Статті в журналах: "Escherichia coli Genetics"

1

Lorenz, E., M. D. Plamann, and G. V. Stauffer. "Escherichia coli." MGG Molecular & General Genetics 250, no. 1 (1996): 81. http://dx.doi.org/10.1007/s004380050053.

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2

Gottesman, S. "Genetics of Proteolysis in Escherichia Coli." Annual Review of Genetics 23, no. 1 (December 1989): 163–98. http://dx.doi.org/10.1146/annurev.ge.23.120189.001115.

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3

Milkman, Roger. "Recombination and Population Structure in Escherichia coli." Genetics 146, no. 3 (July 1, 1997): 745–50. http://dx.doi.org/10.1093/genetics/146.3.745.

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4

Reynolds, Mary G. "Compensatory Evolution in Rifampin-Resistant Escherichia coli." Genetics 156, no. 4 (December 1, 2000): 1471–81. http://dx.doi.org/10.1093/genetics/156.4.1471.

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Abstract This study examines the intrinsic fitness burden associated with RNA polymerase (rpoB) mutations conferring rifampin resistance in Escherichia coli K12 (MG1655) and explores the nature of adaptation to the costs of resistance. Among 28 independent Rifr mutants, the per-generation fitness burden (in the absence of rifampin) ranged from 0 to 28%, with a median of 6.4%. We detected no relationship between the magnitude of the cost and the level of resistance. Adaptation to the costs of rif resistance was studied by following serial transfer cultures for several Rifr mutants both in the presence of rifampin and in the absence. For cultures evolved in the absence of rifampin, single clones isolated after 200 generations were more fit than their ancestor; we saw no association between increased fitness and changes in the level of rifampin resistance; and in all cases, increased fitness was due to compensatory mutations, rather than to reversion to drug sensitivity. However, in the parallel evolution experiments in the presence of rifampin, overall levels of resistance increased as did relative fitness—for all strains save one that had an initially high level of resistance. Among the evolved clones tested, five (of seven) demonstrated increased transcription efficiency (assessed using a semiquantitative RT-PCR protocol). The implications of these results for our understanding of adaptive molecular evolution and the increasing clinical problem of antibiotic resistance are discussed.

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5

Thaler, D. S., G. Tombline, and K. Zahn. "Short-patch reverse transcription in Escherichia coli." Genetics 140, no. 3 (July 1, 1995): 909–15. http://dx.doi.org/10.1093/genetics/140.3.909.

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Abstract Chimeras of RNA and DNA have distinctive physical and biological properties. Chimeric oligonucleotides that contained one, two or three ribonucleotides whose phosphodiester backbone was covalently continuous with DNA were synthesized. Site-directed mutagenesis was used to assess genetic information transfer from the ribonucleotide positions. Transfer was scored by the formation or reversion of an ochre site that also corresponded to a restriction cleavage site. This allowed physical as well as genetic assay of mutational events. Bases attached to the ribonucleotides were able to accurately direct the synthesis of progeny DNA. The results suggest that in vivo DNA polymerases utilize a "running start" on a DNA backbone to continue across a covalent backbone junction into a region of ribonucleotides and then back again onto a normal DNA backbone. The phenomenon is designated short-patch reverse transcription (SPRT) by analogy to short-patch mismatch correction and reverse transcription as the term is generally used. The possibility is considered that SPRT contributes to an unrecognized pathway of mutagenesis.

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6

Friedman-Ohana, Rachel, Iris Karunker, and Amikam Cohen. "Chi-Dependent Intramolecular Recombination in Escherichia coli." Genetics 148, no. 2 (February 1, 1998): 545–57. http://dx.doi.org/10.1093/genetics/148.2.545.

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Abstract Homologous recombination in Escherichia coli is enhanced by a cis-acting octamer sequence named Chi (5′-GCTGGTGG-3′) that interacts with RecBCD. To gain insight into the mechanism of Chi-enhanced recombination, we recruited an experimental system that permits physical monitoring of intramolecular recombination by linear substrates released by in vivo restriction from infecting chimera phage. Recombination of the released substrates depended on recA, recBCD and cis-acting Chi octamers. Recombination proficiency was lowered by a xonA mutation and by mutations that inactivated the RuvABC and RecG resolution enzymes. Activity of Chi sites was influenced by their locations and by the number of Chi octamers at each site. A single Chi site stimulated recombination, but a combination of Chi sites on the two homologs was synergistic. These data suggest a role for Chi at both ends of the linear substrate. Chi was lost in all recombinational exchanges stimulated by a single Chi site. Exchanges in substrates with Chi sites on both homologs occurred in the interval between the sites as well as in the flanking interval. These observations suggest that the generation of circular products by intramolecular recombination involves Chi-dependent processing of one end by RecBCD and pairing of the processed end with its duplex homolog.

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7

Volkert, Michael R., Dinh C. Nguyen, and K. Christopher Beard. "ESCHERICHIA COLI GENE INDUCTION BY ALKYLATION TREATMENT." Genetics 112, no. 1 (January 1, 1986): 11–26. http://dx.doi.org/10.1093/genetics/112.1.11.

