SOS, the formidable strategy of bacteria against aggressions

Baharoglu, Zeynep; Mazel, Didier

doi:10.1111/1574-6976.12077

Cited by 339 publications

(323 citation statements)

References 203 publications

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“…During conjugation, the plasmid enters the new cell as single-stranded DNA (32), producing a transient activation of the SOS response (33). The SOS response is a bacterial stress response triggered by an increase in single-stranded DNA in the cell, which leads to a rise in mutation and recombination rates (34). Activation of the SOS regulon also results in inhibition of cell division, which by definition translates into a decrease in bacterial fitness in the short term (35).…”

Section: Plasmid Receptionmentioning

confidence: 99%

Fitness Costs of Plasmids: a Limit to Plasmid Transmission

2017

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Plasmids mediate the horizontal transmission of genetic information between bacteria, facilitating their adaptation to multiple environmental conditions. An especially important example of the ability of plasmids to catalyze bacterial adaptation and evolution is their instrumental role in the global spread of antibiotic resistance, which constitutes a major threat to public health. Plasmids provide bacteria with new adaptive tools, but they also entail a metabolic burden that, in the absence of selection for plasmid-encoded traits, reduces the competitiveness of the plasmid-carrying clone. Although this fitness reduction can be alleviated over time through compensatory evolution, the initial cost associated with plasmid carriage is the main constraint on the vertical and horizontal replication of these genetic elements. The fitness effects of plasmids therefore have a crucial influence on their ability to associate with new bacterial hosts and consequently on the evolution of plasmid-mediated antibiotic resistance. However, the molecular mechanisms underlying plasmid fitness cost remain poorly understood. Here, we analyze the literature in the field and examine the potential fitness effects produced by plasmids throughout their life cycle in the host bacterium. We also explore the various mechanisms evolved by plasmids and bacteria to minimize the cost entailed by these mobile genetic elements. Finally, we discuss potential future research directions in the field.

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Section: Plasmid Receptionmentioning

confidence: 99%

Fitness Costs of Plasmids: a Limit to Plasmid Transmission

2017

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“…On the other hand, we would more generally expect that, under sublethal stress, nonproducers limit the emergence and spread of resistant cooperators by cheating on public goods production. In addition, should stress responses (29)(30)(31) or the evolution of stress resistance (32)(33)(34) entail costs, such costs could potentially interact with social behaviors and accentuate selection for cheating. Evidence to support or refute such hypotheses is lacking.…”

mentioning

confidence: 99%

Antibiotic stress selects against cooperation in the pathogenic bacterium Pseudomonas aeruginosa

Vasse

Noble

Akhmetzhanov

et al. 2017

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

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Cheats are a pervasive threat to public goods production in natural and human communities, as they benefit from the commons without contributing to it. Although ecological antagonisms such as predation, parasitism, competition, and abiotic environmental stress play key roles in shaping population biology, it is unknown how such stresses generally affect the ability of cheats to undermine cooperation. We used theory and experiments to address this question in the pathogenic bacterium, Pseudomonas aeruginosa. Although public goods producers were selected against in all populations, our competition experiments showed that antibiotics significantly increased the advantage of nonproducers. Moreover, the dominance of nonproducers in mixed cultures was associated with higher resistance to antibiotics than in either monoculture. Mathematical modeling indicates that accentuated costs to producer phenotypes underlie the observed patterns. Mathematical analysis further shows how these patterns should generalize to other taxa with public goods behaviors. Our findings suggest that explaining the maintenance of cooperative public goods behaviors in certain natural systems will be more challenging than previously thought. Our results also have specific implications for the control of pathogenic bacteria using antibiotics and for understanding natural bacterial ecosystems, where subinhibitory concentrations of antimicrobials frequently occur.evolution | cooperation | antibiotics | social behavior | resistance P ublic goods production is a characteristic of a diverse range of taxa, from microbes to humans (1-3). Explaining the persistence of this costly behavior is challenging, because cheats can exploit the commons without contributing. Kin selection theory has proven to be a successful framework for addressing this question, with the central prediction that cooperation is favored by sufficient benefits to, and positive assortment between, cooperators (4-8). For example, recent study in experimental bacterial populations has elucidated mechanisms such as assortment emerging from limited or budding dispersal (9, 10) and kin discrimination (11, 12) that are consistent with kin selection fostering cooperative behaviors (e.g., refs. 8 and 13). However, despite this accumulating consensus, little is known about how social populations respond to differences and variation in abiotic and biotic components of their environment. In particular, it is unclear how ecological antagonisms affect the ability of cheats to invade cooperator communities.Cooperation can be affected by stress directly through differential selection on cooperative phenotypes (14, 15), or by inducing specific plastic behaviors (16-22), especially when cooperation leads to increased stress resistance. However, in the absence of a direct benefit of the cooperative behavior against stress, the ecological and evolutionary outcomes of the interactions between nondefensive public goods and stress responses are less clear and are potentially complex. Cooperation may be infl...

