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Electronic Supplementary Material (ESI) for Analyst. This Journal Is © the Royal Society of Chemistry 2017
Electronic Supplementary Material (ESI) for Analyst. This journal is © The Royal Society of Chemistry 2017 Supplemental Table 2. Proteins Increased in Either Blood or Horizon media Table 2A. Proteins Increased in Spores Produced on Horizon Soil Over Spores Produced on Blood Medium quasi.fdr Protein Protein Class/Name KEGG Pathway Names or Function (if ID Pathways found in KEGG) Amino Acid Metabolism bat00250, bat00280, Alanine, aspartate and glutamate metabolism, bat00410, Valine, leucine and isoleucine degradation, bat00640, beta-Alanine metabolism to acetyl CoA, 4.50E-07 BAS0310 4-aminobutyrate aminotransferase bat00650 Propanoate metabolism, Butanoate metabolism bat00270, bat00330, Cysteine and methionine metabolism, Arginine bat00410, and proline metabolism, beta-Alanine 3.84E-10 BAS5060 spermidine synthase bat00480 metabolism, Glutathione metabolism bat00270, bat00330, Cysteine and methionine metabolism, Arginine bat00410, and proline metabolism, beta-Alanine 2.30E-09 BAS5219 spermidine synthase bat00480 metabolism, Glutathione metabolism bat00250, Alanine, aspartate and glutamate metabolism, 6.94E-07 BAS0561 alanine dehydrogenase bat00430 Taurine and hypotaurine metabolism bat00250, Alanine, aspartate and glutamate metabolism, 5.23E-07 BAS4521 alanine dehydrogenase bat00430 Taurine and hypotaurine metabolism 0.005627 BAS5218 agmatinase, putative bat00330 Arginine and proline metabolism 2,3,4,5-tetrahydropyridine-2- carboxylate N-succinyltransferase, 1.40E-10 BAS3891 putative bat00300 Lysine biosynthesis bat00010, bat00020, Glycolysis -
Supplementary Table S1. Table 1. List of Bacterial Strains Used in This Study Suppl
Supplementary Material Supplementary Tables: Supplementary Table S1. Table 1. List of bacterial strains used in this study Supplementary Table S2. List of plasmids used in this study Supplementary Table 3. List of primers used for mutagenesis of P. intermedia Supplementary Table 4. List of primers used for qRT-PCR analysis in P. intermedia Supplementary Table 5. List of the most highly upregulated genes in P. intermedia OxyR mutant Supplementary Table 6. List of the most highly downregulated genes in P. intermedia OxyR mutant Supplementary Table 7. List of the most highly upregulated genes in P. intermedia grown in iron-deplete conditions Supplementary Table 8. List of the most highly downregulated genes in P. intermedia grown in iron-deplete conditions Supplementary Figures: Supplementary Figure 1. Comparison of the genomic loci encoding OxyR in Prevotella species. Supplementary Figure 2. Distribution of SOD and glutathione peroxidase genes within the genus Prevotella. Supplementary Table S1. Bacterial strains Strain Description Source or reference P. intermedia V3147 Wild type OMA14 isolated from the (1) periodontal pocket of a Japanese patient with periodontitis V3203 OMA14 PIOMA14_I_0073(oxyR)::ermF This study E. coli XL-1 Blue Host strain for cloning Stratagene S17-1 RP-4-2-Tc::Mu aph::Tn7 recA, Smr (2) 1 Supplementary Table S2. Plasmids Plasmid Relevant property Source or reference pUC118 Takara pBSSK pNDR-Dual Clonetech pTCB Apr Tcr, E. coli-Bacteroides shuttle vector (3) plasmid pKD954 Contains the Porpyromonas gulae catalase (4) -
Generate Metabolic Map Poster
Authors: Pallavi Subhraveti Anamika Kothari Quang Ong Ron Caspi An online version of this diagram is available at BioCyc.org. Biosynthetic pathways are positioned in the left of the cytoplasm, degradative pathways on the right, and reactions not assigned to any pathway are in the far right of the cytoplasm. Transporters and membrane proteins are shown on the membrane. Ingrid Keseler Peter D Karp Periplasmic (where appropriate) and extracellular reactions and proteins may also be shown. Pathways are colored according to their cellular function. Csac1394711Cyc: Candidatus Saccharibacteria bacterium RAAC3_TM7_1 Cellular Overview Connections between pathways are omitted for legibility. Tim Holland TM7C00001G0420 TM7C00001G0109 TM7C00001G0953 TM7C00001G0666 TM7C00001G0203 TM7C00001G0886 