the spread of antibiotic resistance. Borgeaud et. al also suggests that chitin-induced expression may also enhance the virulence potential of this pathogen in the human gut. Therefore, any method found to reduce the HGT of V. cholerae may have an added bonus of also reducing the severity or its ability to cause disease.

Borgeaud, S., Metzger, L. C., Scrignari, T., & Blokesch, M. (2015). The type VI secretion system of Vibrio cholerae fosters horizontal gene transfer. Science347(6217), 63-67.
Special thanks to Prof. Blokesch for access to this report

2 comments:

  1. Hi Ben,

    In terms of new methods to fight V. cholerae, do you think there could just be a way to reduce or block competence of it for the chitin? Perhaps by preventing adhesion to the surface? Although even if it could work, I'm not sure how it could be implemented on a large scale!!

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  2. I agree that on a large scale it wouldn't feasible/appropriate to try and control V. cholerae natural competence. If this was possible then it could have wide environmental consequences, maybe affecting chitinous organisms or other bacteria associated with them. In order to reduce any possible evolution of antibiotic resistance in environmental populations I think the best method is to control the amount of antibiotics entering the water e.g. from farm animals. If a method was devised, such as blocking receptor sites or denaturing the TfoX protein etc, then I feel this would have much more use when used in conjunction with regular antibiotics combatting infections in the human gut. This would mean that V. cholerae would have far less potential to become resistant to this antibiotic making the drug more effective as well as, as mentioned above, possibly reducing its virulence. I hope this answers your question!

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