Programmed cell death in bacteria: proteic plasmid stabilization systems

Jensen, Rasmus Bugge; Gerdes, Kenn

doi:10.1111/j.1365-2958.1995.mmi_17020205.x

Cited by 304 publications

(255 citation statements)

References 17 publications

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“…These model plasmids contain several different types of systems that prevent plasmid loss at cell division (Nordstrom & Austin 1989). One such type encodes a differentiation system that leads to the killing of plasmid-free cells and thereby confers plasmid stabilization Jensen & Gerdes 1995). Conversely, true partitioning systems stabilize their replicons by actively distributing the plasmid molecules to the daughter cells, and this becomes essential for very low copy number plasmids.…”

Section: Dna Partitioning Of the Low Copy Number Plasmidsmentioning

confidence: 99%

Towards understanding the molecular basis of bacterial DNA segregation

Leonard

Møller‐Jensen

Löwe

2005

Phil. Trans. R. Soc. B

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Bacteria ensure the fidelity of genetic inheritance by the coordinated control of chromosome segregation and cell division. Here, we review the molecules and mechanisms that govern the correct subcellular positioning and rapid separation of newly replicated chromosomes and plasmids towards the cell poles and, significantly, the emergence of mitotic-like machineries capable of segregating plasmid DNA. We further describe surprising similarities between proteins involved in DNA partitioning (ParA/ParB) and control of cell division (MinD/MinE), suggesting a mechanism for intracellular positioning common to the two processes. Finally, we discuss the role that the bacterial cytoskeleton plays in DNA partitioning and the missing link between prokaryotes and eukaryotes that is bacterial mechano-chemical motor proteins.

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Section: Dna Partitioning Of the Low Copy Number Plasmidsmentioning

confidence: 99%

Towards understanding the molecular basis of bacterial DNA segregation

Leonard

Møller‐Jensen

Löwe

2005

Phil. Trans. R. Soc. B

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“…One possibility to confer a selective replication advantage to bacterial plasmids consists in the generation of aǹ addiction module' (Jensen and Gerdes, 1995;Naito et al, 1995;Yarmolinsky, 1995). If the plasmid encodes both a long-lived toxin and a short-lived antidote, then loss or The bacterium contains pre-formed toxins that are released upon lysis of the bacterium.…”

Section: Addiction Modulesmentioning

confidence: 99%

Mitochondrial implication in apoptosis. Towards an endosymbiont hypothesis of apoptosis evolution

1997

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Recent evidence indicates that a profound alteration in mitochondrial function constitutes an obligatory early event of the apoptotic process. The molecular mechanism accounting for this alteration is mitochondrial permeability transition (PT). PT is both sufficient and necessary for apoptosis to occur. Experiments performed in cell-free systems of apoptosis demonstrate that mitochondria undergoing PT release protease activators that can trigger nuclear manifestations of apoptotis. Bcl-2 and its homologs are endogenous regulators of PT. It appears that some types of necrosis, those inhibited by Bcl-2, involve PT. If PT is a rate-limiting event of both apoptosis and necrosis, then downstream events including caspase activation and the bioenergetic consequences of PT must determine the choice between both modes of cell death. PT without caspase activation would cause necrosis. These findings have important implications for the comprehension of the apoptotic process, for the dichotomy between apoptosis and necrosis, and for the phylogeny of programmed cell death. Apoptosis may have evolved together with the endosymbiotic incorporation of aerobic bacteria (the precursors of mitochondria) into ancestral unicellular eukaryotes.

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“…Nondegenerate primers were designed such that each primer set would specifically amplify the genes of one TA system (9). These include three TA systems that have been previously observed on plasmids from Gram-positive bacteria [ --(20), axe-txe (21), and par (22)], and seven that are representative of the major TA systems from Gram-negative bacteria [parDE (23), ccdAB (24,25), mazEF (26), relBE (27), higBA, (28), vagCD (29), and phd-doc (30)]. The exact primers used and their location on the TA genes are shown in SI Figs.…”

Section: Plasmid-encoded Vancomycinmentioning

confidence: 99%

Toxin–antitoxin systems are ubiquitous and plasmid-encoded in vancomycin-resistant enterococci

Moritz¹,

Hergenrother

2007

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

124

127

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Vancomycin-resistant enterococci (VRE) are common hospital pathogens that are resistant to most major classes of antibiotics. The incidence of VRE is increasing rapidly, to the point where over one-quarter of enterococcal infections in intensive care units are now resistant to vancomycin. The exact mechanism by which VRE maintains its plasmid-encoded resistance genes is ill-defined, and novel targets for the treatment of VRE are lacking. In an effort to identify novel protein targets for the treatment of VRE infections, we probed the plasmids obtained from 75 VRE isolates for the presence of toxin-antitoxin (TA) gene systems. Remarkably, genes for one particular TA pair, the mazEF system (originally identified on the Escherichia coli chromosome), were present on plasmids from 75/75 (100%) of the isolates. Furthermore, mazEF was on the same plasmid as vanA in the vast majority of cases (>90%). Plasmid stability tests and RT-PCR raise the possibility that this plasmidencoded mazEF is indeed functional in enterococci. Given this ubiquity of mazEF in VRE and the deleterious activity of the MazF toxin, disruption of mazEF with pharmacological agents is an attractive strategy for tailored antimicrobial therapy.antibiotics ͉ mazEF ͉ axe-txe ͉ relbE ͉ VRE E nterococci are the leading cause of surgical-site infections and the third leading cause of urinary tract and bloodstream infections (1, 2) and are implicated in bacterial endocarditis, intraabdominal infections, bacteremia, and meningitis (3). The intrinsic resistance of enterococci to cephalosporin and aminoglycoside antibiotics complicates treatment strategies. Historically, vancomycin has been effective in the management of enterococcal infections; however, after nearly 30 years of use, vancomycin-resistant enterococci (VRE) emerged in the mid-1980s. In a short time span, intensive care units in the U.S. have seen a dramatic increase in the percentage of enterococcal infections that are resistant to vancomycin, from 0. 4% in 1989 to 25% in 1999 (3). In fact, in a recent study, 60% of Enterococcus faecium clinical isolates were resistant to vancomycin (4).The genes encoding the elaborate protein systems that mediate vancomycin resistance generally reside on mobile genetic elements within the enterococci. In some cases, plasmids with the various vancomycin resistance gene clusters have been recovered from enterococci (5-8), although the prevalence of plasmid-encoded resistance in VRE has not been defined. Large plasmids often have intricate mechanisms by which they maintain themselves in the bacterial population. Some plasmids contain genes encoding postsegregational killing ''plasmid addiction'' systems (9, 10), in which the plasmid encodes a potent toxin and a labile antitoxin. Provided the plasmid is present, the antitoxin binds to and sequesters the toxin. However, if a plasmid-free daughter cell arises, the unstable antitoxin is degraded, and the toxic protein kills the bacterial cell from within.If toxin-antitoxin (TA) systems are prevalent and functional on ...

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Programmed cell death in bacteria: proteic plasmid stabilization systems

Cited by 304 publications

References 17 publications

Towards understanding the molecular basis of bacterial DNA segregation

Towards understanding the molecular basis of bacterial DNA segregation

Mitochondrial implication in apoptosis. Towards an endosymbiont hypothesis of apoptosis evolution

Toxin–antitoxin systems are ubiquitous and plasmid-encoded in vancomycin-resistant enterococci

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