DOCSLIB.ORG

Supplementary Table 1: List of Modules and Their Associated Kos

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplementary Table 1: List of Modules and Their Associated Kos Supplementary Table 1: List of modules and their associated KOs. Modules Description List of KOs K00656/K00132/K04072/K04073/K00001/K00121/K11440/ MF0001 ethanol production (formate pathway) K13953/K13954 MF0002 ethanol production (CO2 pathway) K00001/K00121/K04072/K11440/K13953/K13954 MF0003 acetylglucosamine degradation K00884/K01443/K02564/K02802/K02803/K02804 MF0004 putrescine degradation K00137/K09251/K09471/K09472 acetylneuraminate and acetylmannosamine MF0005 K01639/K00885/K01788 degradation MF0006 urea degradation K14048/K01941/K01457/K01428/K01429/K01430 MF0007 phenylalanine degradation K00832/K00812/K00813/K11358/K00817 tyrosine degradation (hydroxyphenylacetaldehyde MF0008 K00832/K00812/K00813/K11358/K00817/K00055 pathway) MF0009 tryptophan degradation K01667 MF0010 tyrosine degradation (phenol pathway) K01668 MF0011 aspartate degradation (oxaloacetate pathway) K00812/K00813/K11358 MF0012 aspartate degradation (fumarate pathway) K01744 MF0013 glutamate degradation (crotonyl-CoA pathway) K00260/K15371/K00261/K00262/K01615/K01039/K01040 glutamate degradation (4-aminobutanoate MF0014 K01580 pathway) MF0015 glutamate degradation (methylaspartate pathway) K01846/K04835 MF0016 glycine degradation K00281/K00605/K00382/K00282/K00283 MF0017 alanine degradation (racemase pathway) K01775/K00285 MF0018 proline degradation (glutamate pathway) K13821/K00318/K00294 MF0019 proline degradation (aminopentanoate pathway) K01777/K10793/K10794/K10795/K10796 K00826/K00248/K00249/K01692/K01782/K01825/K00020/ MF0020 valine degradation K00382/K11381/K00140/K00822/K07250 MF0021 leucine degradation K00826/K00249/K13766/K01640/K00382/K11381/K01968 K00826/K00248/K00249/K01692/K01782/K01825/K00626/ MF0022 isoleucine degradation K00632/K00382/K11381 MF0023 methionine degradation (cysteine pathway) K00789/K00558/K01251 MF0024 methionine degradation (mercaptan pathway) K01761 MF0025 alanine degradation (glutamate pathway) K00259 MF0026 cysteine biosynthesis/homocysteine degradation K01697/K01758 MF0027 cysteine degradation K01758/K01760 MF0028 serine degradation K01752/K01753 MF0029 threonine degradation (glycine pathway) K00060/K00639/K01620/K00132/K04072/K04073 MF0030 threonine degradation (formate pathway) K01754/K00656 MF0031 asparagine degradation K01424 MF0032 glutamine degradation (ammonia pathway) K01425 MF0033 cysteine degradation (mercaptopyruvate pathway) K00812/K01011/K00813/K11358 MF0034 glutamine degradation (oxoglutarate pathway) K00265/K00266 arginine degradation (agmatine deiminase MF0035 K01583/K01584/K01585/K02626/K10536/K12251 pathway) arginine degradation (ornithine decarboxylase MF0036 K01476/K01581 pathway) arginine degradation (AST/succinyltransferase MF0037 K00673/K01484/K00840/K06447/K05526 pathway) lysine fermentation to acetate and butyrate (3,6- MF0039 K01843/K01844/K00248 diaminohexanoate pathway) MF0040 lysine degradation (cadaverine pathway) K01582 MF0041 histidine degradation K01745/K01712/K01468/K01479/K01458/K00603/K13990 MF0042 4-aminobutyrate degradation K00823/K07250/K00135/K14534 MF0043 arginine degradation (agmatinase pathway) K01583/K01584/K01585/K02626/K01480 