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ABSTRACT Searches for alkylation-inducible (aid) genes of Escherichia coli have been conducted by screening random fusions of the Mu-dl(ApR lac) phage for fusions showing increased β-galactosidase activity after treatment with methylating agents, but not after treatments with UV-irradiation. In this report we describe gene fusions that are specifically induced by alkylation treatments. Nine new mutants are described, and their properties are compared with the five mutants described previously. The total of 14 fusion mutants map at five distinct genetic loci. They can be further subdivided on the basis of their induction by methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). alkA, aidB and aidD are induced by both agents and appear to be regulated by ada. Neither aidC nor aidI is regulated by ada. Moreover, since aidC is induced only by MNNG and aidI is induced only by MMS, these two genes are likely to be individually regulated. Thus, there appear to be at least three different regulatory mechanisms controlling aid genes.

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8

Cooke, E. Mary. "Escherichia coli – an overview." Journal of Hygiene 95, no. 3 (December 1985): 523–30. http://dx.doi.org/10.1017/s022217240006065x.

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The isolation and description of Bacillus coli commune by Escherich a hundred years ago marked the start of a series of scientific investigations which have led to some of the most important discoveries in microbial pathogenicity and genetics that have been made since that time. It is not difficult to find the reasons why so much effort has been concentrated on this organism. Escherichia coli is present in the gut of all warm-blooded animals generally forming the predominant aerobic flora; it is of medical and veterinary importance being responsible for a variety of infections in the human and animal populations and it has provided a useful tool for geneticists.

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9

Lederberg, Joshua. "Genetic Recombination in Escherichia coli: Disputation at Cold Spring Harbor, 1946–1996." Genetics 144, no. 2 (October 1, 1996): 439–43. http://dx.doi.org/10.1093/genetics/144.2.439.

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10

Guttman, D. S., and D. E. Dykhuizen. "Detecting selective sweeps in naturally occurring Escherichia coli." Genetics 138, no. 4 (December 1, 1994): 993–1003. http://dx.doi.org/10.1093/genetics/138.4.993.

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Abstract The nucleotide sequences of the gapA and pabB genes (separated by approximately 32.5 kb) were determined in 12 natural isolates of Escherichia coli. Three analyses were performed on the data. First, the levels of polymorphism at the loci were compared within and between E. coli and Salmonella strains relative to their degrees of constraint. Second, the gapA and pabB loci were analyzed by the Hudson-Kreitman-Aguadé (HKA) test for selective neutrality. Four additional dispersed genes (crr, putP, trp and gnd) were added to the analysis to provide the necessary frame of reference. Finally, the gene genealogies of gapA and pabB were examined for topological consistency within and between the loci. These lines of evidence indicate that some evolutionary event has recently purged the variability in the region surrounding the gapA and pabB loci in E. coli. This can best be explained by the spread of a selected allele through the global E. coli population by directional selection and the resulting loss in variability in the surrounding regions due to genetic hitchhiking.

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11

Schaaper, R. M., and R. L. Dunn. "Spontaneous mutation in the Escherichia coli lacI gene." Genetics 129, no. 2 (October 1, 1991): 317–26. http://dx.doi.org/10.1093/genetics/129.2.317.

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Abstract To gain more detailed insight into the nature and mechanisms of spontaneous mutations, we undertook a DNA sequence analysis of a large collection of spontaneous mutations in the N-terminal region of the Escherichia coli lacI gene. This region of circa 210 base pairs is the target for dominant lacI mutations (i-d) and is suitable for studies of mutational specificity since it contains a relatively high density of detectable mutable sites. Among 414 independent i-d mutants, 70.8% were base substitutions, 17.2% deletions, 7.7% additions and 4.3% single-base frameshifts. The base substitutions were both transitions (60%) and transversions (40%), the largest single group being G.C----A.T (47% of base substitutions). All four transversions were observed. Among the 71 deletions, a hotspot (37 mutants) was present: an 87-bp deletion presumably directed by an 8-bp repeated sequence at its endpoints. The remaining 34 deletions were distributed among 29 different mutations, either flanked (13/34) or not flanked (21/34) by repeated sequences. The 32 additions comprised 29 different events, with only two containing a direct repeat at the endpoints. The single-base frameshifts were the loss of a single base from either repeated (67%) or nonrepeated (33%) bases. A comparison with the spectrum obtained previously in strains defective in DNA mismatch correction (mutH, mutL, mutS strains) yielded information about the apparent efficiency of mismatch repair. The overall effect was 260-fold but varied substantially among different classes of mutations. An interesting asymmetry was uncovered for the two types of transitions, A.T----G.C and G.C----A.T being reduced by mismatch repair 1340- and 190-fold, respectively. Explanations for this asymmetry and its possible implications for the origins of spontaneous mutations are discussed.

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12

Allgood, N. D., and T. J. Silhavy. "Escherichia coli xonA (sbcB) mutants enhance illegitimate recombination." Genetics 127, no. 4 (April 1, 1991): 671–80. http://dx.doi.org/10.1093/genetics/127.4.671.

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Abstract Mutations of Escherichia coli K-12 were isolated that increase the frequency of deletion formation. Three of these mutations map to the gene sbcB at 43.5 min on the E. coli chromosome. Two types of mutations at sbcB have been previously defined: sbcB-type that suppress both the UV sensitivity and recombination deficiency of recBC mutants, and xonA-type that suppress only the UV sensitivity. Both types are defective for production of exonuclease I activity. The mutations isolated here were similar to xonA alleles of sbcB because they suppressed the UV sensitivity of recBC mutants but did not restore recombination proficiency. Indeed, two previously characterized xonA alleles were shown to increase the frequency of deletion formation, although an sbcB allele did not. This result demonstrates that loss of exonuclease I activity is not sufficient to confer a high deletion phenotype, rather, the product of the sbcB gene possesses some other function that is important for deletion formation. Because deletion formation in this system is recA independent and does not require extensive DNA homology, these mutations affect a pathway of illegitimate recombination.

