Global Regulation by Horizontally Transferred Regulators Establishes the Pathogenicity of Escherichia coli

Enterohemorrhagic Escherichia coli is an emerging pathogen that causes diarrhea and hemolytic uremic syndrome. Much of the genomic information that affects virulence is acquired by horizontal transfer. Genes necessary for attaching and effacing lesions are located in the locus for enterocyte effacement (LEE) pathogenicity island. LEE gene transcription is positively regulated by Ler, which is also encoded by the LEE, and by Pch regulators, which are encoded at other loci. Here we identified genes whose transcription profiles were similar to those of the LEE genes, by comparing the effects of altering ler and pch transcript levels. We assigned these genes into two classes, according to their transcription profiles. By determining the binding profiles for Ler and Pch, we showed that both were involved in regulating one class of genes, but only Pch was involved in regulating the other class. Binding sites were found in the coding region as well as the promoter region of regulated genes, which include genes common to K12 strains as well as 0157-specific genes, suggesting that both act as a global regulator. These results indicate that Ler and Pch orchestrate the transcription of virulence genes, which are captured by horizontal transfer and scattered throughout the chromosome

Exact asymptotic form of the exchange interactions between shallow centers in doped semiconductors

The method developed in [L. P. Gor'kov and L. P. Pitaevskii, Sov. Phys. Dokl. 8, 788 (1964); C. Herring and M. Flicker, Phys. Rev. 134, A362 (1964)] to calculate the asymptotic form of exchange interactions between hydrogen atoms in the ground state is extended to excited states. The approach is then applied to shallow centers in semiconductors. The problem of the asymptotic dependence of the exchange interactions in semiconductors is complicated by the multiple degeneracy of the ground state of an impurity (donor or acceptor) center in valley or band indices, crystalline anisotropy and strong spin-orbital interactions, especially for acceptor centers in III-V and II-VI groups semiconductors. Properties of two coupled centers in the dilute limit can be accessed experimentally, and the knowledge of the exact asymptotic expressions, in addition to being of fundamental interest, must be very helpful for numerical calculations and for interpolation of exchange forces in the case of intermediate concentrations. Our main conclusion concerns the sign of the magnetic interaction -- the ground state of a pair is always non-magnetic. Behavior of the exchange interactions in applied magnetic fields is also discussed

Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains

The type III protein secretion system is an important pathogenicity factor of enteropathogenic and enterohaemorrhagic Escherichia coli pathotypes. The genes encoding this apparatus are located on a pathogenicity island (the locus of enterocyte effacement) and are transcriptionally activated by the master regulator Ler. In each pathotype Ler is also known to regulate genes located elsewhere on the chromosome, but the full extent of the Ler regulon is unclear, especially for enteropathogenic E. coli. The Ler regulon was defined for two strains of E. coli: E2348/69 (enteropathogenic) and EDL933 (enterohaemorrhagic) in mid and late log phases of growth by DNA microarray analysis of the transcriptomes of wild-type and ler mutant versions of each strain. In both strains the Ler regulon is focused on the locus of enterocyte effacement – all major transcriptional units of which are activated by Ler, with the sole exception of the LEE1 operon during mid-log phase growth in E2348/69. However, the Ler regulon does extend more widely and also includes unlinked pathogenicity genes: in E2348/69 more than 50 genes outside of this locus were regulated, including a number of known or potential pathogenicity determinants; in EDL933 only 4 extra-LEE genes, again including known pathogenicity factors, were activated. In E2348/69, where the Ler regulon is clearly growth phase dependent, a number of genes including the plasmid-encoded regulator operon perABC, were found to be negatively regulated by Ler. Negative regulation by Ler of PerC, itself a positive regulator of the ler promoter, suggests a negative feedback loop involving these proteins