MF0044 glycocholate degradation K01442/K00076 MF0045 trehalose degradation K01226/K01194/K05342 MF0046 sucrose degradation K01193/K00847 K01220/K01819/K00917/K08302/K01635/K02786/K02787/ MF0047 lactose and galactose degradation (PTS) K02788 MF0048 lactose degradation K12111/K01190/K12308 MF0049 maltose degradation K00691/K01838 MF0050 melibiose degradation K07406/K07407 MF0051 sucrose degradation (Actinobacteria) K00690/K00847/K01792/K01835 chondroitin sulfate and dermatan sulfate MF0052 K08961 degradation MF0053 allose degradation K00881/K01808 MF0054 arabinose degradation K01804 MF0055 xylose degradation K01805/K00854 MF0056 galactose degradation (Leloir pathway) K01785/K00849/K00965/K01784/K01838 alpha-D-glucose and alpha-D-glucose 1-phosphate MF0057 K00117/K00845/K01053/K01085/K01792/K01835 degradation MF0058 fructose degradation K00882 MF0059 rhamnose degradation K01813/K00848/K01629/K01803 MF0060 ribose degradation K00852 MF0061 mannose degradation K01809 K01176/K07405/K01200/K01208/K00688/K00705/K01187/ MF0062 starch degradation K01178/K01182/K01214 MF0063 fructan degradation K03332 MF0064 pectin degradation K01051/K01184/K01213 pectin degradation - 5-dehydro-4-deoxy-D- MF0065 K01728/K01730/K01815/K00874/K01625 glucuronate degradation MF0066 glycogen metabolism K00975/K00703/K00700/K00688/K01187/K00705 MF0067 PHB production K00023 MF0068 glucarate degradation K01706/K13877/K00042/K01630/K11529 MF0069 galactarate degradation K01708/K13877/K00042/K01630/K11529 MF0070 galactonate degradation K01684/K00883/K01631 MF0071 D-galacturonate degradation K01812/K00041/K01685/K00874 MF0072 ribitol degradation K00875/K01783 MF0073 sorbitol degradation (dehydrogenase) K00008 MF0074 mannitol degradation K00009 sorbitol degradation (phosphotransferase)/sorbose MF0075 K00068 degradation MF0076 arabitol degradation K00854 MF0077 galactitol degradation K00094/K00917/K01635/K08302/K01803 MF0078 xylitol degradation K05351/K00854 MF0079 bifidobacterium shunt K00616/K00615/K01807/K01808/K01783/K01621 K00844/K00845/K01810/K06859/K00850/K01623/K01624/ MF0080 Glycolysis (preparatory phase) K01803 MF0081 Glycolysis (pay-off phase) K00134/K00927/K01834/K01689/K00873 MF0082 pentose phosphate pathway (oxidative branch) K00036/K01057/K07404/K00033 MF0083 pyruvate dehydrogenase complex K00163/K00382/K00627/K00161/K00162 MF0084 pyruvate:ferredoxin oxidoreductase K00169/K00170/K00171/K00172 MF0085 pyruvate:formate lyase K00656 K01647/K01681/K01682/K00031/K00030/K01676/K01679/ K00024/K00116/K00164/K00658/K00382/K01902/K01903/ MF0086 TCA cycle K00239/K00240/K00241/K00242/K00244/K00245/K00246/ K00247/K01677/K01678 K01647/K01681/K01682/K00031/K00030/K01637/K01638/ MF0087 TCA cycle (Mycobacterium pathway) K00024/K00239/K00240/K00241/K00242/K00244/K00245/ K00246/K00247 K01647/K01681/K01682/K00031/K00030/K01676/K01679/ MF0088 TCA cycle (Helicobacter pathway) K00116/K00174/K00175/K00176/K00177/K01028/K01677/ K01678 MF0089 Entner-Doudoroff pathway I K01690/K01625 MF0090 pentose phosphate pathway (non-oxidative branch) K01807/K01808/K01783/K00615/K00616 MF0091 beta-D-glucuronide and D-glucuronate degradation K00040/K00874/K01195/K01686/K01812 K00677/K02535/K02536/K03269/K00748/K00912/K02527/ MF0092 kdo2-lipid A synthesis K02517/K02560 K01938/K01491/K00297/K15023/K05299/K15022/K14138/ MF0093 homoacetogenesis K00196/K00198/K03518/K03519/K03520 MF0094 hydrogen metabolism K00436/K00533/K00534/K06441 MF0095 NADH:ferredoxin oxidoreductase K00529 MF0098 methanogenesis from carbon dioxide K00672/K01499/K00202/K11261/K00441 MF0099 methanol conversion K14080 MF0100 Sulfate reduction (dissimilatory) K00955/K00957/K00956/K00394/K00395/K11180/K11181 MF0101 Sulfate reduction (assimilatory) K00390/K00860/K00955/K00957/K00956/K00380/K00381 K01186/K05970/K01132/K01135/K01137/K01205/K01207/ MF0102 mucin degradation K12373/K01227/K13714/K01206 MF0103 nitrate reduction (assimilatory) K00366/K01915/K00262/K00362 MF0104 nitrate reduction (dissimilatory) K03385 K00368/K00370/K00371/K00374/K00373/K02567/K02568/ MF0105 nitrate reduction (denitrification) K04561 MF0106 anaerobic fatty acid beta-oxidation K06076/K12507/K06445/K00632/K01782 MF0107 glycerol degradation (propanediol pathway) K00086/K06120/K06121 MF0108 glycerol degradation (dihydroxyacetone pathway) K00005/K00863/K01803 MF0109 glycerol degradation (glycerol kinase pathway) K00864/K01126/K00111/K01803/K00112/K00113 MF0110 glyoxylate bypass K01647/K01681/K01682/K01637/K00024/K01596/K01610 MF0111 triacylglycerol degradation K01046 MF0112 acetate to acetyl-CoA K01895 MF0113 acetyl-CoA to acetate K01905/K01067/K00625/K00925 MF0114 acetyl-CoA to crotonyl-CoA K00626/K00023/K01782/K01825/K01715/K01692 MF0115 Crotonyl-coA from succinate K14534/K01902/K01903 MF0116 butyrate production via transferase K00248/K01034/K01035 MF0117 butyrate production via kinase K00248/K00634/K00929 MF0118 formate conversion K05299/K00123/K00124/K00125/K00127/K08348/K08350 MF0119 lactate production K00016/K03777/K03778 MF0120 lactate consumption K00101/K00102 MF0121 propionate production (acrylate pathway) K01026/K00249 MF0122 propionate production (succinate pathway) K01847/K01849/K01848/K05606/K01902/K01903 MF0123 propionate production (propanediol pathway) K00048/K01699/K13919/K13920/K00086/K13922/K13921 MF0124 Fucose degradation K01818/K00879/K01628/K01803 MF0125 propionate production via kinase K13788/K13923/K00932 MF0126 propionate production via transferase K01026 K01596/K01610/K00024/K00116/K01676/K01679/K00873/ MF0127 Succinate production K01958/K01960/K01677/K01678/K00239/K00240/K00241/ K00242/K00244/K00245/K00246/K00247 MF0128 Propionate conversion to succinate K01659/K01720/K01682/K03417 MF0129 catalase K03781/K03782 K00428/K03782/K00432/K00433/K03386/K03564/K11065/ MF0130 peroxidase K07223 MF0131 superoxide dismutase K04564/K04565 MF0132 superoxide reductase K05919 K02523/K00805/K02548/K02551/K08680/K02549/K01911/ MF0133 menaquinone production K01661/K02361/K02552/K11782/K11783/K11784/K11785 M00791 Manganese/zinc transport system K10830/K19971/K19972 M00319 Manganese/zinc/iron transport system K11707/K11708/K11709/K11710 M00241 Vitamin B12 transport system K06073/K06858 M00586 Putative amino-acid transport system K16961/K16962/K16963 M00223 Phosphonate transport system K02041/K02042/K02044 Thiamine biosynthesis, AIR => thiamine- M00127 K00788/K00878/K00941/K00946/K03147/K14153 P/thiamine-2P GABA biosynthesis, eukaryotes, putrescine => M00135 K00128/K00274/K00657
Load more

Recommended publications
  • 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)
    [Show full text]
