TL;DR: Exonuclease function of DNA polymerase from Escherichia colis, discussing hydrolysis of polydeoxyribonucleotides and resistancy of oligonucleotide.
TL;DR: The ClerMonTyping method and its associated web-interface, the ClermonTyper, that allows a given strain sequence to be assigned to E. coli sensu stricto as well as to the seven main E. bacteria phylogroups is developed.
Abstract: The genus Escherichia is composed of Escherichia albertii, E. fergusonii, five cryptic Escherichia clades and E. coli sensu stricto. Furthermore, the E. coli species can be divided into seven main phylogroups termed A, B1, B2, C, D, E and F. As specific lifestyles and/or hosts can be attributed to these species/phylogroups, their identification is meaningful for epidemiological studies. Classical phenotypic tests fail to identify non-sensu stricto E. coli as well as phylogroups. Clermont and colleagues have developed PCR assays that allow the identification of most of these species/phylogroups, the triplex/quadruplex PCR for E. coli phylogroup determination being the most popular. With the growing availability of whole genome sequences, we have developed the ClermonTyping method and its associated web-interface, the ClermonTyper, that allows a given strain sequence to be assigned to E. albertii, E. fergusonii, Escherichia clades I–V, E. coli sensu stricto as well as to the seven main E. coli phylogroups. The ClermonTyping is based on the concept of in vitro PCR assays and maintains the principles of ease of use and speed that prevailed during the development of the in vitro assays. This in silico approach shows 99.4 % concordance with the in vitro PCR assays and 98.8 % with the Mash genome-clustering tool. The very few discrepancies result from various errors occurring mainly from horizontal gene transfers or SNPs in the primers. We propose the ClermonTyper as a freely available resource to the scientific community at: http://clermontyping.iame-research.center/.
TL;DR: It is demonstrated that the HPI of the Y. pestis evolutionary group is disseminated among species of the family Enterobacteriaceae which are pathogenic to humans and prevails in enteroaggregativeEscherichia coli and in E. coli blood culture isolates.
Abstract: The fyuA-irp gene cluster contributes to the virulence of highly pathogenic Yersinia (Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica 1B). The cluster encodes an iron uptake system mediated by the siderophore yersiniabactin and reveals features of a pathogenicity island. Two evolutionary lineages of this “high pathogenicity island” (HPI) can be distinguished on the basis of DNA sequence comparison: a Y. pestis group and a Y. enterocolitica group. In this study we demonstrate that the HPI of the Y. pestis evolutionary group is disseminated among species of the family Enterobacteriaceae which are pathogenic to humans. It prevails in enteroaggregative Escherichia coli and in E. coli blood culture isolates (93 and 80%, respectively), but is rarely found in enteropathogenic E. coli, enteroinvasive E. coli, and enterotoxigenic E. coli isolates. In contrast, the HPI was absent from enterohemorrhagic E. coli, Shigella, and Salmonella enterica strains investigated. Polypeptides encoded by the fyuA, irp1, and irp2 genes located on the HPI could be detected in E. coli strains pathogenic to humans. However, these E. coli strains showed a reduced sensitivity to the bacteriocin pesticin, whose uptake is mediated by the FyuA receptor. Escherichia strains do not possess the hms gene locus thought to be a part of the HPI of Y. pestis. Deletions of the fyuA-irp gene cluster affecting solely the fyuA part of the HPI were identified in 3% of the E. coli strains tested. These results suggest horizontal transfer of the HPI between Y. pestis and some pathogenic E. coli strains.
TL;DR: Evidence that Escherichia fergusonii has evolved at an accelerated rate compared to E. coli is found, suggesting that this species is younger than estimated by the molecular clock method.
Abstract: Extended multilocus sequence typing (MLST) analysis of atypical Escherichia isolates was used to identify five novel phylogenetic clades (CI to CV) among isolates from environmental, human, and animal sources. Analysis of individual housekeeping loci showed that E. coli and its sister clade, CI, remain largely indistinguishable and represent nascent evolutionary lineages. Conversely, clades of similar age (CIII and CIV) were found to be phylogenetically distinct. When all Escherichia lineages (named and unnamed) were evaluated, we found evidence that Escherichia fergusonii has evolved at an accelerated rate compared to E. coli, CI, CIII, CIV, and CV, suggesting that this species is younger than estimated by the molecular clock method. Although the five novel clades were phylogenetically distinct, we were unable to identify a discriminating biochemical marker for all but one of them (CIII) with traditional phenotypic profiling. CIII had a statistically different phenotype from E. coli that resulted from the loss of sucrose and sorbitol fermentation and lysine utilization. The lack of phenotypic distinction has likely hindered the ability to differentiate these clades from typical E. coli, and so their ecological significance and importance for applied and clinical microbiology are yet to be determined. However, our sampling suggests that CIII, CIV, and CV represent environmentally adapted Escherichia lineages that may be more abundant outside the host gastrointestinal tract.
TL;DR: Analysis of the pattern of mutability has made even the bacteria amenable to genetic investigation, and those bacterial viruses which have been most thoroughly investigated genetically belong to a group of seven phages and their mutant forms that comprise the T system.
Abstract: The present understanding of genetic principles has emerged only after exhaustive study of numerous organisms characterized by various levels of organization. Recently the trend has been toward investigations with the simpler organisms as is illustrated by work with fungi (Beadle, 1945a, 1945b; Lindegren, 1945) and several of the protista (Moewus, 1940; Sonneborn, 1946). Analysis of the pattern of mutability has made even the bacteria amenable to genetic investigation (Luria and Delbriick, 1943). Genetic studies have, however, been made with organisms at an even lower level of organization than those mentioned above. Luria (1945) with his experiments on host range mutants and Hershey (1946a, 1946b) with his analysis of plaque size mutants have cleared the way for a more complete inquiry into the genetics of the bacteriophages. Research into the genetics of these organisms may lead to the solution of genetic problems, which other studies have not yet resolved. Those bacterial viruses which have been most thoroughly investigated genetically belong to a group of seven phages and their mutant forms that comprise the T system (Delbrtick, 1946). These phages, named Ti, T2, ... and T7, fall into several subgroups on the basis of serology, electron microscopy, host range, and certain physiological characteristics. One of these subgroups is of particular interest here, the even-numbered phages, T2, T4, and T6. These phages are closely related serologically and show the same characteristic morphology in the electron microscope (Delbruick, 1946). Hershey (1946a, 1946b) has shown that they also have another property in common: all three are capable of mutation from the wild type, r+, to the r type. The former type is characterized by the fact that it forms small plaques with very turbid halos on agar plates. The mutant type, r, forms large plaques with clear. halos. Another characteristic distinguishing r+ from r type, and probably the basic cause of the plaque size difference, is the time required for lysis of visibly turbid cultures. When highly diluted, suspensions of infected bacteria have the same latent period between infection and lysis whether the phage used for infection be of the r+ or the r type. When, however, the infected cultures are visibly turbid, a difference in the latent period occurs. An r-infected culture will clear between 21 and 30 minutes after infection. In contrast to this, a visibly turbid culture infected with r+ phage will not clear between 21 and 30 minutes but will