TM7C00001G0113 TM7C00001G0247 TM7C00001G0735 TM7C00001G0001 TM7C00001G0509 TM7C00001G0264 TM7C00001G0176 TM7C00001G0342 TM7C00001G0055 TM7C00001G0120 TM7C00001G0642 TM7C00001G0837 TM7C00001G0101 TM7C00001G0559 TM7C00001G0810 TM7C00001G0656 TM7C00001G0180 TM7C00001G0742 TM7C00001G0128 TM7C00001G0831 TM7C00001G0517 TM7C00001G0238 TM7C00001G0079 TM7C00001G0111 TM7C00001G0961 TM7C00001G0743 TM7C00001G0893 TM7C00001G0630 TM7C00001G0360 TM7C00001G0616 TM7C00001G0162 TM7C00001G0006 TM7C00001G0365 TM7C00001G0596 TM7C00001G0141 TM7C00001G0689 TM7C00001G0273 TM7C00001G0126 TM7C00001G0717 TM7C00001G0110 TM7C00001G0278 TM7C00001G0734 TM7C00001G0444 TM7C00001G0019 TM7C00001G0381 TM7C00001G0874 TM7C00001G0318 TM7C00001G0451 TM7C00001G0306 TM7C00001G0928 TM7C00001G0622 TM7C00001G0150 TM7C00001G0439 TM7C00001G0233 TM7C00001G0462 TM7C00001G0421 TM7C00001G0220 TM7C00001G0276 TM7C00001G0054 TM7C00001G0419 TM7C00001G0252 TM7C00001G0592 TM7C00001G0628 TM7C00001G0200 TM7C00001G0709 TM7C00001G0025 TM7C00001G0846 TM7C00001G0163 TM7C00001G0142 TM7C00001G0895 TM7C00001G0930 Detoxification Carbohydrate Biosynthesis DNA combined with a 2'- di-trans,octa-cis a 2'- Amino Acid Degradation an L-methionyl- TM7C00001G0190 superpathway of pyrimidine deoxyribonucleotides de novo biosynthesis (E. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Metligdb: a Web-Based Database for the Identification of Chemical Groups
computer programs Journal of Applied MetLigDB: a web-based database for the Crystallography identification of chemical groups to design ISSN 0021-8898 metalloprotein inhibitors Received 12 April 2011 Accepted 10 June 2011 Hwanho Choi,‡ Hongsuk Kang‡ and Hwangseo Park* Department of Bioscience and Biotechnology, Sejong University, 98 Kunja-dong, Kwangjin-ku, Seoul 143-747, Korea. Correspondence e-mail: [email protected] MetLigDB (http://silver.sejong.ac.kr/MetLigDB) is a publicly accessible web- based database through which the interactions between a variety of chelating groups and various central metal ions in the active site of metalloproteins can be explored in detail. Additional information can also be retrieved, including protein and inhibitor names, the amino acid residues coordinated to the central metal ion, and the binding affinity of the inhibitor for the target metalloprotein. Although many metalloproteins have been considered promising targets for drug discovery, it is difficult to discover new inhibitors because of the difficulty in designing a suitable chelating moiety to impair the catalytic activity of the central metal ion. Because both common and specific chelating groups can be identified for varying metal ions and the associated coordination environments, # 2011 International Union of Crystallography MetLigDB is expected to give users insight into designing new inhibitors of Printed in Singapore – all rights reserved metalloproteins for drug discovery. 1. Introduction 2008), the coordination geometry around the metal ion (Castagnetto The importance of metal ions in biological systems is increasingly et al., 2002; Andreini, Bertini, Cavallaro, Holliday & Thornton, 2009), drawing attention, as indicated by the recent emergence of terms such catalytic mechanisms (Andreini, Bertini, Cavallaro, Najmanovich & as metallome and metallomics (Shi & Chance, 2008). -
High Coverage Metabolomics Analysis Reveals Phage-Specific Alterations to Pseudomonas Aeruginosa Physiology During Infection
The ISME Journal (2016) 10, 1823–1835 © 2016 International Society for Microbial Ecology All rights reserved 1751-7362/16 www.nature.com/ismej ORIGINAL ARTICLE High coverage metabolomics analysis reveals phage-specific alterations to Pseudomonas aeruginosa physiology during infection Jeroen De Smet1, Michael Zimmermann2, Maria Kogadeeva2, Pieter-Jan Ceyssens1,3, Wesley Vermaelen1, Bob Blasdel1, Ho Bin Jang1, Uwe Sauer2 and Rob Lavigne1 1Laboratory of Gene Technology, Department of Biosystems, KU Leuven, Heverlee, Belgium; 2Institute of Molecular Systems Biology, Eidgenössische Technische Hochschule (ETH) Zürich, Zürich, Switzerland and 3Unit Bacterial Diseases, Scientific Institute of Public Health (WIV-ISP), Brussels, Belgium Phage-mediated metabolic