  • Progress Toward Understanding the Contribution of Alkali Generation in Dental Biofilms to Inhibition of Dental Caries
    International Journal of Oral Science (2012) 4, 135–140 ß 2012 WCSS. All rights reserved 1674-2818/12 www.nature.com/ijos REVIEW Progress toward understanding the contribution of alkali generation in dental biofilms to inhibition of dental caries Ya-Ling Liu1, Marcelle Nascimento2 and Robert A Burne1 Alkali production by oral bacteria is believed to have a major impact on oral microbial ecology and to be inibitory to the initiation and progression of dental caries. A substantial body of evidence is beginning to accumulate that indicates the modulation of the alkalinogenic potential of dental biofilms may be a promising strategy for caries control. This brief review highlights recent progress toward understanding molecular genetic and physiologic aspects of important alkali-generating pathways in oral bacteria, and the role of alkali production in the ecology of dental biofilms in health and disease. International Journal of Oral Science (2012) 4, 135–140; doi:10.1038/ijos.2012.54; published online 21 September 2012 Keywords: arginine; biofilm; dental caries; microbial ecology; urea INTRODUCTION via the arginine deiminase system (ADS).15–18 Urea is provided con- Dental biofilms, the microbial communities that colonize the surfaces tinuously in salivary secretions and gingival exudates at concentra- of the teeth, exist in a dynamic equilibrium with host defenses and are tions roughly equivalent to those in serum, which range from about 3 generally compatible with the integrity of the tissues they colonize.1–4 to10 mmol?L21 in healthy humans. Urea is rapidly converted to A strong correlation is evident between the compositional and meta- ammonia and CO2 by bacterial ureases (Figure 1), which are produced bolic changes of the dental biofilms and the transition from oral health by a small subset of oral bacteria that includes Streptococcus salivarius, 2,5 to disease states, including dental caries and periodontal disease.
    [Show full text]
  • Paul R Thompson
    Paul R Thompson Department of Biochemistry and Molecular Pharmacology Voice: (508) 856-8492 UMass Medical School FAX: (508) 856-6215 Worcester, MA, 01605 Email: [email protected] PROFESSIONAL PREPARATION Institution Major Area Degree & Year McMaster University Biochemistry Honors B.S.c. – 1994 McMaster University Biochemistry Ph.D. – 2000 Johns Hopkins University SOM Pharmacology PDF – 2000-2003 PROFESSIONAL EXPERIENCE Dates Title Institution Department 2014-present Professor and Director University of Massachusetts Biochemistry and of Chemical Biology Medical School Molecular with tenure Pharmacology 2010-2014 Associate Professor The Scripps Research Chemistry with tenure Institute, Scripps Florida 2009-2010 Associate Professor University of South Carolina Chemistry with Tenure 2004-2008 Assistant Professor University of South Carolina Chemistry 2003-2004 Visiting Assistant Professor University of South Carolina Chemistry 2000-2003 Postdoctoral Fellow Johns University SOM Pharmacology 1994-2000 Teaching and McMaster University Biochemistry Research Assistant 1993-1994 Teaching Assistant McMaster University Chemistry HONORS, AWARDS AND OTHER SIGNIFICANT ACTIVITIES • Consultant to Disarm Therapeutics, 2018 to present • Chair, Bioorganic Chemistry Gordon Research Conference 2017 • Permanent Member, Synthetic Biological Chemistry B (SBCB) Study Section, NIH October 2016- present. • Consultant to Celgene, 2018 to present. • Associate Chair, Bioorganic Chemistry Gordon Research Conference 2017 • Consultant to Bristol Myers Squibb,
