Amino Acid Catabolism in Staphylococcus Aureus
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Joosten, Han M.L.J.; Herst, Patricia M.; Drift, Chris Van Der
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by University of Groningen University of Groningen Characterization of Glutamine-Requiring Mutants of Pseudomonas aeruginosa Janssen, Dick B.; Joosten, Han M.L.J.; Herst, Patricia M.; Drift, Chris van der Published in: Archives of Microbiology IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 1982 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Janssen, D. B., Joosten, H. M. L. J., Herst, P. M., & Drift, C. V. D. (1982). Characterization of Glutamine- Requiring Mutants of Pseudomonas aeruginosa. Archives of Microbiology, 131(4). Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 12-11-2019 JOURNAL OF BACTERIOLOGY, Sept. 1982, p. 1176-1183 Vol. 151, No. -
Amino Acid Disorders 105
AMINO ACID DISORDERS 105 Massaro, A. S. (1995). Trypanosomiasis. In Guide to Clinical tions in biological fluids relatively easy. These Neurology (J. P. Mohrand and J. C. Gautier, Eds.), pp. 663– analyzers separate amino acids either by ion-ex- 667. Churchill Livingstone, New York. Nussenzweig, V., Sonntag, R., Biancalana, A., et al. (1953). Ac¸a˜o change chromatography or by high-pressure liquid de corantes tri-fenil-metaˆnicos sobre o Trypanosoma cruzi in chromatography. The results are plotted as a graph vitro: Emprego da violeta de genciana na profilaxia da (Fig. 1). The concentration of each amino acid can transmissa˜o da mole´stia de chagas por transfusa˜o de sangue. then be calculated from the size of the corresponding O Hospital (Rio de Janeiro) 44, 731–744. peak on the graph. Pagano, M. A., Segura, M. J., DiLorenzo, G. A., et al. (1999). Cerebral tumor-like American trypanosomiasis in Most amino acid disorders can be diagnosed by acquired immunodeficiency syndrome. Ann. Neurol. 45, measuring the concentrations of amino acids in 403–406. blood plasma; however, some disorders of amino Rassi, A., Trancesi, J., and Tranchesi, B. (1982). Doenc¸ade acid transport are more easily recognized through the Chagas. In Doenc¸as Infecciosas e Parasita´rias (R. Veroesi, Ed.), analysis of urine amino acids. Therefore, screening 7th ed., pp. 674–712. Guanabara Koogan, Sa˜o Paulo, Brazil. Spina-Franc¸a, A., and Mattosinho-Franc¸a, L. C. (1988). for amino acid disorders is best done using both South American trypanosomiasis (Chagas’ disease). In blood and urine specimens. Occasionally, analysis of Handbook of Clinical Neurology (P. -
BIOCHEMISTRY of TRYPTOPHAN in HEALTH and DISEASE Contents
Molec. Aspects Med. Vol. 6, pp. 101-197, 1982 0098-2997/82/020101-97548.50/0 Printed in Great Britain. All rights reserved. Copyright © Pergamon Press Ltd. BIOCHEMISTRY OF TRYPTOPHAN IN HEALTH AND DISEASE David A. Bender Courtauld Institute of Biochemistry, The Middlesex Hospital Medical School, London WIP 7PN, U.K. Contents Chapter 1 THE DISCOVERY OF TRYPTOPHAN, ITS PHYSIOLOGICAL SIGNIFICANCE AND METABOLIC FATES 103 Tryptophan and glucose metabolism 105 Xanthurenic acid and insulin 105 The glucose tolerance factor 106 Inhibition of gluconeogenesis by tryptophan metabolites i07 Metabolic fates of tryptophan 108 Protein synthesis 108 Oxidative metabolism Ii0 5-Hydroxyindole synthesis 111 Intestinal bacterial metabolism iii Chapter 2 THE 5-HYDROXYINDOLE PATHWAY OF TRYPTOPHAN METABOLISM; SEROTONIN AND OTHER CENTRALLY ACTIVE TRYPTOPHAN METABOLITES 112 Tryptophan 5-hydroxylase 112 Inhibition of tryptophan hydroxylase and the carcinoid syndrome 116 Aromatic amino acid decarboxylase 118 The specificity of aromatic amino acid decarboxylase 120 Tryptophan metabolism in the pineal gland 121 Monoamine oxidase 124 The uptake of tryptophan into the brain 124 The binding of tryptophan to serum albumin 127 Competition for uptake by other neutral amino acids 129 Changes in tryptophan metabolism in response to food intake 129 Tryptophan uptake into the brain in liver failure 131 Sleep and tryptophan metabolism 134 101 102 D.A. Bender Tryptophan and serotonin in psychiatric disorders 135 Affective disorders 136 Evidence for a deficit of serotonin or tryptophan -