changes in bacteria are hypothesized to markedly alter global nutrient and biogeochemical cycles. Despite their theoretic importance, experimental data on the net metabolic impact of phage infection on the bacterial metabolism remains scarce. In this study, we tracked the dynamics of intracellular metabolites using untargeted high coverage metabolomics in Pseudomo- nas aeruginosa cells infected with lytic bacteriophages from six distinct phage genera. Analysis of the metabolomics data indicates an active interference in the host metabolism. In general, phages elicit an increase in pyrimidine and nucleotide sugar metabolism. Furthermore, clear phage-specific and infection stage-specific responses are observed, ranging from extreme metabolite depletion (for example, phage YuA) to complete reorganization of the metabolism (for example, phage phiKZ). As expected, pathways targeted by the phage-encoded auxiliary metabolic genes (AMGs) were enriched among the metabolites changing during infection. The effect on pyrimidine metabolism of phages encoding AMGs capable of host genome degradation (for example, YuA and LUZ19) was distinct from those lacking nuclease-encoding genes (for example, phiKZ), which demonstrates the link between the encoded set of AMGs of a phage and its impact on host physiology. -
The Microbiota-Produced N-Formyl Peptide Fmlf Promotes Obesity-Induced Glucose
Page 1 of 230 Diabetes Title: The microbiota-produced N-formyl peptide fMLF promotes obesity-induced glucose intolerance Joshua Wollam1, Matthew Riopel1, Yong-Jiang Xu1,2, Andrew M. F. Johnson1, Jachelle M. Ofrecio1, Wei Ying1, Dalila El Ouarrat1, Luisa S. Chan3, Andrew W. Han3, Nadir A. Mahmood3, Caitlin N. Ryan3, Yun Sok Lee1, Jeramie D. Watrous1,2, Mahendra D. Chordia4, Dongfeng Pan4, Mohit Jain1,2, Jerrold M. Olefsky1 * Affiliations: 1 Division of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, La Jolla, California, USA. 2 Department of Pharmacology, University of California, San Diego, La Jolla, California, USA. 3 Second Genome, Inc., South San Francisco, California, USA. 4 Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, VA, USA. * Correspondence to: 858-534-2230, [email protected] Word Count: 4749 Figures: 6 Supplemental Figures: 11 Supplemental Tables: 5 1 Diabetes Publish Ahead of Print, published online April 22, 2019 Diabetes Page 2 of 230 ABSTRACT The composition of the gastrointestinal (GI) microbiota and associated metabolites changes dramatically with diet and the development of obesity. Although many correlations have been described, specific mechanistic links between these changes and glucose homeostasis remain to be defined. Here we show that blood and intestinal levels of the microbiota-produced N-formyl peptide, formyl-methionyl-leucyl-phenylalanine (fMLF), are elevated in high fat diet (HFD)- induced obese mice. Genetic or pharmacological inhibition of the N-formyl peptide receptor Fpr1 leads to increased insulin levels and improved glucose tolerance, dependent upon glucagon- like peptide-1 (GLP-1). Obese Fpr1-knockout (Fpr1-KO) mice also display an altered microbiome, exemplifying the dynamic relationship between host metabolism and microbiota. -
Discovery of a New Genetic Variant of Methionine Aminopeptidase From
Discovery of a New Genetic Variant of Methionine Aminopeptidase from Streptococci with Possible Post- Translational Modifications: Biochemical and Structural Characterization Tarun Arya, Chandan Kishor, Venkateshwarlu Saddanapu, Ravikumar Reddi, Anthony Addlagatta* Centre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Hyderabad, Andhra Pradesh, India Abstract Protein N-terminal methionine excision is an essential co-translational process that occurs in the cytoplasm of all organisms. About 60-70% of the newly synthesized proteins undergo this modification. Enzyme responsible for the removal of initiator methionine is methionine aminopeptidase (MetAP), which is a dinuclear metalloprotease. This protein is conserved through all forms of life from bacteria to human except viruses. MetAP is classified into two isoforms, Type I and II. Removal of the map gene or chemical inhibition is lethal to bacteria and