    [Show full text]
  • Paul R Thompson
    Paul R Thompson Department of Chemistry Voice: (561) 228-2860 The Scripps Research Institute FAX: (561) 228-2918 Jupiter, FL, 33458 Email: [email protected] PROFESSIONAL PREPARATION Institution Major Area Degree & Year McMaster University Biochemistry Honors B.S.c. – 1994 McMaster University Biochemistry Ph.D. – 2000 Johns Hopkins University SOM Pharmacology PDF – 2000-2003 PROFESSIONAL EXPERIENCE Dates Title Institution Department 2010-present Associate Professor The Scripps Research Chemistry with tenure Institute, Scripps Florida 2009-2010 Associate Professor University of South Carolina Chemistry with Tenure 2004-2008 Assistant Professor University of South Carolina Chemistry 2003-2004 Visiting Assistant Professor University of South Carolina Chemistry 2000-2003 Postdoctoral Fellow Johns University SOM Pharmacology 1994-2000 Teaching and McMaster University Biochemistry Research Assistant 1993-1994 Teaching Assistant McMaster University Chemistry HONORS, AWARDS AND OTHER SIGNIFICANT ACTIVITIES Chair, Enzymes, Coenzymes & Metabolic Pathways Gordon Research Conference 2014 Associate Chair, Enzymes, Coenzymes & Metabolic Pathways Gordon Research Conference 2013 Symposium Chair, Chemical Biology: Chemical Answers to Biological Questions, SERMACS 2012 Session Leader, FASEB Conference entitled: "Biological Methylation: From DNA to Histones" 2010 South Carolina Governor’s Young Scientist Award for Excellence in Scientific Research Cofounder Arginomix, 2009 Mail in reviewer, NIH Challenge Grants, June 2009 Camille Dreyfus Teacher Scholar
    [Show full text]
  • 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.
    [Show full text]
  • Q 297 Suppl USE
    The following supplement accompanies the article Atlantic salmon raised with diets low in long-chain polyunsaturated n-3 fatty acids in freshwater have a Mycoplasma dominated gut microbiota at sea Yang Jin, Inga Leena Angell, Simen Rød Sandve, Lars Gustav Snipen, Yngvar Olsen, Knut Rudi* *Corresponding author: [email protected] Aquaculture Environment Interactions 11: 31–39 (2019) Table S1. Composition of high- and low LC-PUFA diets. Stage Fresh water Sea water Feed type High LC-PUFA Low LC-PUFA Fish oil Initial fish weight (g) 0.2 0.4 1 5 15 30 50 0.2 0.4 1 5 15 30 50 80 200 Feed size (mm) 0.6 0.9 1.3 1.7 2.2 2.8 3.5 0.6 0.9 1.3 1.7 2.2 2.8 3.5 3.5 4.9 North Atlantic fishmeal (%) 41 40 40 40 40 30 30 41 40 40 40 40 30 30 35 25 Plant meals (%) 46 45 45 42 40 49 48 46 45 45 42 40 49 48 39 46 Additives (%) 3.3 3.2 3.2 3.5 3.3 3.4 3.9 3.3 3.2 3.2 3.5 3.3 3.4 3.9 2.6 3.3 North Atlantic fish oil (%) 9.9 12 12 15 16 17 18 0 0 0 0 0 1.2 1.2 23 26 Linseed oil (%) 0 0 0 0 0 0 0 6.8 8.1 8.1 9.7 11 10 11 0 0 Palm oil (%) 0 0 0 0 0 0 0 3.2 3.8 3.8 5.4 5.9 5.8 5.9 0 0 Protein (%) 56 55 55 51 49 47 47 56 55 55 51 49 47 47 44 41 Fat (%) 16 18 18 21 22 22 22 16 18 18 21 22 22 22 28 31 EPA+DHA (% diet) 2.2 2.4 2.4 2.9 3.1 3.1 3.1 0.7 0.7 0.7 0.7 0.7 0.7 0.7 4 4.2 Table S2.