Characterization of the Metal Ion Binding Site in the Anti-Terminator Protein, Hutp, of Bacillus Subtilis Thirumananseri Kumarevel, Hiroshi Mizuno1 and Penmetcha K
Published online September 28, 2005 5494–5502 Nucleic Acids Research, 2005, Vol. 33, No. 17 doi:10.1093/nar/gki868 Characterization of the metal ion binding site in the anti-terminator protein, HutP, of Bacillus subtilis Thirumananseri Kumarevel, Hiroshi Mizuno1 and Penmetcha K. R. Kumar* Institute for Biological Resources and Functions, National Institute of Advanced Industrial Science and Technology (AIST), Central 6, Tsukuba, Ibaraki 305-8566, Japan and 1NEC Soft Ltd, 1-18-6, Shinkiba, Koto-ku, Tokyo 106-8608, Japan Downloaded from https://academic.oup.com/nar/article-abstract/33/17/5494/1067798 by guest on 06 March 2019 Received July 10, 2005; Revised August 22, 2005; Accepted September 9, 2005 PDB ID: 1WRN, 1WRO and 1WPT ABSTRACT terminator structure (+459 to +571 nt, Figure 1) in between the hutP and hutH genes, and regulates the transcription of the HutP is an RNA-binding protein that regulates the hut operon by an anti-termination mechanism (1–3). Several expression of the histidine utilization (hut) operon bacterial proteins that regulate anti-terminator/terminator in Bacillus subtilis, by binding to cis-acting regulatory structures have been described, including TRAP, PyrR, sequences on hut mRNA. It requires L-histidine and LacT, BglG, SacT and GlpP (4–10). One such protein is an Mg21 ion for binding to the specific sequence the hutP gene product, HutP, of B.subtilis. HutP is a 16.2 within the hut mRNA. In the present study, we show kDa protein that shares 60% sequence identity with that several divalent cations can mediate the HutP– the HutP proteins found in other Bacillus species, such as RNA interactions. -
Histidinaemia in Mouse and Man
Arch Dis Child: first published as 10.1136/adc.49.7.545 on 1 July 1974. Downloaded from Archives of Disease in Childhood, 1974, 49, 545. Histidinaemia in mouse and man GRAHAME BULFIELD and HENRIK KACSER From the Department of Genetics, University of Edinburgh Bulfield, G., and Kacser, H. (1974). Archives of Disease in Childhood, 49, 545. Histidinaemia in mouse and man. A recently discovered mutant in the mouse was found to have very low levels of histidase. It is an autosomal recessive. In its enzymic and metabolic properties it appears to be a homologue ofhuman histidinaemia. While the homozygous mouse mutants show no overt abnormalities, offspring of histidinaemic mothers display a balance defect resulting in circling behaviour. This is associated with vestibular damage during in utero development. Mental retardation caused by human maternal phenylketonuria may have a similar aetiology. There are well recognized advantages in studying histidine and its derivatives. The enzymic and animal models in the investigation of human metabolic changes in both mouse and human diseases. The increasing number of disorders in mutants appear to be the same. In addition, man which are reported to have a genetic basis maternal histidinaemia in the mouse has a terato- (McKusick, 1971; Raine, 1972) makes it desirable to genic effect on the developing inner ear which results find and investigate animal homologues with the in abnormal behaviour of the affected offspring. same genic lesions. The genetically most in- These findings may be relevant to the aetiology of vestigated laboratory mammal is the mouse, with human histidinaemia. over 500 known mutants (Green, 1966; Searle, 1973). -
Bacterial Selenoproteins: a Role in Pathogenesis and Targets for Antimicrobial Development
