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Mehta, Preeti; Casjens, Sherwood; Krishnaswamy, S.

doi:10.1186/1471-2180-4-4

Cited by 51 publications

(33 citation statements)

References 59 publications

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“…This prophage lies at position 1,195,432 bp to 1,210,646 bp [33] on the chromosome and contains 24 putative ORFs, many of which have unknown function [34]. Exposure to UV radiation consistently activates excision of this element [35]–[36], probably through induction of the SOS response [37].…”

Section: Discussionmentioning

confidence: 99%

Genetic Basis of Growth Adaptation of Escherichia coli after Deletion of pgi, a Major Metabolic Gene

et al. 2010

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Bacterial survival requires adaptation to different environmental perturbations such as exposure to antibiotics, changes in temperature or oxygen levels, DNA damage, and alternative nutrient sources. During adaptation, bacteria often develop beneficial mutations that confer increased fitness in the new environment. Adaptation to the loss of a major non-essential gene product that cripples growth, however, has not been studied at the whole-genome level. We investigated the ability of Escherichia coli K-12 MG1655 to overcome the loss of phosphoglucose isomerase (pgi) by adaptively evolving ten replicates of E. coli lacking pgi for 50 days in glucose M9 minimal medium and by characterizing endpoint clones through whole-genome re-sequencing and phenotype profiling. We found that 1) the growth rates for all ten endpoint clones increased approximately 3-fold over the 50-day period; 2) two to five mutations arose during adaptation, most frequently in the NADH/NADPH transhydrogenases udhA and pntAB and in the stress-associated sigma factor rpoS; and 3) despite similar growth rates, at least three distinct endpoint phenotypes developed as defined by different rates of acetate and formate secretion. These results demonstrate that E. coli can adapt to the loss of a major metabolic gene product with only a handful of mutations and that adaptation can result in multiple, alternative phenotypes.

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Section: Discussionmentioning

confidence: 99%

Genetic Basis of Growth Adaptation of Escherichia coli after Deletion of pgi, a Major Metabolic Gene

et al. 2010

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“…SOS, SlmA, and MinC independence was also shown in exponential-phase cells growing slowly with one replicating chromosome and incubated at constant temperature. The inhibition was very unlikely to result from a fourth inhibitor, the SfiC product of the defective lambdoid prophage e14 (46,79,80) present in strain MG1655 (81), because SfiC induction is SOS dependent (46,79). These results bring to light a new mechanism of E. coli division control which is independent of SOS, SlmA-mediated nucleoid occlusion, and the Min proteins.…”

Section: Discussionmentioning

confidence: 99%

A Replication-Inhibited Unsegregated Nucleoid at Mid-Cell Blocks Z-Ring Formation and Cell Division Independently of SOS and the SlmA Nucleoid Occlusion Protein in Escherichia coli

Cambridge¹,

Blinkova²,

Magnan³

et al. 2013

Journal of Bacteriology

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Chromosome replication and cell division of Escherichia coli are coordinated with growth such that wild-type cells divide once and only once after each replication cycle. To investigate the nature of this coordination, the effects of inhibiting replication on Z-ring formation and cell division were tested in both synchronized and exponentially growing cells with only one replicating chromosome. When replication elongation was blocked by hydroxyurea or nalidixic acid, arrested cells contained one partially replicated, compact nucleoid located mid-cell. Cell division was strongly inhibited at or before the level of Z-ring formation. DNA cross-linking by mitomycin C delayed segregation, and the accumulation of about two chromosome equivalents at mid-cell also blocked Z-ring formation and cell division. Z-ring inhibition occurred independently of SOS, SlmA-mediated nucleoid occlusion, and MinCDE proteins and did not result from a decreased FtsZ protein concentration. We propose that the presence of a compact, incompletely replicated nucleoid or unsegregated chromosome masses at the normal mid-cell division site inhibits Z-ring formation and that the SOS system, SlmA, and MinC are not required for this inhibition. Bacterial DNA replication and cell division are coordinated with growth so that a single, timely division follows each genome duplication. This rule, however, is complicated by the fact that cells can divide rapidly, with the replication and division machinery operating continuously and concurrently (e.g., see reference 1). Division at mid-cell, which occurs with high precision (2, 3), begins with polymerization of the FtsZ protein into a circumferential ring on the cytoplasmic membrane inner surface (4). Although division frequency is ultimately determined by growth rate (5, 6), regulatory mechanisms control both the location and timing of FtsZ ring assembly (for recent reviews, see the works of de Boer [7], Chien et al. [8], Lutkenhaus et al. [9], and Egan and Vollmer [10]).Placement of Z rings mid-cell depends on negative activities of the Min proteins and nucleoid occlusion. The MinC protein of Escherichia coli binds to FtsZ, preventing Z-ring assembly at all positions except at mid-cell, where its time-averaged concentration is lowest (11-13). The nucleoid occlusion (14) proteins SlmA and Noc, of E. coli and Bacillus subtilis, respectively (15, 16), bind DNA at specific sequences and prevent division over replicating nucleoids in rapidly growing cells. SlmA prevents Z-ring formation by also binding FtsZ (17, 18); the Noc protein functions similarly but has not been shown to bind FtsZ directly (19). Because the SlmA and Noc DNA binding sites are absent from the terminus domain, which is replicated last and in the cell center (20-23), nucleoid occlusion contributes to both spatial and temporal control of Z-ring formation (17)(18)(19)). An slmA null mutant which is also min null frequently forms Z-ring-like structures over nucleoids when grown in LB medium (15). However, the SlmA protein might not be the ...

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“…Whole-genome search for inversions in clonal populations of MGY grown under standard conditions revealed one locus exhibiting clear PV by inversion. The inverted locus resides inside a remnant of a defective prophage known as e14 [ 33 ]. This prophage is known to harbor an invertase gene, pinE , which regulates the inversion of a neighboring invertible segment.…”

Section: Resultsmentioning

confidence: 99%

Systematic identification and quantification of phase variation in commensal and pathogenic Escherichia coli

et al. 2014

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Bacteria have been shown to generate constant genetic variation in a process termed phase variation. We present a tool based on whole genome sequencing that allows detection and quantification of coexisting genotypes mediated by genomic inversions in bacterial cultures. We tested our method on widely used strains of Escherichia coli, and detected stable and reproducible phase variation in several invertible loci. These are shown here to be responsible for maintaining constant variation in populations grown from a single colony. Applying this tool on other bacterial strains can shed light on how pathogens adjust to hostile environments by diversifying their genomes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-014-0112-4) contains supplementary material, which is available to authorized users.

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Cited by 51 publications

References 59 publications

Genetic Basis of Growth Adaptation of Escherichia coli after Deletion of pgi, a Major Metabolic Gene

Genetic Basis of Growth Adaptation of Escherichia coli after Deletion of pgi, a Major Metabolic Gene

A Replication-Inhibited Unsegregated Nucleoid at Mid-Cell Blocks Z-Ring Formation and Cell Division Independently of SOS and the SlmA Nucleoid Occlusion Protein in Escherichia coli

Systematic identification and quantification of phase variation in commensal and pathogenic Escherichia coli

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