    [Show full text]
  • Occurrence of Agmatine Pathway for Putrescine Synthesis in Selenomonas Ruminatium
    Biosci. Biotechnol. Biochem., 72 (2), 445–455, 2008 Occurrence of Agmatine Pathway for Putrescine Synthesis in Selenomonas ruminatium Shaofu LIAO,1;* Phuntip POONPAIROJ,1;** Kyong-Cheol KO,1;*** Yumiko TAKATUSKA,1;**** y Yoshihiro YAMAGUCHI,1;***** Naoki ABE,1 Jun KANEKO,1 and Yoshiyuki KAMIO2; 1Laboratory of Applied Microbiology, Department of Microbial Biotechnology, Graduate School of Agricultural Science, Tohoku University, 1-1 Amamiyamachi, Aobaku, Sendai 981-8555, Japan 2Department of Human Health and Nutrition, Graduate School of Comprehensive Human Sciences, Shokei Gakuin University, 4-10-1 Yurigaoka, Natori 981-1295, Japan Received August 28, 2007; Accepted November 16, 2007; Online Publication, February 7, 2008 [doi:10.1271/bbb.70550] Selenomonas ruminantium synthesizes cadaverine and Polyamines such as putrescine, cadaverine, and putrescine from L-lysine and L-ornithine as the essential spermidine are essential constituents of peptidoglycan constituents of its peptidoglycan by a constitutive lysine/ and they play a significant role in the maintenance of the ornithine decarboxylase (LDC/ODC). S. ruminantium integrity of the cell envelope in Selenomonas ruminan- grew normally in the presence of the specific inhibitor tium, Veillonella parvulla, V. alcalescens, and Anaero- for LDC/ODC, DL- -difluoromethylornithine, when vibrio lipolytica.1–3) When S. ruminantium and two arginine was supplied in the medium. In this study, species of Veillonella are grown in a medium supple- we discovered the presence of arginine decarboxylase mented with putrescine or cadaverine, putrescine and (ADC), the key enzyme in agmatine pathway for cadaverine respectively link covalently to the -carbox- putrescine synthesis, in S. ruminantium. We purified yl group of the D-glutamic acid residue of the peptido- and characterized ADC and cloned its gene (adc) from glycan, which is catalyzed by diamine:lipid intermediate S.
    [Show full text]
  • 12) United States Patent (10
    US007635572B2 (12) UnitedO States Patent (10) Patent No.: US 7,635,572 B2 Zhou et al. (45) Date of Patent: Dec. 22, 2009 (54) METHODS FOR CONDUCTING ASSAYS FOR 5,506,121 A 4/1996 Skerra et al. ENZYME ACTIVITY ON PROTEIN 5,510,270 A 4/1996 Fodor et al. MICROARRAYS 5,512,492 A 4/1996 Herron et al. 5,516,635 A 5/1996 Ekins et al. (75) Inventors: Fang X. Zhou, New Haven, CT (US); 5,532,128 A 7/1996 Eggers Barry Schweitzer, Cheshire, CT (US) 5,538,897 A 7/1996 Yates, III et al. s s 5,541,070 A 7/1996 Kauvar (73) Assignee: Life Technologies Corporation, .. S.E. al Carlsbad, CA (US) 5,585,069 A 12/1996 Zanzucchi et al. 5,585,639 A 12/1996 Dorsel et al. (*) Notice: Subject to any disclaimer, the term of this 5,593,838 A 1/1997 Zanzucchi et al. patent is extended or adjusted under 35 5,605,662 A 2f1997 Heller et al. U.S.C. 154(b) by 0 days. 5,620,850 A 4/1997 Bamdad et al. 5,624,711 A 4/1997 Sundberg et al. (21) Appl. No.: 10/865,431 5,627,369 A 5/1997 Vestal et al. 5,629,213 A 5/1997 Kornguth et al. (22) Filed: Jun. 9, 2004 (Continued) (65) Prior Publication Data FOREIGN PATENT DOCUMENTS US 2005/O118665 A1 Jun. 2, 2005 EP 596421 10, 1993 EP 0619321 12/1994 (51) Int. Cl. EP O664452 7, 1995 CI2O 1/50 (2006.01) EP O818467 1, 1998 (52) U.S.