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13

McKane, M., and R. Milkman. "Transduction, restriction and recombination patterns in Escherichia coli." Genetics 139, no. 1 (January 1, 1995): 35–43. http://dx.doi.org/10.1093/genetics/139.1.35.

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Abstract Chromosomal DNA from several Escherichia coli reference (ECOR) strains was transduced by bacteriophage P1 into E. coli strain K12 W3110 trpA33. Recombination patterns of the transductants were determined by restriction fragment length polymorphism over a 40-kb region centering on a single marker (trpA+) in the tryptophan operon. These experiments demonstrate that transduction between different strains of E. coli can result in recombinational replacements that are small in comparison to the entrant molecule (replacements average 8-14 kb, whereas P1 packages approximately 100 kb) often in a series of discrete segments. The transduction patterns generated resemble the natural mosaic sequence patterns of the ECOR strains described in previous work. Extensive polymorphisms in the restriction-modification systems of the ECOR strains are a possible explanation for the sequence patterns in nature. To test this possibility two transductants were back-transduced into strain K12 W3110 trpA33. The resulting patterns were strikingly different from the original transductions. The size of the replacements was greater, and no multiple replacements were observed, suggesting a role for restriction-modification systems in the transduction patterns and perhaps for the mosaic sequence patterns in nature.

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14

Schaaper, Roel M. "Antimutator Mutants in Bacteriophage T4 and Escherichia coli." Genetics 148, no. 4 (April 1, 1998): 1579–85. http://dx.doi.org/10.1093/genetics/148.4.1579.

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Abstract Antimutators are mutant strains that have reduced mutation rates compared to the corresponding wild-type strain. Their existence, along with mutator mutants that have higher mutation rates compared to the wild-type strain, are powerful evidence that mutation rates are genetically controlled. Compared to mutator mutants, antimutators have a very distinguishing property. Because they prevent normally occurring mutations, they, uniquely, are capable of providing insight into the mechanisms of spontaneous mutations. In this review, antimutator mutants are discussed in bacteriophage T4 and the bacterium Escherichia coli, with regard to their properties, possible mechanisms, and implications for the sources of spontaneous mutations in these two organisms.

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15

Otsuka, Yuichi, and Tetsuro Yonesaki. "A Novel Endoribonuclease, RNase LS, in Escherichia coli." Genetics 169, no. 1 (January 2005): 13–20. http://dx.doi.org/10.1534/genetics.104.033290.

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16

Bichara, Marc, Isabelle Pinet, Sylvie Schumacher, and Robert P. P. Fuchs. "Mechanisms of Dinucleotide Repeat Instability in Escherichia coli." Genetics 154, no. 2 (February 1, 2000): 533–42. http://dx.doi.org/10.1093/genetics/154.2.533.

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Abstract The high level of polymorphism of microsatellites has been used for a variety of purposes such as positional cloning of genes associated with diseases, forensic medicine, and phylogenetic studies. The discovery that microsatellites are associated with human diseases, not only as markers of risk but also directly in disease pathogenesis, has triggered a renewed interest in understanding the mechanism of their instability. In this work we have investigated the role of DNA replication, long patch mismatch repair, and transcription on the genetic instability of all possible combinations of dinucleotide repeats in Escherichia coli. We show that the (GpC) and (ApT) self-complementary sequence repeats are the most unstable and that the mode of replication plays an important role in their instability. We also found that long patch mismatch repair is involved in avoiding both short deletion and expansion events and also in instabilities resulting from the processing of bulges of 6 to 8 bp for the (GpT/ApC)- and (ApG/CpT)-containing repeats. For each dinucleotide sequence repeat, we propose models for instability that involve the possible participation of unusual secondary structures.

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17

Eichenbaum, Zehava, and Zvi Livneh. "UV Light Induces IS10 Transposition in Escherichia coli." Genetics 149, no. 3 (July 1, 1998): 1173–81. http://dx.doi.org/10.1093/genetics/149.3.1173.

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Abstract A new mutagenesis assay system based on the phage 434 cI gene carried on a low-copy number plasmid was used to investigate the effect of UV light on intermolecular transposition of IS10. Inactivation of the target gene by IS10 insertion was detected by the expression of the tet gene from the phage 434 PR promoter, followed by Southern blot analysis of plasmids isolated from TetR colonies. UV irradiation of cells harboring the target plasmid and a donor plasmid carrying an IS10 element led to an increase of up to 28-fold in IS10 transposition. Each UV-induced transposition of IS10 was accompanied by fusion of the donor and acceptor plasmid into a cointegrate structure, due to coupled homologous recombination at the insertion site, similar to the situation in spontaneous IS10 transposition. UV radiation also induced transposition of IS10 from the chromosome to the target plasmid, leading almost exclusively to the integration of the target plasmid into the chromosome. UV induction of IS10 transposition did not depend on the umuC and uvrA gene product, but it was not observed in lexA3 and ΔrecA strains, indicating that the SOS stress response is involved in regulating UV-induced transposition. IS10 transposition, known to increase the fitness of Escherichia coli, may have been recruited under the SOS response to assist in increasing cell survival under hostile environmental conditions. To our knowledge, this is the first report on the induction of transposition by a DNA-damaging agent and the SOS stress response in bacteria.