University of Central Florida STARS Electronic Theses and Dissertations, 2004-2019 2009 Bacterial Selenoproteins: A Role In Pathogenesis And Targets For Antimicrobial Development Sarah Rosario University of Central Florida Part of the Medical Sciences Commons Find similar works at: https://stars.library.ucf.edu/etd University of Central Florida Libraries http://library.ucf.edu This Doctoral Dissertation (Open Access) is brought to you for free and open access by STARS. It has been accepted for inclusion in Electronic Theses and Dissertations, 2004-2019 by an authorized administrator of STARS. For more information, please contact [email protected]. STARS Citation Rosario, Sarah, "Bacterial Selenoproteins: A Role In Pathogenesis And Targets For Antimicrobial Development" (2009). Electronic Theses and Dissertations, 2004-2019. 3822. https://stars.library.ucf.edu/etd/3822 BACTERIAL SELENOPROTEINS: A ROLE IN PATHOGENESIS AND TARGETS FOR ANTIMICROBIAL DEVELOPMENT. by SARAH E. ROSARIO B.S. Florida State University, 2000 M.P.H. University of South Florida, 2002 A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Burnett School of Biomedical Sciences in the College of Medicine at the University of Central Florida Orlando, Florida Summer Term 2009 Major Professor: William T. Self © 2009 Sarah E. Rosario ii ABSTRACT Selenoproteins are unique proteins in which selenocysteine is inserted into the polypeptide chain by highly specialized translational machinery. They exist within all three kingdoms of life. The functions of these proteins in biology are still being defined. In particular, the importance of selenoproteins in pathogenic microorganisms has received little attention. We first established that a nosocomial pathogen, Clostridium difficile, utilizes a selenoenzyme dependent pathway for energy metabolism. -
Exploring the Application of Ecological Theory to the Human Gut Microbiota Using Complex Defined Microbial Communities As Models
Exploring the application of ecological theory to the human gut microbiota using complex defined microbial communities as models by Kaitlyn Oliphant A Thesis presented to the The University of Guelph In partial fulfillment of requirements for the degree of Doctor of Philosophy in Molecular and Cellular Biology Guelph, Ontario, Canada © Kaitlyn Oliphant, December, 2018 ABSTRACT EXPLORING THE APPLICATION OF ECOLOGICAL THEORY TO THE HUMAN GUT MICROBIOTA USING COMPLEX DEFINED MICROBIAL COMMUNITIES AS MODELS Kaitlyn Oliphant Advisor: University of Guelph, 2018 Dr. Emma Allen-Vercoe The ecosystem of microorganisms that inhabit the human gastrointestinal tract, termed the gut microbiota, critically maintains host homeostasis. Alterations in species structure and metabolic behaviour of the gut microbiota are thus unsurprisingly exhibited in patients of gastrointestinal disorders when compared to the healthy population. Therefore, strategies that aim to remediate such gut microbiota through microbial supplementation have been attempted, with variable clinical success. Clearly, more knowledge of how to assemble a health promoting gut microbiota is required, which could be drawn upon from the framework of ecological theory. Current theories suggest that the forces driving microbial community assembly include historical contingency, dispersal limitation, stochasticity and environmental selection. Environmental selection additionally encompasses habitat filtering, i.e., host-microbe interactions, and species assortment, i.e., microbe-microbe interactions. I propose to explore the application of this theory to the human gut microbiota, and I hypothesize that microbial ecological theory can be replicated utilizing complex defined microbial communities. To address my hypothesis, I first built upon existing methods to assess microbial community composition and behaviour, then applied such tools to human fecal-derived defined microbial communities cultured in bioreactors, for example, by using marker gene sequencing and metabonomics. -
Inborn Errors of Metabolism in Adults: a Diagnostic Approach to Neurological and Psychiatric Presentations
71 2 Inborn Errors of Metabolism in Adults: A Diagnostic Approach to Neurological and Psychiatric Presentations Fanny Mochel, Frédéric Sedel 2.1 Differences Between Paediatric and Adult Phenotypes – 72 2.2 General Approach to IEM In Adulthood – 72 2.3 Specific Approaches to Neuro metabolic Presentations in Adults – 76 References – 89 J.