An analog implementation of pulse-width-modulation based sliding mode controller for dc-dc boost converters

Author name used in this publication: Chi K. TseRefereed conference paper2006-2007 > Academic research: refereed > Refereed conference paperVersion of RecordPublishe

Mutual Regulation of CRP and N(epsilon)-Lysine Acetylation in Escherichia Coli

Post-translational modifications, such as N(epsilon)-lysine acetylation, are known to alter the behavior of transcriptional regulators in eukaryotes, but very little is known about the consequences of acetylation on transcriptional regulation in bacteria. Here, I provide evidence that a global transcriptional regulator of carbon metabolism, cAMP Receptor Protein (CRP), promotes both enzymatic and non-enzymatic lysine acetylation in E. coli. Non-enzymatic lysine acetylation occurs when cells ferment acetate, such as during growth on high concentrations of glucose. Intriguingly, CRP can be non-enzymatically acetylated on several lysines, including lysine 100 (K100). I provide evidence that neutralization of the K100 positive charge, as would occur upon K100 acetylation, has a dual effect on CRP activity. First, K100 neutralization decreases CRP activity at some Class II promoters. This decreased activity likely results from disruption of the interaction between Activating Region 2 (AR2) of CRP and the RNA polymerase alpha subunit N-terminal domain. Second, K100 neutralization increases the CRP half-life, leading to increased CRP steady state levels. Due to increased steady state levels, CRP activity is increased at some Class I promoters, in which CRP does not require AR2. Taken together, I propose that CRP promotes global acetylation, including CRP K100 acetylation, when cells are grown on glucose by positively regulating non-enzymatic acetylation. A consequence of K100 acetylation may be inverse regulation of Class II and Class I promoters under these conditions. This mechanism may help regulate carbon flux though central metabolism

Comparative genome analysis identifies few traits unique to the Escherichia coli ST131 H30Rx clade and extensive mosaicism at the capsule locus

Background: E.coli ST131 is a globally disseminated clone of multi-drug resistant E. coli responsible for that vast majority of global extra-intestinal E. coli infections. Recent global genomic epidemiological studies have highlighted the highly clonal nature of this group of bacteria, however there appears to be inconsistency in some phenotypes associated with the clone, in particular capsule types as determined by K-antigen testing both biochemically and by PCR. Results: We performed improved quality assemblies on ten ST131 genomes previously sequenced by our group and compared them to a new reference genome sequence JJ1886 to identify the capsule loci across the drug-resistant clone H30Rx. Our data shows considerable genetic diversity within the capsule locus of H30Rx clone strains which is mirrored by classical K antigen testing. The varying capsule locus types appear to be randomly distributed across the H30Rx phylogeny suggesting multiple recombination events at this locus, but that this capsule heterogeneity has little to no effect on virulence associated phenotypes in vitro. Conclusions: Our data provides a framework for determining the capsular genetics of E. coli ST131 and further beyond to ExPEC strains, and highlights how capsular mosaicism may be an important strategy in becoming a successful globally disseminated human pathogen

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