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18

Vulić, Marin, and Roberto Kolter. "Evolutionary Cheating in Escherichia coli Stationary Phase Cultures." Genetics 158, no. 2 (June 1, 2001): 519–26. http://dx.doi.org/10.1093/genetics/158.2.519.

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Abstract Starved cultures of Escherichia coli are highly dynamic, undergoing frequent population shifts. The shifts result from the spread of mutants able to grow under conditions that impose growth arrest on the ancestral population. To analyze competitive interactions underlying this dynamic we measured the survival of a typical mutant and the wild type during such population shifts. Here we show that the survival advantage of the mutant at any given time during a takeover is inversely dependent on its frequency in the population, its growth adversely affects the survival of the wild type, and its ability to survive in stationary phase at fixation is lower than that of its ancestor. These mutants do not enter, or exit early, the nondividing stationary-phase state, cooperatively maintained by the wild type. Thus they end up overrepresented as compared to their initial frequency at the onset of the stationary phase, and subsequently they increase disproportionately their contribution in terms of progeny to the succeeding generation in the next growth cycle, which is a case of evolutionary cheating. If analyzed through the game theory framework, these results might be explained by the prisoner’s dilemma type of conflict, which predicts that selfish defection is favored over cooperation.

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19

Koga, Mitsunori, Yuichi Otsuka, Sébastien Lemire, and Tetsuro Yonesaki. "Escherichia coli rnlAandrnlBCompose a Novel Toxin–Antitoxin System." Genetics 187, no. 1 (October 26, 2010): 123–30. http://dx.doi.org/10.1534/genetics.110.121798.

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20

Tenaillon, Olivier, David Skurnik, Bertrand Picard, and Erick Denamur. "The population genetics of commensal Escherichia coli." Nature Reviews Microbiology 8, no. 3 (March 2010): 207–17. http://dx.doi.org/10.1038/nrmicro2298.

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21

Denamur, Erick, Olivier Clermont, Stéphane Bonacorsi, and David Gordon. "The population genetics of pathogenic Escherichia coli." Nature Reviews Microbiology 19, no. 1 (August 21, 2020): 37–54. http://dx.doi.org/10.1038/s41579-020-0416-x.

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22

Zhulin, Igor B. "Classic Spotlight: Genetics of Escherichia coli Chemotaxis." Journal of Bacteriology 198, no. 22 (October 21, 2016): 3041. http://dx.doi.org/10.1128/jb.00687-16.

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23

Lutkenhaus, Joe. "Escherichia coli cell division." Current Opinion in Genetics & Development 3, no. 5 (October 1993): 783–88. http://dx.doi.org/10.1016/s0959-437x(05)80099-1.

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24

Minakami, H., and I. Fridovich. "Alcohols Protect Escherichia coli against Cold Shock." Experimental Biology and Medicine 197, no. 2 (June 1, 1991): 168–74. http://dx.doi.org/10.3181/00379727-197-43240.

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25

Slavchenko, I. Yu, E. V. Boreyko, N. V. Vorobey, T. G. Gavrysh, E. N. Pehota, and V. A. Kordyum. "Overexpression and purification of methionine aminopeptidase from Escherichia coli." Biopolymers and Cell 19, no. 3 (May 20, 2003): 274–80. http://dx.doi.org/10.7124/bc.00065c.

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26

Radman, M., and R. Wagner. "Mismatch Repair in Escherichia Coli." Annual Review of Genetics 20, no. 1 (December 1986): 523–38. http://dx.doi.org/10.1146/annurev.ge.20.120186.002515.

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27

Marinus, M. G. "DNA Methylation in Escherichia Coli." Annual Review of Genetics 21, no. 1 (December 1987): 113–31. http://dx.doi.org/10.1146/annurev.ge.21.120187.000553.

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28

Miller, Jeffrey H. "Mutators in Escherichia coli." Mutation Research/DNA Repair 409, no. 3 (December 1998): 99–106. http://dx.doi.org/10.1016/s0921-8777(98)00049-4.

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29

Cairns, J., and P. L. Foster. "Adaptive reversion of a frameshift mutation in Escherichia coli." Genetics 128, no. 4 (August 1, 1991): 695–701. http://dx.doi.org/10.1093/genetics/128.4.695.

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Abstract Mutation rates are generally thought not to be influenced by selective forces. This doctrine rests on the results of certain classical studies of the mutations that make bacteria resistant to phages and antibiotics. We have studied a strain of Escherichia coli which constitutively expresses a lacI-lacZ fusion containing a frameshift mutation that renders it Lac-. Reversion to Lac+ is a rare event during exponential growth but occurs in stationary cultures when lactose is the only source of energy. No revertants accumulate in the absence of lactose, or in the presence of lactose if there is another, unfulfilled requirement for growth. The mechanism for such mutation in stationary phase is not known, but it requires some function of RecA which is apparently not required for mutation during exponential growth.

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30

Schofield, M. A., R. Agbunag, and J. H. Miller. "DNA inversions between short inverted repeats in Escherichia coli." Genetics 132, no. 2 (October 1, 1992): 295–302. http://dx.doi.org/10.1093/genetics/132.2.295.

