Generated by SRI International Pathway Tools Version 25.0, Authors S

Total Page:16

File Type:pdf, Size:1020Kb

Generated by SRI International Pathway Tools Version 25.0, Authors S Authors: Pallavi Subhraveti Peter D Karp Ingrid Keseler 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. Anamika Kothari Periplasmic (where appropriate) and extracellular reactions and proteins may also be shown. Pathways are colored according to their cellular function. Gcf_000442315Cyc: Rubellimicrobium thermophilum DSM 16684 Cellular Overview Connections between pathways are omitted for legibility. Ron Caspi lipid II (meso phosphate diaminopimelate sn-glycerol containing) phosphate dCTP 3-phosphate predicted ABC RS07495 RS12165 RS03605 transporter RS13105 of phosphate lipid II (meso dCTP sn-glycerol diaminopimelate phosphate 3-phosphate containing) phosphate Secondary Metabolite Degradation Storage Compound Biosynthesis Tetrapyrrole Biosynthesis Hormone Biosynthesis Aromatic Compound Aldehyde Degradation UDP-N-acetyl- Biosynthesis undecaprenyl- a mature (4R)-4-hydroxy- an L-glutamyl- a [protein]-L- queuosine at Macromolecule Modification myo-inositol degradation I α-D-glucosamine adenosylcobinamide a purine L-canavanine 5'-deoxyadenosine sec Metabolic Regulator Biosynthesis Amine and Polyamine Biosynthesis polyhydroxybutanoate biosynthesis siroheme biosynthesis methylglyoxal degradation I diphospho-N- peptidoglycan 2-oxoglutarate Gln β-isoaspartate glu position 34 ser a tRNA indole-3-acetate 4-deoxy-L-threo-hex-4- D-fructuronate degradation L-idonate ribonucleoside (n) [tRNA ] ATP roseoflavin chorismate biosynthesis I acetylmuramoyl- (meso-DAP protein-L- of a tRNA Asp enopyranuronate degradation degradation Asp-tRNA(Asn) 5'-phosphate Aminoacyl-tRNA Charging glutaminyl-tRNA gln biosynthesis via transamidation biosynthesis tRNA-uridine 2-thiolation and selenation (bacteria) L-alanyl-γ-D- 5'-triphosphate containing) isoaspartate O- ppGpp metabolism spermidine biosynthesis III acetyl-CoA uroporphyrinogen-III myo-inositol S-methyl-5'- /Glu-tRNA(Gln) trehalose biosynthesis I putrescine spermidine biosynthesis I IV (bacteria) D-erythrose 4-deoxy-L-threo-hex- D-fructuronate methylglyoxal glutamyl-L-lysyl- Arginase/agmatinase/ bifunctional methyltransferase: trehalose siroheme synthase: (indole-3-yl) 4-enopyranuronate L-idonate lactoylglutathione lyase: bifunctional formimionoglutamate thioadenosine 4-hydroxy-2- amidotransferase tRNA glutamyl- serine- biosynthesis I acetyl-CoA C- 4-phosphate inositol 2- D-alanyl-D-alanine RUTHE_RS00520 bifunctional glu biosynthesis V RUTHE_RS00605 acetonitrile cys D-mannonate L-idonate 5- RUTHE_RS06270 UDP-N- adenosylcobinamide lytic hydrolase phosphorylase: oxoglutarate subunit GatB: gatB Q(34) synthetase -tRNA pppGpp D-glucopyranose arg SAM acyltransferase: dehydrogenase: protein-L- riboflavin kinase/ UDP-α-D-glucose SAM uroporphyrinogen-III oxidoreductase: dehydrogenase: acetylglucosamine- kinase/ transglycosylase arginase family: mtnP aldolase/2- Asp-tRNA(Asn) GluQRS: ligase: a glycogen 6-phosphate RUTHE_RS13365 3-deoxy- iolG lactoylglutathione lyase: isoaspartate(D- FAD synthetase: bifunctional (p)ppGpp arg C-methyltransferase: RUTHE_RS11770 RUTHE_RS11800 -N-acetylmuramyl- adenosylcobinamide- domain-containing RUTHE_RS02820 dehydro-3-deoxy- /Glu-tRNA(Gln) RUTHE_RS04050 