    [Show full text]
  • Supplementary Figure 1. Rpod Sequence Alignment. Protein Sequence Alignment Was Performed for Rpod from Three Species, Pseudoruegeria Sp
    J. Microbiol. Biotechnol. https://doi.org/10.4014/jmb.1911.11006 J. Microbiol. Biotechnol. https://doi.org/10.4014/jmb.2003.03025 Supplementary Figure 1. RpoD sequence alignment. Protein sequence alignment was performed for RpoD from three species, Pseudoruegeria sp. M32A2M (FPS10_24745, this study), Ruegeria pomeroyi (NCBI RefSeq: WP_011047484.1), and Escherichia coli (NCBI RefSeq: NP_417539.1). Multalin version 5.4.1 was used for the analysis. Subregion 2 and 4 are represented in a rectangle, and the helix-turn-helix motif in subregion 4 is highlighted in red. The amino acid degeneration from any of the three was highlighted in light gray and the sequence degeneration between Pseudoruegeria sp. M32A2M and R. pomeroyi is highlighted in dark gray. The substituted two amino acids into HTH motif (K578Q and D581S) against E. coli were marked as asterisk. Supplementary Table 1. Genome assembly statistics Categories Pseudoruegeria sp. M32A2M Number of scaffolds less than 1,000 bp 0 Number of scaffolds between 1,000 bp –10,000 bp 39 Number of scaffolds between 10,000 bp – 100,000 bp 38 Number of scaffolds larger than 100,000 bp 14 Number of scaffolds 91 Total assembled length (bp) 5,466,515 G+C contents (%) 62.4 N50 (bp) 249,384 Minimum length of scaffold (bp) 1,015 Maximum length of scaffold (bp) 733,566 Total Ns included in the draft genome 2,158 Supplementary Table 2. The list of gene annotation and its functional categorization in Pseudoruegeria sp.
    [Show full text]
  • POLSKIE TOWARZYSTWO BIOCHEMICZNE Postępy Biochemii
    POLSKIE TOWARZYSTWO BIOCHEMICZNE Postępy Biochemii http://rcin.org.pl WSKAZÓWKI DLA AUTORÓW Kwartalnik „Postępy Biochemii” publikuje artykuły monograficzne omawiające wąskie tematy, oraz artykuły przeglądowe referujące szersze zagadnienia z biochemii i nauk pokrewnych. Artykuły pierwszego typu winny w sposób syntetyczny omawiać wybrany temat na podstawie możliwie pełnego piśmiennictwa z kilku ostatnich lat, a artykuły drugiego typu na podstawie piśmiennictwa z ostatnich dwu lat. Objętość takich artykułów nie powinna przekraczać 25 stron maszynopisu (nie licząc ilustracji i piśmiennictwa). Kwartalnik publikuje także artykuły typu minireviews, do 10 stron maszynopisu, z dziedziny zainteresowań autora, opracowane na podstawie najnow­ szego piśmiennictwa, wystarczającego dla zilustrowania problemu. Ponadto kwartalnik publikuje krótkie noty, do 5 stron maszynopisu, informujące o nowych, interesujących osiągnięciach biochemii i nauk pokrewnych, oraz noty przybliżające historię badań w zakresie różnych dziedzin biochemii. Przekazanie artykułu do Redakcji jest równoznaczne z oświadczeniem, że nadesłana praca nie była i nie będzie publikowana w innym czasopiśmie, jeżeli zostanie ogłoszona w „Postępach Biochemii”. Autorzy artykułu odpowiadają za prawidłowość i ścisłość podanych informacji. Autorów obowiązuje korekta autorska. Koszty zmian tekstu w korekcie (poza poprawieniem błędów drukarskich) ponoszą autorzy. Artykuły honoruje się według obowiązujących stawek. Autorzy otrzymują bezpłatnie 25 odbitek swego artykułu; zamówienia na dodatkowe odbitki (płatne) należy zgłosić pisemnie odsyłając pracę po korekcie autorskiej. Redakcja prosi autorów o przestrzeganie następujących wskazówek: Forma maszynopisu: maszynopis pracy i wszelkie załączniki należy nadsyłać w dwu egzem­ plarzach. Maszynopis powinien być napisany jednostronnie, z podwójną interlinią, z marginesem ok. 4 cm po lewej i ok. 1 cm po prawej stronie; nie może zawierać więcej niż 60 znaków w jednym wierszu nie więcej niż 30 wierszy na stronie zgodnie z Normą Polską.
