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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. -
Amino Acid Catabolism in Staphylococcus Aureus
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Fall 12-16-2016 Amino Acid Catabolism in Staphylococcus aureus Cortney Halsey University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Bacteriology Commons Recommended Citation Halsey, Cortney, "Amino Acid Catabolism in Staphylococcus aureus" (2016). Theses & Dissertations. 160. https://digitalcommons.unmc.edu/etd/160 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. Amino Acid Catabolism in Staphylococcus aureus By Cortney R. Halsey A DISSERTATION Presented to the Faculty of The Graduate College in the University of Nebraska In Partial Fulfillment of the Requirements For the Degree of Doctor of Philosophy Pathology and Microbiology Under the Supervision of Dr. Paul D. Fey University of Nebraska Medical Center Omaha, Nebraska October 2016 Supervisory Committee: Kenneth Bayles, Ph.D. Steven Carson, Ph.D. Paul Dunman, Ph.D. Rakesh Singh, Ph.D. ii Acknowledgements First and foremost, I would like to thank my mentor, Dr. Paul Fey, whose patience and support over the past six years has been critical to my success as a graduate student. Paul has given me opportunities to grow as a scientist and person, for which I will be forever thankful. I would also like to thank Dr. Ken Bayles, Dr. Steven Carson, Dr. Paul Dunman, and Dr. Rakesh Singh for serving on my supervisory committee. -
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 -
Folate Deficiency in the Livers of Diethylnitrosamine Treated Rats1
[CANCER RESEARCH 36, 2775-2779, August 1976] Folate Deficiency in the Livers of Diethylnitrosamine treated Rats1 Yoon Sook Shin Buehring,2 Lionel A. Poirier, and E. L. R. Stokstad Department of Nutritional Sciences, University of California, Berkeley, California 94720 (V. S. S. B., E. L. R. 5,1, and Carcinogen Metabolism and Toxicology Branch, National Cancer Institute, Bethesda, Maryland 20014 fL. A. P.] SUMMARY activities of such agents as 2-acetylaminofluorene (22), N, N-dimethyl-4-aminoazobenzene (7, 19), DENA (27, 28), The effects of diethylnitrosamine on the metabolism of methylcholanthrene (24, 25), and 7,12-dimethyl folic acid and related compounds in rat liver were investi benz(a)anthracene (ii). Furthermore, the lipotropes methi gated. The administration, in the drinking water, of diethyl onine, vitamin B@9,andfolic acid are all prospective targets nitrosamine to rats for 3 weeks led to decreased hepatic . of the electrophilic activated form of 1 or more chemical levels of folate, S-adenosylmethionine, and 5-methyltetra carcinogens (12, 16, 20). The metabolic interrelations hyd rofolate :homocysteine methyltransferase . Liver methyl among the various lipotropes are very complex, and it is enetetrahydrofolate reductase levels were unaffected by ad impossible to alter the tissue levels or metabolism of one ministration of diethylnitrosamine. The polyglutamate frac without simultaneously altering the metabolism of each of tion of hepatic folates obtained from rats treated with dieth the others (3-5, 13, 42). We therefore decided to investigate ylnitrosamine for 3 weeks prior to injection with [3H]folate in detail the mechanism responsible for the folic acid defi contained less radioactivity than did the polyglutamate frac ciency observed in DENA-treated rats. -
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). -
Folate Deficiency and Formiminoglutamic Acid Excretion During Chronic Diethylnitrosamine Administration to Rats1
[CANCER RF.SF.ARCH 33, 383-388. February 1973] Folate Deficiency and Formiminoglutamic Acid Excretion during Chronic Diethylnitrosamine Administration to Rats1 Lionel A. Poirier2 and V. Michael Whitehead Institut du Cancer de Montréal,Hôpital Notre-Dame et Départementde Biochimie, Universitéde MontréalIL. A. P.l, and Department of Haematology, and Medii! University Medical Clinic, Montreal General Hospital ¡V.M. W./. Montréal,QuébecCanada SUMMARY restricted to certain constituents of the nucleic acids and proteins (3. 