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MacA, a Diheme c-Type Cytochrome Involved in Fe(III) Reduction by Geobacter sulfurreducens. Jessica E. Butler, 2004.A 36-kDa diheme c-type cytochrome abundant in Fe(III)-respiring Geobacter sulfurreducens, designated MacA, was more highly expressed during growth with Fe(III) as the electron acceptor than with fumarate . Although MacA has homology to proteins with in vitro peroxidase activity, deletion of macA had no impact on response to oxidative stress . However, the capacity for Fe(III) reduction was greatly diminished, indicating that MacA, which is predicted to be localized in the periplasm, is a key intermediate in electron transfer to Fe(III) . Decreased Bioavailability of Rifampin and Other Antituberculosis Drugs in Patients with Advanced Human Immunodeficiency Virus Disease. Prema Gurumurthy, 2004.We evaluated the effects of human immunodeficiency virus (HIV) disease on pharmacokinetics of antituberculosis medications by measuring concentrations of isoniazid and rifampin in blood and of pyrazinamide and ethambutol in urine . Peak concentration and exposure were reduced for rifampin, and rapid acetylators of isoniazid had lower drug levels . HIV and HIV-tuberculosis patients who have diarrhea and cryptosporidial infection exhibit decreased bioavailability of antituberculosis drugs . DksA Affects ppGpp Induction of RpoS at a Translational Level. Larissa Brown, 2002.The RpoS sigma factor (also called  S or
38) is known to regulate at least 50 genes in response to environmental sources of stress or during entry into stationary phase . Regulation of RpoS abundance and activity is complex, with many factors participating at multiple levels . One factor is the nutritional stress signal ppGpp . The absence of ppGpp blocks or delays the induction of rpoS during entry into stationary phase . Artificially inducing ppGpp, without starvation, is known to induce rpoS during the log phase 25- to 50-fold . Induction of ppGpp is found to have only minor effects on rpoS transcript abundance or on RpoS protein stability; instead, the efficiency of rpoS mRNA translation is increased by ppGpp as judged by both RpoS pulse-labeling and promoter-independent effects on lacZ fusions . DksA is found to affect RpoS abundance in a manner related to ppGpp . Deleting dksA blocks rpoS induction by ppGpp . Overproduction of DksA induces rpoS but not ppGpp . Deleting dksA neither alters regulation of ppGpp in response to amino acid starvation nor nullifies the inhibitory effects of ppGpp on stable RNA synthesis . Although this suggests that dksA is epistatic to ppGpp, inducing ppGpp does not induce DksA . A dksA deletion does display a subset of the same multiple-amino-acid requirements found for ppGpp0 mutants, but overproducing DksA does not satisfy ppGpp0 requirements . Sequenced spontaneous extragenic suppressors of dksA polyauxotrophy are frequently the same T563P rpoB allele that suppresses a ppGpp0 phenotype . We propose that DksA functions downstream of ppGpp but indirectly regulates rpoS induction .
Replication-Dependent Recruitment of the ß-Subunit of DNA Polymerase III from Cytosolic Spaces to Replication Forks in Escherichia coli. Toshinari Onogi, 2002.The ß-subunit of DNA polymerase III is located as one or two condensed clusters within the nucleoid-occupied space in exponentially growing cells of Escherichia coli . When chromosome replication is terminated after incubation at nonpermissive temperature in a temperature-sensitive dnaC mutant, the ß-subunit is located in the cytosolic spaces of the cell poles . Regulation of Sialic Acid Catabolism by the DNA Binding Protein NanR in Escherichia coli. Kathryn A. Kalivoda, 2003.All Escherichia coli strains so far examined possess a chromosomally encoded nanATEK-yhcH operon for the catabolism of sialic acids . These unique nine-carbon sugars are synthesized primarily by higher eukaryotes and can be used as carbon, nitrogen, and energy sources by a variety of microbial pathogens or commensals . The gene nanR, located immediately upstream of the operon, encodes a protein of the FadR/GntR family that represses nan expression in trans . S1 analysis identified the nan transcriptional start, and DNA footprint analysis showed that NanR binds to a region of  30 bp covering the promoter region . Native (nondenaturing) polyacrylamide gel electrophoresis, mass spectrometry, and chemical cross-linking indicated that NanR forms homodimers in solution . The region protected by NanR contains three tandem repeats of the hexameric sequence GGTATA . Gel shift analysis with purified hexahistidine-tagged or native NanR detected three retarded complexes, suggesting that NanR binds sequentially to the three repeats . Artificial operators carrying different numbers of repeats formed the corresponding number of complexes . Among the sugars tested that were predicted to be products of the nan-encoded system, only the exogenous addition of sialic acid resulted in the dramatic induction of a chromosomal nanA-lacZ fusion or displaced NanR from its operator in vitro . Titration of NanR by the nan promoter region or artificial operators carrying different numbers of the GGTATA repeat on plasmids in this fusion strain supported the binding of the regulator to target DNA in vivo . Together, the results indicate that GGTATA is important for NanR binding, but the precise mechanism remains to be determined .
Comparison of Shiga Toxin Production by Hemolytic-Uremic Syndrome-Associated and Bovine-Associated Shiga Toxin-Producing Escherichia coli Isolates. Jenny M. Ritchie, 2003.There is considerable diversity among Shiga toxin (Stx)-producing Escherichia coli (STEC) bacteria, and only a subset of these organisms are thought to be human pathogens . The characteristics that distinguish STEC bacteria that give rise to human disease are not well understood . Stxs, the principal virulence determinants of STEC, are thought to account for hemolytic-uremic syndrome (HUS), a severe clinical consequence of STEC infection . Stxs are typically bacteriophage encoded, and their production has been shown to be enhanced by prophage-inducing agents such as mitomycin C in a limited number of clinical STEC isolates . Low iron concentrations also enhance Stx production by some clinical isolates; however, little is known regarding whether and to what extent these stimuli regulate Stx production by STEC associated with cattle, the principal environmental reservoir of STEC . In this study, we investigated whether toxin production differed between HUS- and bovine-associated STEC strains . Basal production of Stx by HUS-associated STEC exceeded that of bovine-associated STEC . In addition, following mitomycin C treatment, Stx2 production by HUS-associated STEC was significantly greater than that by bovine-associated STEC . Unexpectedly, mitomycin C treatment had a minimal effect on Stx1 production by both HUS- and bovine-associated STEC . However, Stx1 production was induced by growth in low-iron medium, and induction was more marked for HUS-associated STEC than for bovine-associated STEC . These observations reveal that disease-associated and bovine-associated STEC bacteria differ in their basal and inducible Stx production characteristics .
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