Adaptation Genomics of a Small-Colony Variant in a Pseudomonas chlororaphis 30-84 Biofilm

Wang, Dongping; Dorosky, Robert J.; Han, Cliff; Lo, Chien-Chi; Dichosa, Armand E. K.; Chain, Patrick; Yu, Jae Hyeon; Pierson, Leland S.; Pierson, Elizabeth A.

doi:10.1128/aem.02617-14

Cited by 40 publications

(36 citation statements)

References 43 publications

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“…This study, as well as those of others (Koh et al, 2007;Singh et al, 2009;Workentine et al, 2010;Cooper et al, 2014;Wang et al, 2015), have shown that the production of morphotypic variants is commonly associated with biofilm formation, where mutations are induced by stresses such as starvation and oxidative stress (Bjedov et al, 2003).…”

Section: Discussionsupporting

confidence: 69%

Interspecific diversity reduces and functionally substitutes for intraspecific variation in biofilm communities

et al. 2015

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Diversity has a key role in the dynamics and resilience of communities and both interspecific (species) and intraspecific (genotypic) diversity can have important effects on community structure and function. However, a critical and unresolved question for understanding the ecology of a community is to what extent these two levels of diversity are functionally substitutable? Here we show, for a mixed-species biofilm community composed of Pseudomonas aeruginosa, P. protegens and Klebsiella pneumoniae, that increased interspecific diversity reduces and functionally substitutes for intraspecific diversity in mediating tolerance to stress. Biofilm populations generated high percentages of genotypic variants, which were largely absent in biofilm communities. Biofilms with either high intra-or interspecific diversity were more tolerant to SDS stress than biofilms with no or low diversity. Unexpectedly, genotypic variants decreased the tolerance of biofilm communities when experimentally introduced into the communities. For example, substituting P. protegens wild type with its genotypic variant within biofilm communities decreased SDS tolerance by twofold, apparently due to perturbation of interspecific interactions. A decrease in variant frequency was also observed when biofilm populations were exposed to cell-free effluents from another species, suggesting that extracellular factors have a role in selection against the appearance of intraspecific variants. This work demonstrates the functional substitution of inter-and intraspecific diversity for an emergent property of biofilms. It also provides a potential explanation for a long-standing paradox in microbiology, in which morphotypic variants are common in laboratory grown biofilm populations, but are rare in diverse, environmental biofilm communities.

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Section: Discussionsupporting

confidence: 69%

Interspecific diversity reduces and functionally substitutes for intraspecific variation in biofilm communities

et al. 2015

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“…SCV formation is also observed in P. aeruginosa strains (Coggan and Wolfgang, 2012;Drenkard and Ausubel, 2002) and Pc30-84 (Wang et al, 2015). These variants show modifications in the genes that increase the levels of c-di-GMP, consistent with a battery of phenotype changes focused on a loss of motility and but a gain of strong biofilm formation (Römling et al, 2013;Valentini and Filloux, 2016).…”

Section: Gacs-dependent But Rpos-independentmentioning

confidence: 72%

“…3. Gac/Rsm regulation was reported to act central role on biofilm formation in pathogenic P. aeruginosa isolates (Frangipani et al, 2014) and in Pc isolate 30-84 (Wang et al, 2015). To understand biofilm formation in PcO6, we have studied two of the processes involved, cell motility and extracellular matrix production.…”

Section: Root Colonization and Biofilm Formationmentioning

confidence: 99%

The Gac/Rsm Signaling Pathway of a Biocontrol Bacterium, Pseudomonas chlororaphis O6

Anderson

Kang

Kim

2017

Research in Plant Disease

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Pseudomonas chlororaphis O6, isolated from the roots of dryland, field-grown commercial wheat in the USA, enhances plant health and therefore it is used in agriculture as a biofertilizer and biocontrol agent. The metabolites produced by this pseudomonad stimulate plant growth through direct antagonism of pathogens and by inducing systemic resistance in the plant. Studies upon P. chlororaphis O6 identify the pathways through which defined bacterial metabolites generate protection against pathogenic microbes, insects, and nematodes. P. chlororaphis O6 also triggers plant resistance to drought and salinity stresses. The beneficial determinants are produced from bacterial cells as they form biofilms during root colonization. Molecular control these processes in P. chlororaphis O6 involves the global regulatory Gac/Rsm signaling cascade with cross-talk between other global regulatory pathways. The Gac/Rsm regulon allows for coordinate phasing of expression of the genes that encode these beneficial traits among a community of cells. This review provides insights on the Gac/Rsm regulon in expression of beneficial traits of the P. chlororaphis O6 which can contribute to help yield enhancement and quality in agricultural production.