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Abstract Using site-specific mutagenesis in vitro, we have constructed Escherichia coli strains that allow the detection of the inversion of an 800-bp segment in the lac region. The invertible segment is bounded by inverted repeats of either 12 or 23 bp. Inversions occurring at these inverted repeats will restore the Lac+ phenotype. Inversions can be detected at both short homologies at frequencies ranging from 0.5 x 10(-8) to 1 x 10(-7). These events, which have been verified by DNA sequence analysis, are reduced up to 1000-fold in strains deficient for either RecA, RecB or RecC. They are not reduced in strains deficient in the RecF, J pathway. These results show that the RecB,C,D system can mediate rearrangements at short sequence repeats, and probably plays a major role in cellular rearrangements.

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31

Dean, A. M. "Selection and neutrality in lactose operons of Escherichia coli." Genetics 123, no. 3 (November 1, 1989): 441–54. http://dx.doi.org/10.1093/genetics/123.3.441.

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Abstract The kinetics of the permeases and beta-galactosidases of six lactose operons which had been transduced into a common genetic background from natural isolates of Escherichia coli were investigated. The fitnesses conferred by the operons were determined using chemostat competition experiments in which lactose was the sole growth-limiting factor. The cell wall is demonstrated to impose a resistance to the diffusion of galactosides at low substrate concentrations. A steady state model of the flux of lactose through the metabolic pathway (diffusion, uptake and hydrolysis) is shown to be proportional to fitness. This metabolic model is used to explain why an approximately twofold range in activity among the permease alleles confers a 13% range in fitness, whereas a similar range in activity among alleles of the beta-galactosidase confers a 0.5% range in fitness. This metabolic model implies that selection need not be maximized when a resource is scarce.

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32

Hill, C. W., G. Feulner, M. S. Brody, S. Zhao, A. B. Sadosky, and C. H. Sandt. "Correlation of Rhs elements with Escherichia coli population structure." Genetics 141, no. 1 (September 1, 1995): 15–24. http://dx.doi.org/10.1093/genetics/141.1.15.

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Abstract The Rhs family of composite genetic elements was assessed for variation among independent Escherichia coli strains of the ECOR reference collection. The location and content of the RhsA-B-C-F subfamily correlates highly with the clonal structure of the ECOR collection. This correlation exists at several levels: the presence of Rhs core homology in the strain, the location of the Rhs elements present, and the identity of the Rhs core-extensions associated with each element. A provocative finding was that an identical 1518-bp segment, covering core-extension-b1 and its associated downstream open reading frame, is present in two distinct clonal groups, but in association with different Rhs elements. The sequence identity of this segment when contrasted with the divergence of other chromosomal segments suggests that shuffling of Rhs core extensions has been a relatively recent variation. Nevertheless the copies of core-extension-b1 were placed within the respective Rhs elements before the emergence of the clonal groups. In the course of this analysis, two new Rhs elements absent from E. coli K-12 were discovered: RhsF, a fourth member of the RhsA-B-C-F subfamily, and RhsG, the prototype of a third Rhs subfamily.

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33

Döring, Volker, and Philippe Marlière. "Reassigning Cysteine in the Genetic Code of Escherichia coli." Genetics 150, no. 2 (October 1, 1998): 543–51. http://dx.doi.org/10.1093/genetics/150.2.543.

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Abstract We investigated directed deviations from the universal genetic code. Mutant tRNAs that incorporate cysteine at positions corresponding to the isoleucine AUU, AUC, and AUA and methionine AUG codons were introduced in Escherichia coli K12. Missense mutations at the cysteine catalytic site of thymidylate synthase were systematically crossed with synthetic suppressor tRNACys genes coexpressed from compatible plasmids. Strains harboring complementary codon/anticodon associations could be stably propagated as thymidine prototrophs. A plasmid-encoded tRNACys reading the codon AUA persisted for more than 500 generations in a strain requiring its suppressor activity for thymidylate biosynthesis, but was eliminated from a strain not requiring it. Cysteine miscoding at the codon AUA was also enforced in the active site of amidase, an enzyme found in Helicobacter pylori and not present in wild-type E. coli. Propagating the amidase missense mutation in E. coli with an aliphatic amide as nitrogen source required the overproduction of Cys-tRNA synthetase together with the complementary suppressor tRNACys. The toxicity of cysteine miscoding was low in all our strains. The small size and amphiphilic character of this amino acid may render it acceptable as a replacement at most protein positions and thus apt to overcome the steric and polar constraints that limit evolution of the genetic code.

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34

Le Gac, Mickaël, Michelle D. Brazas, Melanie Bertrand, Jabus G. Tyerman, Christine C. Spencer, Robert E. W. Hancock, and Michael Doebeli. "Metabolic Changes Associated With Adaptive Diversification in Escherichia coli." Genetics 178, no. 2 (February 2008): 1049–60. http://dx.doi.org/10.1534/genetics.107.082040.

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35

Yamamoto, K., N. Takahashi, H. Yoshikura, and I. Kobayashi. "Homologous recombination involving a large heterology in Escherichia coli." Genetics 119, no. 4 (August 1, 1988): 759–69. http://dx.doi.org/10.1093/genetics/119.4.759.