to human cell lines, suggesting that MetAP could be a good drug target. In the present study we describe the discovery of a new genetic variant of the Type I MetAP that is present predominantly in the streptococci bacteria. There are two inserts (insert one: 27 amino acids and insert two: four residues) within the catalytic domain. Possible glycosylation and phosphorylation posttranslational modification sites are identified in the ‘insert one’. Biochemical characterization suggests that this enzyme behaves similar to other MetAPs in terms of substrate specificity. Crystal structure Type Ia MetAP from Streptococcus pneumoniae (SpMetAP1a) revealed that it contains two molecules in the asymmetric unit and well ordered inserts with structural features that corroborate the possible posttranslational modification. Both the new inserts found in the SpMetAP1a structurally align with the P-X-X-P motif found in the M. -
Metalloenzymes: Native Co-Factor Or Experimental Artifact? Marcy Hernick* Department of Biochemistry, Virginia Tech, Blacksburg, VA 24061, USA
nalytic A al & B y i tr o s c i h e Hernick, Biochem Anal Biochem 2012, 1:6 m m e Biochemistry & i h s c t r o DOI: 10.4172/2161-1009.1000e120 i y B ISSN: 2161-1009 Analytical Biochemistry Editorial Open Access Metalloenzymes: Native Co-factor or Experimental Artifact? Marcy Hernick* Department of Biochemistry, Virginia Tech, Blacksburg, VA 24061, USA There has been much interest in the biochemical characterization metallohydrolases. Superoxide dismutase (SOD) is an example of a of metalloenzymes, owing in part to past successes in targeting metalloenzyme that utilizes Mn2+, Fe2+, or Mn/Fe as native co-factors metalloenzymes for the development of therapeutic agents. It is across different species [16-20]. (Note: The cited references offer just a estimated that ~10% of approved drugs target metalloenzymes, [1] such small sampling of the research examining SOD co-factor preferences). as carbonic anhydrase, matrix metalloprotesases, and angiotensin- These detailed studies on SOD reinforce the important contributions converting enzyme [2-5]. Inhibitors of metalloenzymes typically that metal ion availability and experimental conditions have on contain a metal-binding group that targets the catalytic metal ion, identifying the native co-factor(s) preferences of metalloenzymes. and therefore, inhibitor affinity is affected by changes to the catalytic In addition to metalloenzymes that prefer a single co-factor as metal ion. Consequently, the development of therapeutically effective described above, there are also increasing numbers of cambialistic inhibitors requires that the biologically relevant form(s) of the enzyme enzymes that can utilize multiple co-factors in vivo has been identified. -
Exploration of the Core Metabolism of Symbiotic Bacteria
Klein et al. BMC Genomics 2012, 13:438 http://www.biomedcentral.com/1471-2164/13/438 RESEARCH ARTICLE Open Access Exploration of the core metabolism of symbiotic bacteria Cecilia Coimbra Klein1,2,5*, Ludovic Cottret3, Janice Kielbassa1,2, Hubert Charles1,4, Christian Gautier1,2, Ana Tereza Ribeiro de Vasconcelos1,2,5, Vincent Lacroix1,2 and Marie-France Sagot1,2* Abstract Background: A large number of genome-scale metabolic networks is now available for many organisms, mostly bacteria. Previous works on minimal gene sets, when analysing host-dependent bacteria, found small common sets of metabolic genes. When such analyses are restricted to bacteria with similar lifestyles, larger portions of metabolism are expected to be shared and their composition is worth investigating. Here we report a comparative analysis of the small molecule metabolism of symbiotic bacteria, exploring common and variable portions as well as the contribution of different lifestyle groups to the reduction of a common set of metabolic capabilities. Results: We found no reaction shared by all the bacteria analysed. Disregarding those with the smallest genomes, we still do not find a reaction core, however we did find a core of biochemical capabilities. While obligate intracellular symbionts have no core of reactions within their group, extracellular and cell-associated symbionts do have a small core composed of disconnected fragments. In agreement with previous findings in Escherichia coli, their cores are enriched in biosynthetic processes whereas the variable metabolisms have similar ratios of biosynthetic and degradation reactions. Conversely, the variable metabolism of obligate intracellular symbionts is enriched in anabolism. Conclusion: Even when removing the symbionts with the most reduced genomes, there is no core of reactions common to the analysed symbiotic bacteria. -