-M. Saudubray et al. (Eds.), Inborn Metabolic Diseases, DOI 10.1007/978-3-662-49771-5_2, © Springer-Verlag Berlin Heidelberg 2016 72 Chapter 2 · Inborn Errors of Metabolism in Adults: A Diagnostic Approach to Neurological and Psychiatric Presentations Late-onset forms of IEM presenting initially in adulthood are of- In addition, some clinical signs are highly suggestive of a ten unrecognised, so that their exact prevalence is unknown [1]. particular IEM or of a particular group of IEM. Some of these Most often they have psychiatric or neurological manifestations, ‘red flags’ are listed in . Table 2.2. 2 including atypical psychosis or depression, unexplained coma, Unfortunately, in many circumstances, highly specific peripheral neuropathy, cerebellar ataxia, spastic paraparesis, de- signs or symptoms are lacking and the presentation is that of mentia, movement disorders and epilepsy [2][3][4][5]. a less specific neurological or psychiatric disorder (epilepsy, Physicians caring for adult patients with IEM are also involved in cognitive decline, psychiatric signs). In such situations, the the management of those with early onset forms who reach diagnostic approach is based on the type of clinical signs, their adulthood. The transfer of such patients from paediatric to adult clinical course (acute, acute-relapsing, with diurnal variations, care raises a number of medical, dietetic and social concerns. -
Characterization of the Metal Ion Binding Site in the Anti-Terminator Protein, Hutp, of Bacillus Subtilis Thirumananseri Kumarevel, Hiroshi Mizuno1 and Penmetcha K
5494–5502 Nucleic Acids Research, 2005, Vol. 33, No. 17 doi:10.1093/nar/gki868 Characterization of the metal ion binding site in the anti-terminator protein, HutP, of Bacillus subtilis Thirumananseri Kumarevel, Hiroshi Mizuno1 and Penmetcha K. R. Kumar* Institute for Biological Resources and Functions, National Institute of Advanced Industrial Science and Technology (AIST), Central 6, Tsukuba, Ibaraki 305-8566, Japan and 1NEC Soft Ltd, 1-18-6, Shinkiba, Koto-ku, Tokyo 106-8608, Japan Received July 10, 2005; Revised August 22, 2005; Accepted September 9, 2005 PDB ID: 1WRN, 1WRO and 1WPT ABSTRACT terminator structure (+459 to +571 nt, Figure 1) in between the hutP and hutH genes, and regulates the transcription of the HutP is an RNA-binding protein that regulates the hut operon by an anti-termination mechanism (1–3). Several expression of the histidine utilization (hut) operon bacterial proteins that regulate anti-terminator/terminator in Bacillus subtilis, by binding to cis-acting regulatory structures have been described, including TRAP, PyrR, sequences on hut mRNA. It requires L-histidine and LacT, BglG, SacT and GlpP (4–10). One such protein is an Mg21 ion for binding to the specific sequence the hutP gene product, HutP, of B.subtilis. HutP is a 16.2 within the hut mRNA. In the present study, we show kDa protein that shares 60% sequence identity with that several divalent cations can mediate the HutP– the HutP proteins found in other Bacillus species, such as RNA interactions. The best divalent cations were Bacillus halodurans (11), Bacillus cereus (12) and Bacillus Mn21,Zn21 and Cd21, followed by Mg21,Co21 and anthracis (13). -
Paweł Mateusz Mordaka Reductions Using Clostridium Sporogenes
Department of Chemical and Environmental Engineering Paweł Mateusz Mordaka Reductions using Clostridium sporogenes Thesis submitted to the University of Nottingham for the degree of Doctor of Philosophy December 2013 ABSTRACT Pawel Mateusz Mordaka Reductions using Clostridium sporogenes Clostridium sporogenes was previously shown to be an extraordinary source for unusual reductases. It can catalyze reduction of wide a range of substrates such as nitroalkenes, enoates and nitro compounds, and can be used to generate chiral products. In preliminary studies, the ClosTron gene knock-out system for Clostridia was used to inactivate the fldZ gene assumed to encode the enzyme responsible for reduction of cinnamic acid in the reductive branch of L-phenylalanine fermentation via the Stickland reaction. Biotransformations with the fldZ mutant showed that C. sporogenes possesses multiple enzymatic activities, reducing enoates, β,β- and α,β-disubstituted nitroalkenes with different yields and enantioselectivities. The fldZ reductase was found to be responsible for reduction of cinnamic acid, (E)-1-nitro-2-phenylpropene, (E)-2-nitro-1- phenylpropene and β-nitrostyrene. However, the mutant