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“…As previously postulated by Bagdasarian et al (1986Bagdasarian et al ( , 1992 for the PsiB protein, UmuDpR may protect the plasmid conjugative transfer process, which involves the transient formation of single-stranded DNA, which may trigger the potentially deleterious SOS response. Thus, the SOS response not only involves activities to survive or to change, but also includes actions devoted to sharing information with neighbouring cells (Baharoglu & Mazel, 2014). Possession of an SOS response repressor could be evolutionarily advantageous for the conjugative pUM505 plasmid.…”

Section: Umudpr Regulates Expression Of Sos Genesmentioning

confidence: 99%

A plasmid-encoded UmuD homologue regulates expression of Pseudomonas aeruginosa SOS genes

Díaz-Magaña¹,

Alva-Murillo

Chávez-Moctezuma

et al. 2015

Microbiology

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The Pseudomonas aeruginosa plasmid pUM505 contains the umuDC operon that encodes proteins similar to error-prone repair DNA polymerase V. The umuC gene appears to be truncated and its product is probably not functional. The umuD gene, renamed umuDpR, possesses an SOS box overlapped with a Sigma factor 70 type promoter; accordingly, transcriptional fusions revealed that the umuDpR gene promoter is activated by mitomycin C. The predicted sequence of the UmuDpR protein displays 23 % identity with the Ps. aeruginosa SOS-response LexA repressor. The umuDpR gene caused increased MMC sensitivity when transferred to the Ps. aeruginosa PAO1 strain. As expected, PAO1-derived knockout lexA 2 mutant PW6037 showed resistance to MMC; however, when the umuDpR gene was transferred to PW6037, MMC resistance level was reduced. These data suggested that UmuDpR represses the expression of SOS genes, as LexA does. To test whether UmuDpR exerts regulatory functions, expression of PAO1 SOS genes was evaluated by reverse transcription quantitative PCR assays in the lexA 2 mutant with or without the pUC_umuD recombinant plasmid. Expression of lexA, imuA and recA genes increased 3.4-5.3 times in the lexA 2 mutant, relative to transcription of the corresponding genes in the lexA + strain, but decreased significantly in the lexA 2 /umuDpR transformant. These results confirmed that the UmuDpR protein is a repressor of Ps. aeruginosa SOS genes controlled by LexA. Electrophoretic mobility shift assays, however, did not show binding of UmuDpR to 59 regions of SOS genes, suggesting an indirect mechanism of regulation.

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SOS, the formidable strategy of bacteria against aggressions

Cited by 339 publications

References 203 publications

Fitness Costs of Plasmids: a Limit to Plasmid Transmission

Fitness Costs of Plasmids: a Limit to Plasmid Transmission

Antibiotic stress selects against cooperation in the pathogenic bacterium Pseudomonas aeruginosa

A plasmid-encoded UmuD homologue regulates expression of Pseudomonas aeruginosa SOS genes

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