21, 23, 38) and to glycogen (11). Of the 4 Elevated levels of the histidine catabolito essential dietary compounds involved in the transfer of formiminoglutamic acid were excreted into the urine of rats 1-carbon units in vivo, 3 [methionine (19, 28, 32), folie acid that were given both 0.01% diethylnitrosamine in their (13), and vitamin B,2 (16)] can behave as classical drinking water for 1 to 5 weeks and an injection of a loading nucleophiles. Of these nucleophiles, only methionine dose of histidine. Similar histidine loading of control rats that reportedly is attacked in vivo by hepatocarcinogens (23, 24). received no carcinogen did not produce an elevation in urinary The limited quantities and the multiplicity of forms of both formiminoglutamic acid excretion. The elevation in urinary vitamin B12 and folie acid in the liver would make the direct formiminoglutamic acid excretion caused by chronic demonstration of such an interaction in vivo quite difficult. diethylnitrosamine administration was prevented by high Since each of the essential 1-carbon compounds or their dietary levels of the methyl donors, methionine, betaine, and derivatives alters the course of carcinogenesis (9, 18, 22, 24, choline; high dietary levels of folate and vitamin B12, either 31 , 33), the possible interrelationship between alone or in combination, had no significant effect on the hepatocarcinogenesis and the metabolism of 1-carbon elevated formiminoglutamic acid excretion caused by compounds is currently under investigation in these diethylnitrosamine. -
Interpretive Guide
INTERPRETIVE GUIDE Contents INTRODUCTION .........................................................................1 NUTREVAL BIOMARKERS ...........................................................5 Metabolic Analysis Markers ....................................................5 Malabsorption and Dysbiosis Markers .....................................5 Cellular Energy & Mitochondrial Metabolites ..........................6 Neurotransmitter Metabolites ...............................................8 Vitamin Markers ....................................................................9 Toxin & Detoxification Markers ..............................................9 Amino Acids ..........................................................................10 Essential and Metabolic Fatty Acids .........................................13 Cardiovascular Risk ................................................................15 Oxidative Stress Markers ........................................................16 Elemental Markers ................................................................17 Toxic Elements .......................................................................18 INTERPRETATION-AT-A-GLANCE .................................................19 REFERENCES .............................................................................23 INTRODUCTION A shortage of any nutrient can lead to biochemical NutrEval profile evaluates several important biochemical disturbances that affect healthy cellular and tissue pathways to help determine nutrient -
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. -
Methyltransferase in Normal and Leukemic Leukocytes
Studies on N5-Methyltetrahydrofolate-Homocysteine Methyltransferase in Normal and Leukemic Leukocytes RENATE PEYTREMANN, JANET THORNDiKE, and WInI.AM S. BECK From the Department of Medicine, Harvard Medical School, and the Hematology Research Laboratory of the Massachusetts General Hospital, Boston, Massachusetts 02114 system A B S T R A C T A cobalamin-dependent N5-methyltetra- reducing CH3-FH4 + L-homocysteine hydrofolate-homocysteine methyltransferase (methyl- cobalamin,rcaing SAMsAm transferase) was demonstrated in unfractionated ex- FH4 + methionine. (1) tracts of human normal and leukemic leukocytes. Ac- Analogous enzymes have been characterized in Esche- tivity was substantially reduced in the absence of an richia coli added cobalamin derivative. Presumably, this residual (2-4) and in various cells of animal origin activity reflects the level (5-15). Some evidence suggests that a major function endogeneous of holoenzyme. of the enzyme is the maintenance of Enzyme activity was notably higher in lymphoid cells methionine levels in tissues. According to other evidence, the pathway has an than in myeloid cells. Thus, mean specific activities essential role in producing FH4, which can enter into (+SD) were: chronic lymphocytic leukemia lympho- essential transfers of "one-carbon" units in various normal cytes, 2.15+1.16; lymphocytes, 0.91+0.59; nor- other pathways, e.g., the folate-dependent synthesis of mal mature granulocytes, chronic myelo- 0.15+0.10; thymidylate (16). Doubtless, both views are correct, cytic leukemia granulocytes, barely detectable activity. the relative importance of the two Properties functions differing of leukocyte enzymes resembled those of perhaps under different conditions. methyltransferases previously studied in bacteria and Despite extensive discussion of an hypothesis that other animal cells. -