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“…Therefore, the role of fusA, which codes for an elongation factor, in the initial protection against tobramycin can be understood in terms of its function in biofilm formation by Pseudomonas chlororaphis (31). The rplB gene codes for a 50S ribosome-associated L2 protein that is known to be involved in bactobolin resistance (32).…”

Section: Discussionmentioning

confidence: 99%

Dynamics of Mutations during Development of Resistance by Pseudomonas aeruginosa against Five Antibiotics

Feng

Jonker

Moustakas

et al. 2016

Antimicrob Agents Chemother

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cPseudomonas aeruginosa is an opportunistic pathogen that causes considerable morbidity and mortality, specifically during intensive care. Antibiotic-resistant variants of this organism are more difficult to treat and cause substantial extra costs compared to susceptible strains. In the laboratory, P. aeruginosa rapidly developed resistance to five medically relevant antibiotics upon exposure to stepwise increasing concentrations. At several time points during the acquisition of resistance, samples were taken for whole-genome sequencing. The increase in the MIC of ciprofloxacin was linked to specific mutations in gyrA, parC, and gyrB, appearing sequentially. In the case of tobramycin, mutations in fusA, HP02880, rplB, and capD were induced. The MICs of the beta-lactam compounds meropenem and ceftazidime and the combination of piperacillin and tazobactam correlated linearly with beta-lactamase activity but not always with individual mutations. The genes that were mutated during the development of beta-lactam resistance differed for each antibiotic. A quantitative relationship between the frequency of mutations and the increase in resistance could not be established for any of the antibiotics. When the adapted strains are grown in the absence of the antibiotic, some mutations remained and others were reversed, but this reversal did not necessarily lower the MIC. The increased MIC came at the cost of moderately reduced cellular functions or a somewhat lower growth rate. In all cases except ciprofloxacin, the increase in resistance seems to be the result of complex interactions among several cellular systems rather than individual mutations.T he medical consequences of antibiotic resistance, such as fewer options for and increased costs of treating infectious diseases, are well recognized. The pathway to resistance consists of sequential mutations or acquisition of resistance genes driven by the selective pressure caused by antibiotic exposure (1). Once resistance has been acquired, the cell rarely reverses to become sensitive again, compensating for the metabolic costs instead (2, 3). The increased level of resistance caused by an antibiotic treatment typically prescribed by primary care physicians is very noticeable when subsequent further treatment is necessary (4). Hence, in order to limit the development of resistance when antibiotics have to be used, treatment protocols need to be devised to prevent this side effect. Rational design of such protocols requires knowledge of the molecular mechanisms that cause resistance. One of the central questions is whether similar mechanisms are operational for all drugs or whether resistance to each drug is induced in a distinct manner. Other basic questions center on evolutionary pathways to clinically significant resistance and the persistence of molecular changes after treatment.Molecular changes that cause the development and persistence of drug resistance can be identified by combining experimental evolution and whole-genome sequencing (WGS), provided that the proper c...

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Adaptation Genomics of a Small-Colony Variant in a Pseudomonas chlororaphis 30-84 Biofilm

Cited by 40 publications

References 43 publications

Interspecific diversity reduces and functionally substitutes for intraspecific variation in biofilm communities

Interspecific diversity reduces and functionally substitutes for intraspecific variation in biofilm communities

The Gac/Rsm Signaling Pathway of a Biocontrol Bacterium, Pseudomonas chlororaphis O6

Dynamics of Mutations during Development of Resistance by Pseudomonas aeruginosa against Five Antibiotics

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