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Type 6 Secretion System–Mediated Immunity to Type 4 Secretion System–Mediated Gene Transfer

Science
11 Oct 2013
Vol 342, Issue 6155
pp. 250-253

Bacterial Détente?

Type VI secretion systems (T6SS) correspond to dynamic intracellular organelles that are functionally analogous to contractile bacteriophage tails. The T6SS of several bacteria species have been found to be responsible for antagonistic behavior that likely reflects the translocation of toxic proteins (effectors) between cells. Pseudomonas aeruginosa is able to sense exogenous T6SS attack and assemble its own T6SS apparatus to launch a retaliatory attack aimed directly at the attacker. Now, Ho et al. (p. 250) describe how exogenous attack is sensed in a process that involves membrane disruption and suggest that the T6SS provides a general cellular defense mechanism against not only T6SS but also conjugative DNA elements delivered via the type IV secretion system involved in mating pair formation.

Abstract

Gram-negative bacteria use the type VI secretion system (T6SS) to translocate toxic effector proteins into adjacent cells. The Pseudomonas aeruginosa H1-locus T6SS assembles in response to exogenous T6SS attack by other bacteria. We found that this lethal T6SS counterattack also occurs in response to the mating pair formation (Mpf) system encoded by broad-host-range IncPα conjugative plasmid RP4 present in adjacent donor cells. This T6SS response was eliminated by disruption of Mpf structural genes but not components required only for DNA transfer. Because T6SS activity was also strongly induced by membrane-disrupting natural product polymyxin B, we conclude that RP4 induces “donor-directed T6SS attacks” at sites corresponding to Mpf-mediated membrane perturbations in recipient P. aeruginosa cells to potentially block acquisition of parasitic foreign DNA.

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Supplementary Material

Summary

Materials and Methods
Table S1
References (30, 31)
Movies S1 and S2

Resources

File (1243745s1.mp4)
File (1243745s2.mp4)
File (ho-sm.pdf)

References and Notes

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Information

Published In

Science
Volume 342 | Issue 6155
11 October 2013

Submission history

Received: 25 July 2013
Accepted: 6 September 2013
Published in print: 11 October 2013

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Acknowledgments

Supporting movies and table can be found in the supplementary materials. This work was supported by National Institute of Allergy and Infectious Diseases grants AI-018045 and AI-26289 to J.J.M.

Authors

Affiliations

Brian T. Ho
Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Marek Basler
Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
John J. Mekalanos* [email protected]
Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.

Notes

*
Corresponding author. E-mail: [email protected]

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