could still reduce (E)-2-nitro-1- phenylpropene, β-nitrostyrene and cinnamic acid confirming the presence of other C=C double bond reductases in C. sporogenes. The analysis of the C. sporogenes genome sequence allowed identification of two hypothetical genes encoding proteins with homology to flavin-containing C=C double bond reductases, fldZ 2-enoate reductase and OYE-like reductase, which were subsequently cloned, overexpressed in E. coli under anaerobic conditions and tested for reduction of unsaturated compounds. The activity tests showed that fldZ possesses a narrow substrate range and can reduce only aromatic enoates such as cinnamic acid or p-coumaric acid. -
PHYSIOLOGICAL and ECOLOGICAL INVESTIGATIONS of CLOSTRIDIUM DIFFICILE by Catherine D. R
PHYSIOLOGICAL AND ECOLOGICAL INVESTIGATIONS OF CLOSTRIDIUM DIFFICILE By Catherine D. Robinson A DISSERTATION Submitted to Michigan State University in partial fulfillment of the requirements for the degree of Microbiology and Molecular Genetics- Doctor of Philosophy 2014 ABSTRACT PHYSIOLOGICAL AND ECOLOGICAL INVESTIGATIONS OF CLOSTRIDIUM DIFFICILE By Catherine D. Robinson Disease caused by Clostridium difficile is currently the most prevalent nosocomial infection and leading cause of antibiotic-associated diarrhea. It is clear that the intestinal microbiota plays a role in preventing C. difficile infection in the absence of antibiotics; however, the mechanisms involved in this protective function are poorly understood. Since antibiotic administration is an inducing factor of C. difficile infection, treatment employing antibiotics often results in recurrent disease, yet it is still the primary line of treatment. Therefore, a central goal of research in this area is to better define the role of the intestinal microbiota in suppression of disease, and ultimately develop alternative ways to prevent and treat C. difficile infection. In this thesis, I present a novel in vitro model that was developed to study complex fecal communities. This in vitro model is a continuous-culture system that utilizes arrays of small-volume reactors; it is unique in its simple set-up and high replication. We adapted this model to operate as a C. difficile infection model, where in vivo C. difficile invasion dynamics are replicated in that the fecal communities established in the reactors are resistant to C. difficile growth unless disrupted by antibiotic administration. We then go on to use this model to show that newly emerged, epidemic strains of C. -
Discovery and Characterization of a Prominent Gut Microbial Glycyl Radical Enzyme Responsible for 4-Hydroxyproline Metabolism
Discovery and Characterization of a Prominent Gut Microbial Glycyl Radical Enzyme Responsible for 4-Hydroxyproline Metabolism The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Huang, Yue. 2019. Discovery and Characterization of a Prominent Gut Microbial Glycyl Radical Enzyme Responsible for 4- Hydroxyproline Metabolism. Doctoral dissertation, Harvard University, Graduate School of Arts & Sciences. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:41121269 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Discovery and characterization of a prominent gut microbial glycyl radical enzyme responsible for 4-hydroxyproline metabolism A dissertation presented by Yue Huang to the Committee on Higher Degrees in Chemical Biology in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Chemical Biology Harvard University Cambridge, Massachusetts October 2018 © 2018 – Yue Huang All rights reserved Dissertation advisor: Professor Emily P. Balskus Yue Huang Discovery and characterization of a prominent gut microbial glycyl radical enzyme responsible for 4-hydroxyproline metabolism Abstract The human gut is one of the most densely populated microbial habitat on Earth and the gut microbiota is extremely important in maintaining health and disease states. Advances in sequencing technologies have enabled us to gain a better understanding of microbiome compositions, but the majority of microbial genes are not functionally annotated. Therefore, the molecular basis by which gut microbes influence human health remains largely unknown.