Structure and Function of Metallohydrolases in the Arginase- Deacetylase Family
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2016 Structure and Function of Metallohydrolases in the Arginase- Deacetylase Family Yang Hai University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Biochemistry Commons Recommended Citation Hai, Yang, "Structure and Function of Metallohydrolases in the Arginase-Deacetylase Family" (2016). Publicly Accessible Penn Dissertations. 1753. https://repository.upenn.edu/edissertations/1753 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1753 For more information, please contact [email protected]. Structure and Function of Metallohydrolases in the Arginase-Deacetylase Family Abstract Arginases and deacetylases are metallohydrolases that catalyze two distinct chemical transformations. The arginases catalyze the hydrolysis of the guanidinium group of arginine by using a hydroxide ion 2+ 2+ bridging the binuclear manganese cluster (Mn A-Mn B) for nucleophilic attack. The deacetylases catalyze the hydrolysis of amide bonds by using a mononuclear Zn2+-ion activated water molecule as the nucleophile. Despite the diverse functions, metallohydrolases of the arginase-deacetylase superfamily 2+ share the same characteristic α/β hydrolase core fold and a conserved metal binding site (the Mn B site in arginase corresponds to the catalytic Zn2+ site in deacetylase) which is essential for catalysis in both enzymes. We report crystal structure of formiminoglutamase from the parasitic protozoan Trypanosoma cruzi and confirm that formiminoglutamase is a Mn2+-requiring hydrolase that belongs to the arginase- deacetylase superfamily. We also report the crystal structure of an arginase-like protein from Trypanosoma brucei (TbARG) with unknown function. Although its biological role remains enigmatic, the 2+ evolutionarily more conserved Mn B site can be readily restored in TbARG through side-directed mutagenesis. -
Endogenous Lipid Chemoattractants and Extracellular Matrix Proteins
ENDOGENOUS LIPID CHEMOATTRACTANTS AND EXTRACELLULAR MATRIX PROTEINS INVOLVED IN DEVELOPMENT OF MYXOCOCCUS XANTHUS by PATRICK DAVID CURTIS (Under the Direction of Lawrence J. Shimkets) ABSTRACT The soil bacterium Myxococcus xanthus is a model organism to study multicellular development and biofilm formation. When starved, swarms of M. xanthus cells aggregate into a multicellular architecture called a fruiting body, wherein cells differentiate into metabolically dormant myxospores. Fruiting body formation requires directed cell movement and production of an extracellular matrix (ECM) to facilitate cell-contact dependent motility (Social motility), and biofilm formation. M. xanthus displays chemotaxis towards phospholipids derived from its membrane containing the rare fatty acid 16:1ω5c. This study demonstrates that 16:1ω5c is primarily found at the sn-1 position within the major membrane phospholipid, phosphatidylethanolamine (PE), which is contrary to the established dogma of fatty acid localization in Gram-negative bacteria. Additionally, 16:1ω5c at the sn-1 position stimulates chemotaxis stronger than 16:1ω5c located at the sn-2 position. These results suggest that the endogenous lipid chemoattractants may serve as a self-recognition system. Chemotaxis towards a self-recognition marker could facilitate movement of cells into aggregation centers. Lipid chemotaxis is dependent on the ECM-associated zinc metalloprotease FibA, suggesting that the ECM may harbor protein components of extracellular signaling pathways. Protein components of prokaryotic biofilms are largely unexplored. Twenty one putative ECM-associated proteins were identified, including FibA. Many are novel proteins. A large portion of the putative ECM proteins have lipoprotein secretion signals, unusual for extracellular proteins. An MXAN4860 pilA mutant displays a 24 hour delay in fruiting body formation and sporulation compared to the pilA parent, indicating that MXAN4860 functions in the FibA-mediated developmental pathway previously described.