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The pseudomonas quinolone signal (PQS) balances life and death in Pseudomonas aeruginosa populations.

Häussler S, Becker T - PLoS Pathog. (2008)

Bottom Line: We propose that this dual function fragments populations into less and more stress tolerant members which respond differentially to developing stresses in deteriorating habitats.This suggests that a little poison may be generically beneficial to populations, in promoting survival of the fittest, and in contributing to bacterial multi-cellular behavior.It further identifies PQS as an essential mediator of the shaping of the population structure of Pseudomonas and of its response to and survival in hostile environmental conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell Biology, Helmholtz Center for Infection Research, Braunschweig, Germany. susanne.haeussler@helmholtz-hzi.de

ABSTRACT
When environmental conditions deteriorate and become inhospitable, generic survival strategies for populations of bacteria may be to enter a dormant state that slows down metabolism, to develop a general tolerance to hostile parameters that characterize the habitat, and to impose a regime to eliminate damaged members. Here, we provide evidence that the pseudomonas quinolone signal (PQS) mediates induction of all of these phenotypes. For individual cells, PQS, an interbacterial signaling molecule of Pseudomonas aeruginosa, has both deleterious and beneficial activities: on the one hand, it acts as a pro-oxidant and sensitizes the bacteria towards oxidative and other stresses and, on the other, it efficiently induces a protective anti-oxidative stress response. We propose that this dual function fragments populations into less and more stress tolerant members which respond differentially to developing stresses in deteriorating habitats. This suggests that a little poison may be generically beneficial to populations, in promoting survival of the fittest, and in contributing to bacterial multi-cellular behavior. It further identifies PQS as an essential mediator of the shaping of the population structure of Pseudomonas and of its response to and survival in hostile environmental conditions.

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Killing curves upon exposure to UV irradiation.Wild-type PAO1, the pqsA mutant, the pqsH mutant and the pqsA mutant complemented with pLG10 were grown overnight in LB, and diluted in DeMoss medium [40]. The cells were UV irradiated while shaking, and aliquots were removed at 10s intervals. The exogenous addition of 100 µM PQS to the pqsA mutant cultures 4 h before exposure to UV radiation restored UV tolerance, whereas PQS addition immediately before the UV stress did not show any effect. Serial dilutions were plated on LB agar to determine the viable cell count. The UV killing assays were performed three times with independent cultures, and the outcome of one representative experiment is shown.
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ppat-1000166-g010: Killing curves upon exposure to UV irradiation.Wild-type PAO1, the pqsA mutant, the pqsH mutant and the pqsA mutant complemented with pLG10 were grown overnight in LB, and diluted in DeMoss medium [40]. The cells were UV irradiated while shaking, and aliquots were removed at 10s intervals. The exogenous addition of 100 µM PQS to the pqsA mutant cultures 4 h before exposure to UV radiation restored UV tolerance, whereas PQS addition immediately before the UV stress did not show any effect. Serial dilutions were plated on LB agar to determine the viable cell count. The UV killing assays were performed three times with independent cultures, and the outcome of one representative experiment is shown.

Mentions: Since we could show in this study that PQS can induce oxidative DNA damage we wondered whether this DNA damage may trigger DNA repair and thus induce UV-tolerance. Therefore we applied UV-stress and monitored bacterial survival (Figure 10). Wild-type cells showed killing patterns, characterized by roughly 7 log units of killing over 60 s of UV irradiation. The pqsH and the pqsA mutant were hypersensitive to UV and were killed almost completely within 20–30 s of irradiation. The exogenous addition of 100 µM PQS and the expression of the pqsA-E operon in trans partially restored UV tolerance in the pqsA mutant.


The pseudomonas quinolone signal (PQS) balances life and death in Pseudomonas aeruginosa populations.

Häussler S, Becker T - PLoS Pathog. (2008)

Killing curves upon exposure to UV irradiation.Wild-type PAO1, the pqsA mutant, the pqsH mutant and the pqsA mutant complemented with pLG10 were grown overnight in LB, and diluted in DeMoss medium [40]. The cells were UV irradiated while shaking, and aliquots were removed at 10s intervals. The exogenous addition of 100 µM PQS to the pqsA mutant cultures 4 h before exposure to UV radiation restored UV tolerance, whereas PQS addition immediately before the UV stress did not show any effect. Serial dilutions were plated on LB agar to determine the viable cell count. The UV killing assays were performed three times with independent cultures, and the outcome of one representative experiment is shown.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2533401&req=5

ppat-1000166-g010: Killing curves upon exposure to UV irradiation.Wild-type PAO1, the pqsA mutant, the pqsH mutant and the pqsA mutant complemented with pLG10 were grown overnight in LB, and diluted in DeMoss medium [40]. The cells were UV irradiated while shaking, and aliquots were removed at 10s intervals. The exogenous addition of 100 µM PQS to the pqsA mutant cultures 4 h before exposure to UV radiation restored UV tolerance, whereas PQS addition immediately before the UV stress did not show any effect. Serial dilutions were plated on LB agar to determine the viable cell count. The UV killing assays were performed three times with independent cultures, and the outcome of one representative experiment is shown.
Mentions: Since we could show in this study that PQS can induce oxidative DNA damage we wondered whether this DNA damage may trigger DNA repair and thus induce UV-tolerance. Therefore we applied UV-stress and monitored bacterial survival (Figure 10). Wild-type cells showed killing patterns, characterized by roughly 7 log units of killing over 60 s of UV irradiation. The pqsH and the pqsA mutant were hypersensitive to UV and were killed almost completely within 20–30 s of irradiation. The exogenous addition of 100 µM PQS and the expression of the pqsA-E operon in trans partially restored UV tolerance in the pqsA mutant.

Bottom Line: We propose that this dual function fragments populations into less and more stress tolerant members which respond differentially to developing stresses in deteriorating habitats.This suggests that a little poison may be generically beneficial to populations, in promoting survival of the fittest, and in contributing to bacterial multi-cellular behavior.It further identifies PQS as an essential mediator of the shaping of the population structure of Pseudomonas and of its response to and survival in hostile environmental conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell Biology, Helmholtz Center for Infection Research, Braunschweig, Germany. susanne.haeussler@helmholtz-hzi.de

ABSTRACT
When environmental conditions deteriorate and become inhospitable, generic survival strategies for populations of bacteria may be to enter a dormant state that slows down metabolism, to develop a general tolerance to hostile parameters that characterize the habitat, and to impose a regime to eliminate damaged members. Here, we provide evidence that the pseudomonas quinolone signal (PQS) mediates induction of all of these phenotypes. For individual cells, PQS, an interbacterial signaling molecule of Pseudomonas aeruginosa, has both deleterious and beneficial activities: on the one hand, it acts as a pro-oxidant and sensitizes the bacteria towards oxidative and other stresses and, on the other, it efficiently induces a protective anti-oxidative stress response. We propose that this dual function fragments populations into less and more stress tolerant members which respond differentially to developing stresses in deteriorating habitats. This suggests that a little poison may be generically beneficial to populations, in promoting survival of the fittest, and in contributing to bacterial multi-cellular behavior. It further identifies PQS as an essential mediator of the shaping of the population structure of Pseudomonas and of its response to and survival in hostile environmental conditions.

Show MeSH
Related in: MedlinePlus