serS isoamylase: (indol-3-yl) D-arabino- 5-dehydro-4-deoxy- 5-dehydro- RUTHE_RS06595 aspartate) O- RUTHE_RS03210 synthetase/guanosine- [+ 2 isozymes] cobA scyllo-inosose (R)-S-lactoylglutathione (pentapeptide) phosphate protein: phosphogluconate amidotransferase guanosine 3'- glgX trehalose-6- acetamide heptulosonate D-glucuronate D-mannonate D-gluconate arginase: rocF α methyltransferase: 3',5'-bis(diphosphate) 3'- precorrin-1 pyrophosphoryl- guanylyltransferase: RUTHE_RS01915 5-deoxy- -ribose aldolase: eda subunit GatC: gatC glutamyl- diphosphate 5'- a maltodextrin phosphate acetoacetyl-CoA 7-phosphate adenine RUTHE_RS00315 roseoflavin an L-seryl- an L-glutamyl- pyrophosphohydrolase: agmatine amidase: an [L-cysteine desulfurase]- myo-inosose-2 5-dehydro- mannonate hydroxyacylglutathione undecaprenol N- cobU [+ 5 isozymes] 1-phosphate an L-glutaminyl- a protein L-β- queuosine at triphosphate 3'- synthase: 3-dehydroquinate Gln [tRNA sec ] Gln agmatine dAdoMet uroporphyrinogen-III RUTHE_RS08370 S-sulfanyl-L-cysteine dehydratase: iolE 4-deoxy-D- acetylglucosamine [tRNA ] adenine [tRNA ] RUTHE_RS04610 diphosphatase: malto- RUTHE_RS07565 putrescine dAdoMet synthase: dehydratase: D-galactonate degradation hydrolase: gloB urea isoaspartate position 34 Arginase/agmatinase/ C-methyltransferase: glucuronate adenosyl- L-canaline Asp dinucleotide oligosyltrehalose 3D-(3,5/4)- uxuA transferase: a mature GlcNAc-1,6- glyoxylate pyruvate α-methyl ester of a tRNA Asp-tRNA(Asn) RUTHE_RS04610 formimionoglutamate cobA (indol-3-yl)acetate RUTHE_RS04375 isomerase: D-gluconate cobinamide synthase: treY α,α-trehalose polyamine trihydroxycyclohexane- (R)-lactate ditrans,octacisRUTHE_RS03610- UDP a purine peptidoglycan anhMurNAc- /Glu-tRNA(Gln) hydrolase polyamine (3R)-3- kduI 2-dehydro-3- D-galactonate phosphate (n) gln aminopropyltransferase: 3-dehydroquinate 1,2-dione gluconokinase: undecaprenyldiphospho- (meso-DAP L-Ala-γ-D-Glu- amidotransferase a maltooligosyl- 6-phosphate arginase family: aminopropyltransferase: hydroxybutanoyl- poly-[(R)-3- precorrin-2 a [TusA sulfur-carrier protein]- deoxy-D-gluconate ribonucleoside speE 3D-(3,5/4)- 3-deoxy-D-glycero- D-galactonate RUTHE_RS10490 N-acetyl-(N-acetyl-β-D- containing) DAP-D-Ala subunit GatB: gatB GTP ppGpp trehalose trehalose- RUTHE_RS02820 speE CoA hydroxybutanoate] type II 3- S-sulfanyl-L-cysteine 5'-diphosphate Asp-tRNA(Asn) siroheme synthase: trihydroxycyclohexane- 2,5-hexodiulosonate dehydratase: D-gluconate glucosaminyl)muramoyl- Asp-tRNA(Asn) malto- phosphatase: 1 dehydroquinate /Glu-tRNA(Gln) N -(3- [+ 2 isozymes] class I poly(R)- RUTHE_RS00605 1,2-dione acylhydrolase 2-dehydro- RUTHE_RS02350 6-phosphate L-alanyl-γ-D-glutamyl-L- /Glu-tRNA(Gln) oligosyltrehalose otsB aminopropyl) dehydratase: aroQ pyruvate a reduced amidotransferase nucleoside- bifunctional (p)ppGpp putrescine spermidine hydroxyalkanoic (decyclizing): iolD 3-deoxy-D- 2-dehydro-3-deoxy- lysyl-D-alanyl-D-alanine amidotransferase trehalohydrolase: α α agmatine KDGP H O c-type subunit GatB: gatB diphosphate kinase: synthetase/guanosine- , -trehalose acid synthase: sirohydrochlorin 3-dehydroshikimate a [TusD sulfur-carrier protein]- gluconate 5- D-galactonate 2 cytochrome- subunit GatC: gatC treZ 5-deoxy-D-glucuronate cytochrome [+ 3 isozymes] RUTHE_RS14460 3',5'-bis(diphosphate) 