Surface Analyses and Immune Reactivities of Major Cell Wall-Associated Proteins of Group a Streptococcus Jason N
INFECTION AND IMMUNITY, May 2005, p. 3137–3146 Vol. 73, No. 5 0019-9567/05/$08.00ϩ0 doi:10.1128/IAI.73.5.3137–3146.2005 Copyright © 2005, American Society for Microbiology. All Rights Reserved. Surface Analyses and Immune Reactivities of Major Cell Wall-Associated Proteins of Group A Streptococcus Jason N. Cole,1 Ruben D. Ramirez,1 Bart J. Currie,2 Stuart J. Cordwell,3 Steven P. Djordjevic,4 and Mark J. Walker1* School of Biological Sciences, University of Wollongong, Wollongong, NSW,1 Menzies School Downloaded from of Health Research, Charles Darwin University, Darwin, NT,2 Australian Proteome Analysis Facility, Macquarie University, Sydney, NSW,3 and NSW Agriculture, Elizabeth Macarthur Agricultural Institute, Camden, NSW,4 Australia Received 9 December 2004/Accepted 27 December 2004 A proteomic analysis was undertaken to identify cell wall-associated proteins of Streptococcus pyogenes. Seventy-four distinct cell wall-associated proteins were identified, 66 of which were novel. Thirty-three proteins were immunoreactive with pooled S. pyogenes-reactive human antisera. Biotinylation of the GAS cell surface http://iai.asm.org/ identified 23 cell wall-associated proteins that are surface exposed. The gram-positive human pathogen Streptococcus pyogenes undergone posttranslational modifications. It remains to be (group A streptococcus; GAS) is the etiologic agent of numer- determined whether or not these modifications are physiolog- ous suppurative diseases, ranging from mild skin infections, ical or an artifact caused by urea carbamylation, deamidation, such as pharyngitis, scarlet fever, impetigo, and cellulitis, to or immobilized pH gradient strip overload. With the exception severe invasive diseases such as septicemia, streptococcal toxic of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) on October 19, 2015 by University of Queensland Library shock syndrome, and necrotizing fasciitis (8). -
Challenges of Antibacterial Discovery Lynn L
CLINICAL MICROBIOLOGY REVIEWS, Jan. 2011, p. 71–109 Vol. 24, No. 1 0893-8512/11/$12.00 doi:10.1128/CMR.00030-10 Copyright © 2011, American Society for Microbiology. All Rights Reserved. Challenges of Antibacterial Discovery Lynn L. Silver* LL Silver Consulting, LLC, 955 S. Springfield Ave., Unit C403, Springfield, New Jersey 07081 INTRODUCTION .........................................................................................................................................................72 The Discovery Void...................................................................................................................................................72 Class Modifications versus Novel Classes.............................................................................................................72 BACKGROUND............................................................................................................................................................72 Early Screening—a Brief and Biased Philosophical History .............................................................................72 The Rate-Limiting Steps of Antibacterial Discovery ...........................................................................................74 The Multitarget Hypothesis ....................................................................................................................................74 ANTIBACTERIAL RESISTANCE ..............................................................................................................................75