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Abstract Recombination between two different deletion alleles of a gene (neo) for neomycin and kanamycin resistance was studied in an Escherichia coli sbcA- recB-C- strain. The two homologous regions were in an inverted orientation on the same plasmid molecule. Kanamycin-resistant plasmids were selected and analyzed. The rate of recombination to form kanamycin-resistant plasmids was decreased by mutations in the recE, recF and recJ genes, but was not decreased by a mutation in the recA gene. It was found that these plasmids often possessed one wild-type kanamycin-resistant allele (neo+) while the other neo allele was still in its original (deletion) form. Among kanamycin-resistant plasmids with one wild-type and one parental allele it was often found that the region between the inverted repeats had been flipped (turned around) with respect to sites outside the inverted repeats. These results were interpreted as follows. Gene conversion, analogous to gene conversion in eukaryotic meiosis, is responsible for a unidirectional transfer of information from one neo deletion allele to the other. The flipping of the region between the inverted repeats is interpreted as analogous to the crossing over associated with gene conversion in eukaryotic meiosis. In contrast with a rec+ strain, these products cannot be explained by two rounds of reciprocal crossing over involving a dimeric form as an intermediate. In the accompanying paper we present evidence that gene conversion by double-strand gap repair takes place in the same E. coli strain.

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36

Klig, L. S., D. L. Oxender, and C. Yanofsky. "Second-site revertants of Escherichia coli trp repressor mutants." Genetics 120, no. 3 (November 1, 1988): 651–55. http://dx.doi.org/10.1093/genetics/120.3.651.

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Abstract Second-site reversion studies were performed with five missense mutants with defects in the trp repressor of Escherichia coli. These mutants were altered throughout the gene. The same unidirectional mutagen used in the isolation of these mutants, hydroxylamine, was used in reversion studies, to increase the likelihood that the revertants obtained would have second-site changes. Most of the second-site revertants were found to have the same amino acid substitutions detected previously as superrepressor changes. These second-site revertant repressors were more active in vivo than their parental mutant repressors, in the presence or absence of exogenous tryptophan. Apparently superrepressor changes at many locations in this protein can act globally to increase the activity of mutant repressors.

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37

Pogliano, K. J., and J. Beckwith. "The Cs sec mutants of Escherichia coli reflect the cold sensitivity of protein export itself." Genetics 133, no. 4 (April 1, 1993): 763–73. http://dx.doi.org/10.1093/genetics/133.4.763.

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Abstract We have found that temperature can have a striking effect upon protein export in Escherichia coli, suggesting that there is a cold-sensitive step in the protein export pathway. Cs mutations comprise the largest class of mutations affecting the membrane-localized Sec proteins SecD, SecE, SecF and SecY. Although some of these mutations could encode cold-labile proteins, this is unlikely to account for the Cs phenotype of most export mutants, as mutations which simply produce lower amounts of SecE protein have the same phenotype. Certain signal sequence mutations affecting maltose binding protein are also cold sensitive for export. These effects appear to arise by a specific interaction of cold with certain export defects. We believe that the Cs sec mutations are representative of a large class of conditional lethal mutations, whose conditional phenotype reflects an underlying thermal sensitivity of the process in which they are involved.

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38

Liu, Bin, Axel Furevi, Andrei V. Perepelov, Xi Guo, Hengchun Cao, Quan Wang, Peter R. Reeves, Yuriy A. Knirel, Lei Wang, and Göran Widmalm. "Structure and genetics of Escherichia coli O antigens." FEMS Microbiology Reviews 44, no. 6 (November 28, 2019): 655–83. http://dx.doi.org/10.1093/femsre/fuz028.

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ABSTRACT Escherichia coli includes clonal groups of both commensal and pathogenic strains, with some of the latter causing serious infectious diseases. O antigen variation is current standard in defining strains for taxonomy and epidemiology, providing the basis for many serotyping schemes for Gram-negative bacteria. This review covers the diversity in E. coli O antigen structures and gene clusters, and the genetic basis for the structural diversity. Of the 187 formally defined O antigens, six (O31, O47, O67, O72, O94 and O122) have since been removed and three (O34, O89 and O144) strains do not produce any O antigen. Therefore, structures are presented for 176 of the 181 E. coli O antigens, some of which include subgroups. Most (93%) of these O antigens are synthesized via the Wzx/Wzy pathway, 11 via the ABC transporter pathway, with O20, O57 and O60 still uncharacterized due to failure to find their O antigen gene clusters. Biosynthetic pathways are given for 38 of the 49 sugars found in E. coli O antigens, and several pairs or groups of the E. coli antigens that have related structures show close relationships of the O antigen gene clusters within clades, thereby highlighting the genetic basis of the evolution of diversity.

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39

Bisercić, M., and H. Ochman. "Natural populations of Escherichia coli and Salmonella typhimurium harbor the same classes of insertion sequences." Genetics 133, no. 3 (March 1, 1993): 449–54. http://dx.doi.org/10.1093/genetics/133.3.449.

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Abstract Despite their close phylogenetic relationship, Escherichia coli and Salmonella typhimurium were long considered as having distinct classes of transposable elements maintained by either host-related factors or very restricted gene exchange. In this study, genetically diverse collections of E. coli and S. typhimurium (subgroup I) were surveyed for the presence of several classes of insertion sequences by Southern blot analysis and the polymerase chain reaction. A majority of salmonellae contained IS1 or IS3, elements originally recovered from E. coli, while IS200, a Salmonella-specific element, was present in about 20% of the tested strains of E. coli. Based on restriction mapping, the extent of sequence divergence between copies of IS200 from E. coli and S. typhimurium is on the order of that observed in comparisons of chromosomally encoded genes from these taxa. This suggests that copies of IS200 have not been recently transferred between E. coli and S. typhimurium and that the element was present in the common ancestor to both species. IS200 is polymorphic within E. coli but homogeneous among isolates of S. typhimurium, providing evidence that these species might differ in their rates of transfer and turnover of insertion sequences.

