Genetics of Pseudomonas.

Holloway, B. W.

doi:10.1128/mmbr.33.3.419-443.1969

Cited by 190 publications

(71 citation statements)

References 89 publications

(146 reference statements)

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“…Once direct evidence for the existence of extrachromosomal DNA in bacteria was established, the early years of plasmid biology were dominated by the characterization of their basic properties including size, the fundamentals of incompatibility, entry exclusion and the replication and transfer genes they carried (Novick, 1969). The link between plasmids and resistance genes was noted very early and resulted in P. aeruginosa emerging as a major focus of genetic study in the Gram negatives (Holloway, 1969). The reasons for this included the fact that it is a significant opportunistic pathogen and a common cause of nosocomial infections.…”

Section: Plasmidsmentioning

confidence: 99%

Gene flow, mobile genetic elements and the recruitment of antibiotic resistance genes into Gram-negative pathogens

2011

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Antibiotics were one of the great discoveries of the 20th century. However, resistance appeared even in the earliest years of the antibiotic era. Antibiotic resistance continues to become worse, despite the ever-increasing resources devoted to combat the problem. One of the most important factors in the development of resistance to antibiotics is the remarkable ability of bacteria to share genetic resources via Lateral Gene Transfer (LGT). LGT occurs on a global scale, such that in theory, any gene in any organism anywhere in the microbial biosphere might be mobilized and spread. With sufficiently strong selection, any gene may spread to a point where it establishes a global presence. From an antibiotic resistance perspective, this means that a resistance phenotype can appear in a diverse range of infections around the globe nearly simultaneously. We discuss the forces and agents that make this LGT possible and argue that the problem of resistance can ultimately only be managed by understanding the problem from a broad ecological and evolutionary perspective. We also argue that human activities are exacerbating the problem by increasing the tempo of LGT and bacterial evolution for many traits that are important to humans.

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Section: Plasmidsmentioning

confidence: 99%

Gene flow, mobile genetic elements and the recruitment of antibiotic resistance genes into Gram-negative pathogens

2011

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“…The pathogen Pseudomonas aeruginosa (PA) (Holloway, 1969) is capable of aerobic or anaerobic growth. The latter is either via anaerobic respiration, using an inorganic oxynitrogen terminal electron acceptor (Gennis and Stewart, 1996), or slow growth by arginine substrate level phosphorylation (Mercenier et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Two-pronged survival strategy for the major cystic fibrosis pathogen, Pseudomonas aeruginosa, lacking the capacity to degrade nitric oxide during anaerobic respiration

Yoon

Karabulut

Lipscomb

et al. 2007

EMBO J

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Protection from NO gas, a toxic byproduct of anaerobic respiration in Pseudomonas aeruginosa, is mediated by nitric oxide (NO) reductase (NOR), the norCB gene product. Nevertheless, a norCB mutant that accumulated approximately 13.6 microM NO paradoxically survived anaerobic growth. Transcription of genes encoding nitrate and nitrite reductases, the enzymes responsible for NO production, was reduced >50- and 2.5-fold in the norCB mutant. This was due, in part, to a predicted compromise of the [4Fe-4S](2+) cluster in the anaerobic regulator ANR by physiological NO levels, resulting in an inability to bind to its cognate promoter DNA sequences. Remarkably, two O(2)-dependent dioxygenases, homogentisate-1,2-dioxygenase (HmgA) and 4-hydroxyphenylpyruvate dioxygenase (Hpd), were derepressed in the norCB mutant. Electron paramagnetic resonance studies showed that HmgA and Hpd bound NO avidly, and helped protect the norCB mutant in anaerobic biofilms. These data suggest that protection of a P. aeruginosa norCB mutant against anaerobic NO toxicity occurs by both control of NO supply and reassignment of metabolic enzymes to the task of NO sequestration.

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“…Table 9. Interference by the R factor of Ps2-72 strain with the recombinant formations mediated by the FP5 factor mosome transfers mediated by sex factors and that of a transfer of the sex factor themselves in P. aeruginosa seem, as pointed out by Holloway [7], Holloway et al [8] and Pemberton and Holloway [14], distinct from those observed in enteric bacteria. Further investigations are necessary.…”

Section: Discussionmentioning

confidence: 86%

“…Ps5-70 is not sensitive to both phages F116 and G101, two widely used generalized transducing phages of P. aeruginosa [7,8].…”

Section: Evidences For Maleness Of Strain Ps5-70mentioning

confidence: 99%

“…Genetics of Pseudomonas aeruginosa has been established, and has been extended over the last fifteen years by Holloway and his collaborators [7,8]. Two distinct methods which have been employed in those studies for genetic exchanges among P. aeruginosa strains are conjugation mediated by a sex factor, and transduction using some generalized transducing phages [7,8]. The sex factor of P. aeruginosa so far investigated in detail is the FP2 factor which originated in strain 2 (strain PAT) [6].…”

mentioning

confidence: 99%

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FP5 Factor, an Undescribed Sex Factor of Pseudomonas aeruginosa

Matsui

Tazaki

1973

Japanese Journal of Microbiology

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A Pseudomonas aeruginosa, strain Ps5–70 which was mercury‐resistant, was found to have a sex factor. This sex factor, designated as FP5 factor, mediated chromosome transfer by conjugation. Crosses between Ps5–70, FP5+ and PAO, FP2+ strain of Holloway were fertile, and Ps5–70 acted as the donor. Some of the recombinants between FP5+ and FP5– strains displayed maleness, and those recombinants usually acquired mercury resistance. So, transferability of FP5 factor itself and a very close association between the two determinants of FP5, one for fertility and the other for mercury resistance, were proved similar to the FP2 factor. Female sublines of Ps5–70 which behaved as recipients in intrastrain crosses were obtainable from cultures multiplied in the presence of acriflavin. Those females still retained mercury resistance. An R factor originated in P. aeruginosa interfered with the recombinant formation mediated by FP5 factor when the two episomes coexisted within a single cell.

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Genetics of Pseudomonas.

Cited by 190 publications

References 89 publications

Gene flow, mobile genetic elements and the recruitment of antibiotic resistance genes into Gram-negative pathogens

Gene flow, mobile genetic elements and the recruitment of antibiotic resistance genes into Gram-negative pathogens

Two-pronged survival strategy for the major cystic fibrosis pathogen, Pseudomonas aeruginosa, lacking the capacity to degrade nitric oxide during anaerobic respiration

FP5 Factor, an Undescribed Sex Factor of Pseudomonas aeruginosa

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