    [Show full text]
  • Polyamines Mitigate Antibiotic Inhibition of A.Actinomycetemcomitans Growth
    Polyamines Mitigate Antibiotic Inhibition of A.actinomycetemcomitans Growth THESIS Presented in Partial Fulfillment of the Requirements for the Degree Master of Science in the Graduate School of The Ohio State University By Allan Wattimena Graduate Program in Dentistry The Ohio State University 2017 Master's Examination Committee: Dr John Walters, Advisor Dr Purnima Kumar Dr Sara Palmer Dr Shareef Dabdoub Copyright by Allan Wattimena 2017 Abstract Polyamines are ubiquitous polycationic molecules that are present in all prokaryotic and eukaryotic cells. They are the breakdown products of amino acids and are important modulators of cell growth, stress and cell proliferation. Polyamines are present in higher concentrations in the periodontal pocket and may affect antibiotic resistance of bacterial biofilms. The effect of polyamines was investigated with amoxicillin (AMX), azithromycin (AZM) and doxycycline (DOX) on the growth of Aggregatibacter actinomycetemcomitans (A.a.) Y4 strain. Bacteria were grown in brain heart infusion broth under the following conditions: 1) A.a. only, 2) A.a. + antibiotic, 3) A.a. + antibiotic + polyamine mix (1.4mM putrescine, 0.4mM spermidine, 0.4mM spermine). Growth curve analysis, MIC determination and metatranscriptomic analysis were carried out. The presence of exogenous polyamines produced a small, but significant increase in growth of A.a. Polyamines mitigated the inhibitory effect of AMX, AZM and DOX on A.a. growth. Metatranscriptomic analysis revealed differing transcriptomic profiles when comparing AMX and AZM in the presence of polyamines. Polyamines produced a transient mitigation of AMX inhibition, but did not have a significant effect on gene transcription. Many gene transcription changes were seen when polyamines were in the presence of AZM.
    [Show full text]
  • Supplemental Figure S1. the Map of the JCVI-Syn1.0 Genome Showing
    Supplemental Figure S1. The map of the JCVI-syn1.0 genome showing candidate non- essential genes uncovered in the current study (blue) and regions deleted in the seven- and eight-deletion strains (green). The deleted regions include restriction enzyme genes deleted in the JCVI-syn1.0 ∆1-6 genome. Supplemental Figure S2. Distribution of transposon-hit genes by functional category. The numbers of genes hit by transposons five times or more (“hit”) are shown in blue and those hit less than five times (“not hit”) are shown in red. Only disruptive transposon insertions (see Methods) are included in this analysis. Functional categories are based on a published study (Gibson et al., 2010). The category NULL includes 41 RNA genes and 19 non-conserved hypothetical protein genes. Notably, none of the RNA genes was hit five or more times by transposons (Supplemental Table S2). Supplemental Figure S3. Pulsed-field gel electrophoresis analysis of reduced genomes. (A) XhoI digest. The expected bands were 586 kb, 259 kb, and 217 kb for the starting strain (syn1.0 ∆1–6 strain), 533 kb, 231 kb, and 198 kb for the eight-cluster deletion strains, and 533 kb, 231 kb, and 210 kb for the seven-cluster deletion strains. The actual result was consistent with the expected result. (B) NaeI digest. The expected bands that would be visible in this analysis were 520 kb, 450 kb, 73 kb, and 18 kb for the starting strain, 446 kb, 424 kb, 73 kb, and 18 kb for the eight-cluster deletion strains, and 458 kb, 424 kb, 73 kb, and 18 kb for the seven-cluster deletion strains.
    [Show full text]