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40

Timoshenko, A. V., L. K. Gerasimova, L. I. Kolupaeva, and S. N. Cherenkevich. "Intercellular aggregation of thymocytes and bacterial cells Escherichia coli." Biopolymers and Cell 7, no. 3 (May 20, 1991): 98–102. http://dx.doi.org/10.7124/bc.0002d8.

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41

Sukhodolets, V. V. "Unequal crossing-over in Escherichia coli." Russian Journal of Genetics 42, no. 11 (November 2006): 1285–93. http://dx.doi.org/10.1134/s102279540611010x.

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42

Boyd, E. Fidelma, Charles W. Hill, Stephen M. Rich, and Daniel L. Hartl. "Mosaic Structure of Plasmids From Natural Populations of Escherichia coli." Genetics 143, no. 3 (July 1, 1996): 1091–100. http://dx.doi.org/10.1093/genetics/143.3.1091.

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Abstract The distribution of plasmids related to the fertility factor F was examined in the ECOR reference collection of Escherichia coli. Probes specific for four F-related genes were isolated and used to survey the collection by DNA hybridization. To estimate the genetic diversity of genes in F-like plasmids, DNA sequences were obtained for four plasmid genes. The phylogenetic relationships among the plasmids in the ECOR strains is very different from that of the strains themselves. This finding supports the view that plasmid transfer has been frequent within and between the major groups of ECOR. Furthermore, the sequences indicate that recombination between genes in plasmids takes place at a considerably higher frequency than that observed for chromosomal genes. The plasmid genes, and by inference the plasmids themselves, are mosaic in structure with different regions acquired from different sources. Comparison of gene sequences from a variety of naturally occurring plasmids suggested a plausible donor of some of the recombinant regions as well as implicating a chi site in the mechanism of genetic exchange. The relatively high rate of recombination in F-plasmid genes suggests that conjugational gene transfer may play a greater role in bacterial population structure than previously appreciated.

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43

Saveson, Catherine J., and Susan T. Lovett. "Enhanced Deletion Formation by Aberrant DNA Replication in Escherichia coli." Genetics 146, no. 2 (June 1, 1997): 457–70. http://dx.doi.org/10.1093/genetics/146.2.457.

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Repeated genes and sequences are prone to genetic rearrangements including deletions. We have investigated deletion formation in Escherichia coli strains mutant for various replication functions. Deletion was selected between 787 base pair tandem repeats carried either on a ColE1-derived plasmid or on the E. coli chromosome. Only mutations in functions associated with DNA Polymerase III elevated deletion rates in our assays. Especially large increases were observed in strains mutant in dnaQ the ϵ editing subunit of Pol III, and dnuB, the replication fork helicase. Mutations in several other functions also altered deletion formation: the α polymerase (dnaE), the γ clamp loader complex (holC, dnaX), and the β clamp (dnaN) subunits of Pol III and the primosomal proteins, dnaC and priA. Aberrant replication stimulated deletions through several pathways. Whereas the elevation in dnaB strains was mostly recA- and lexA-dependent, that in dnaQ strains was mostly recA- and lexA-independent. Deletion product analysis suggested that slipped mispairing, producing monomeric replicon products, may be preferentially increased in a dnaQ mutant and sister-strand exchange, producing dimeric replicon products, may be elevated in dnaE mutants. We conclude that aberrant Polymerase III replication can stimulate deletion events through several mechanisms of deletion and via both recA-dependent and independent pathways.

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44

Milkman, R., and M. M. Bridges. "Molecular Evolution of the Escherichia Coli Chromosome. III. Clonal Frames." Genetics 126, no. 4 (December 1, 1990): 1139. http://dx.doi.org/10.1093/genetics/126.4.1139.

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45

Milkman, R., and M. M. Bridges. "Molecular evolution of the Escherichia coli chromosome. III. Clonal frames." Genetics 126, no. 3 (November 1, 1990): 505–17. http://dx.doi.org/10.1093/genetics/126.3.505.

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Abstract PCR fragments, 1500-bp, from 15 previously sequenced regions in the Escherichia coli chromosome have been compared by restriction analysis in a large set of wild (ECOR) strains. Prior published observations of segmental clonality are confirmed: each of several sequence types is shared by a number of strains. The rate of recombinational replacement and the average size of the replacements are estimated in a set of closely related strains in which a clonal frame is dotted with occasional stretches of DNA belonging to other clones. A clonal hierarchy is described. Some new comparative sequencing data are presented.

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46

Milkman, R., and M. M. Bridges. "Molecular evolution of the Escherichia coli chromosome. IV. Sequence comparisons." Genetics 133, no. 3 (March 1, 1993): 455–68. http://dx.doi.org/10.1093/genetics/133.3.455.

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Abstract DNA sequences have been compared in a 4,400-bp region for Escherichia coli K12 and 36 ECOR strains. Discontinuities in degree of similarity, previously inferred, are confirmed in detail. Three clonal frames are described on the basis of the present local high-resolution data, as well as previous analyses of restriction fragment length polymorphism (RFLP) and of multilocus enzyme electrophoresis (MLEE) covering small regions more widely dispersed on the chromosome. These three approaches show important consistency. The data illustrate the fact that, in the limited context of intraspecific genomic sequence variation, clonality and homology are synonymous. Two estimable quantitative properties are defined: recency of common ancestry (the reciprocal of the log10 of the number of generations since the most recent common ancestor), and the number of nucleotide pairs over which a given recency of common ancestry applies. In principle, these parameters are measures of the degree and physical extent of homology. The small size of apparent recombinational replacements, together with the observation that they occasionally occur in discontinuous series, raises the question of whether they result from the superimposition of replacements of much larger size (as expected from an elementary interpretation of conjugation and transduction in experimental E. coli systems) or via an alternative mechanism. Length polymorphisms of several sorts are described.

