Composite Fermions in a weakly density modulated 2DEG: Directive evidence of a periodic magnetic field around n=1/2

We investigate the magnetoresistance of a weakly density modulated high mobility two- dimensional electron system around filling factor . The density modulation with periods a between 300 nm and 500 nm was generated by in situ interferometric illumination. At low B we found commensurability oscillations of the magnetoresistance characteristic for transport in weak electrostatic potentials with minima positions on the magnetic field axis given by 2RC=(ë-1/4)a. Here 2RC is the electron cyclotron diameter at the Fermi- energy and ë an integer. In contrast, we find clear magnetic commensurability features around filling factor with a pronounced minimum for a composite fermion cyclotron radius RC,CF matching 1.25a. This gives direct evidence that the density modulation results in a modulated effective magnetic field for composite fermions. The experimental ñxx-traces around are well described by novel model calculations, based on a semiclassical solution of the Boltzmann equation, taking into account anisotropic scattering

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