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47

Harvey, S., and C. W. Hill. "Exchange of spacer regions between rRNA operons in Escherichia coli." Genetics 125, no. 4 (August 1, 1990): 683–90. http://dx.doi.org/10.1093/genetics/125.4.683.

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Abstract The Escherichia coli rRNA operons each have one of two types of spacer separating the 16S and 23S coding regions. The spacers of four operons encode tRNA(Glu2) and the other three encode both tRNA(Ile) and tRNA(Ala1B). We have prepared a series of mutants in which the spacer region of a particular rrn operon has been replaced by the opposite type. Included among these were a mutant retaining only a single copy of the tRNA(Glu2) spacer (at rrnG) and another retaining only a single copy of the tRNA(Ile)-tRNA(Ala1B) spacer (at rrnA). While both mutants grew more slowly than controls, the mutant deficient in tRNA(Glu2) spacers was more severely affected. At a frequency of 6 X 10(-5), these mutants phenotypically reverted to faster growing types by increasing the copy number of the deficient spacer. In most of these phenotypic revertants, the deficient spacer type appeared in a rrn operon which previously contained the surplus type, bringing the ratio of spacer types closer to normal. In a few cases, these spacer changes were accompanied by an inversion of the chromosomal material between the donor and recipient rrn operons. Two examples of inversion of one-half of the E. coli chromosome between rrnG and rrnH were observed. The correlation of spacer change with inversion indicated that, in these particular cases, the change was due to an intrachromatid gene conversion event accompanied by a reciprocal crossover rather than reciprocal exchange between sister chromatids.

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48

Fijalkowska, I. J., R. L. Dunn, and R. M. Schaaper. "Mutants of Escherichia coli with increased fidelity of DNA replication." Genetics 134, no. 4 (August 1, 1993): 1023–30. http://dx.doi.org/10.1093/genetics/134.4.1023.

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Abstract To improve our understanding of the role of DNA replication fidelity in mutagenesis, we undertook a search for Escherichia coli antimutator strains with increased fidelity of DNA replication. The region between 4 and 5 min of the E. coli chromosome was mutagenized using localized mutagenesis mediated by bacteriophage P1. This region contains the dnaE and dnaQ genes, which encode, respectively, the DNA polymerase (alpha subunit) and 3' exonucleolytic proofreading activity (epsilon subunit) of DNA polymerase III holoenzyme, the enzyme primarily responsible for replicating the bacterial chromosome. The mutated bacteria were screened for antimutator phenotype in a strain defective in DNA mismatch repair (mutL), using a papillation assay based on the reversion of the galK2 mutation. In a mutL strain, mutations result primarily from DNA replication errors. Among 10,000 colonies, seven mutants were obtained whose level of papillation was reduced 5-30-fold. These mutants also displayed decreased mutation frequencies for rifampicin or nalidixic acid resistance as well as for other markers. Mapping by P1 transduction and complementation showed each to reside in dnaE. These observations support the idea that the mutants represent antimutators which replicate their DNA with increased fidelity. Mutation rates were reduced in both mutL and mutT backgrounds, but mutagenesis by ultraviolet light was not significantly affected, suggesting that the antimutator effect may be largely restricted to normal DNA replication.

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49

Kazic, T., and D. E. Berg. "Context effects in the formation of deletions in Escherichia coli." Genetics 126, no. 1 (September 1, 1990): 17–24. http://dx.doi.org/10.1093/genetics/126.1.17.

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Abstract We have examined the frequency with which identical deletions are formed in different chromosomal contexts. A panel of six mutant bla genes containing palindrome/direct repeat structures were moved from pBR322 to three locations: at lambda att, at chromosomal lac, and at F'lac. Deletion of the palindromes and one of the direct repeats results in reversion to Ampr. The frequency of deletion for all alleles declines beyond the reduction in copy number when they are moved from the multicopy plasmid environment to a single-copy chromosome. The magnitude of the declines varies in an allele-specific and location-specific manner. Our data support the hypothesis that context can influence the frequency of mutation independent of the immediate DNA sequence.

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50

Smith, Bradley T., and Graham C. Walker. "Mutagenesis and More: umuDC and the Escherichia coli SOS Response." Genetics 148, no. 4 (April 1, 1998): 1599–610. http://dx.doi.org/10.1093/genetics/148.4.1599.

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Abstract The cellular response to DNA damage that has been most extensively studied is the SOS response of Escherichia coli. Analyses of the SOS response have led to new insights into the transcriptional and posttranslational regulation of processes that increase cell survival after DNA damage as well as insights into DNA-damage-induced mutagenesis, i.e., SOS mutagenesis. SOS mutagenesis requires the recA and umuDC gene products and has as its mechanistic basis the alteration of DNA polymerase III such that it becomes capable of replicating DNA containing miscoding and noncoding lesions. Ongoing investigations of the mechanisms underlying SOS mutagenesis, as well as recent observations suggesting that the umuDC operon may have a role in the regulation of the E. coli cell cycle after DNA damage has occurred, are discussed.

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