3'- phaC S-sulfanyl-L-cysteine dehydrogenase 2-dehydro-3- c oxidase, an oxidized a 5-phosphooxy- UDP-N-acetyl- undecaprenyldiphospho- a DNA containing UDP-N-acetyl- phosphoenol pyrophosphohydrolase: α,α-trehalose siroheme synthase: shikimate 5- KduD: kduD a nucleoside an L-aspartyl- oleoyl-CoA H O 34 O cbb3-type c-type L-glutamyl- bifunctional deoxygalactonokinase: D-sorbitol degradation I α-D-glucosamine N-acetylmuramoyl-L- an apurinic/ α D-glt H O 3'-AMP ala 2 a cytidine lys 2 ammonium a ribonucleic acid -D-muramoyl- 2 Asn pyruvate UDP-N-acetyl- Gln RUTHE_RS04610 poly-[(R)-3- RUTHE_RS00605 dehydrogenase: triphosphate GTP [tRNA ] dGDP Ile2 acytochrome reduced [tRNA ] 2-dehydro-3- 4-hydroxy-2- RUTHE_RS08865 alanyl-γ-D-glutamyl-meso apyrimidinic site L-alanine α-D-muramate in tRNA spermidine hydroxybutanoate] RUTHE_RS12865 2-dehydro-3-deoxy- Asp-tRNA(Asn) 5'/3'-nucleotidase H O c-type siroheme a [TusE sulfur carrier 5-dehydro-2- deoxy-D-gluconate oxoglutarate D-sorbitol -2,6-diaminopimeloyl- SurE: surE 2 cytochrome Asp-tRNA(Asn) a uridine 34 in tRNA D-galactonate /Glu-tRNA(Gln) tol-pal system- ancytochrome oxidized shikimate protein]-S-sulfanylcysteine deoxy-D-gluconate aldolase/2- L-iditol 2- D-alanyl-D-alanine endonuclease DNA- tRNA c oxidase /Glu-tRNA(Gln) GDP 6-phosphate UDP-N- GTPase amidotransferase bifunctional 2',3'- UDP-N- associated O c-type dehydro-3-deoxy- directed RNA 2 5-dehydro-2- dehydrogenase: III: nth acetylmuramoyl- HflX: hflX subunit GatB: gatB pyruvate cyclic-nucleotide 2'- acetylmuramate-- acyl-CoA lysidine(34) a reduced amidotransferase shikimate kinase: phosphogluconate UDP-N- polymerase: cytochrome tRNA 2-thiouridine(34) deoxygluconokinase: 2-dehydro-3-deoxy-6- RUTHE_RS10505 bifunctional DNA- L-alanine--D- [+ 2 isozymes] Asp-tRNA(Asn) kinase: pyk phosphodiesterase/ L-alanine ligase: thioesterase: synthetase H O c-type subunit GatB: gatB RUTHE_RS04380 aldolase: eda keto-D-fructose acetylglucosamine- rpoB rpoC 2 synthase MnmA: mnmA iolC KDGP phosphogalactonate formamidopyrimidine glutamate ligase: /Glu-tRNA(Gln) 3'-nucleotidase: RUTHE_RS03615 ybgC TilS: tilS cytochrome Asp-tRNA(Asn) -N-acetylmuramyl- RS12765 an oxidized shikimate 3- 5-dehydro-2-deoxy-D- aldolase: glycosylase/ DNA-directed RUTHE_RS06155 amidotransferase RUTHE_RS11010 /Glu-tRNA(Gln) D-glyceraldehyde (pentapeptide) phosphate H + O c-type phosphate a 2-thiouridine 34 in tRNA gluconate 6-phosphate pyruvate RUTHE_RS08860 DNA-(apurinic RNA polymerase GDP subunit GatC: gatC pyruvate UDP-N-acetyl- a lysidine 34 2 amidotransferase bifunctional 3-phosphate pyrophosphoryl- an L-asparaginyl- dGTP adenosine H + RS00710 cytochromeH + 3-phosphoshikimate 1- or apyrimidinic subunit alpha: UDP-N-acetyl- α-D-muramoyl- oleate in tRNA Ile2 subunit GatC: gatC 4-hydroxy-2- undecaprenol N- Asn tRNA uridine-5- D-glyceraldehyde β-D-fructofuranose
Recommended publications
  • METACYC ID Description A0AR23 GO:0004842 (Ubiquitin-Protein Ligase
    Electronic Supplementary Material (ESI) for Integrative Biology This journal is © The Royal Society of Chemistry 2012 Heat Stress Responsive Zostera marina Genes, Southern Population (α=0.
    [Show full text]
  • Gene Symbol Gene Description ACVR1B Activin a Receptor, Type IB
    Table S1. Kinase clones included in human kinase cDNA library for yeast two-hybrid screening Gene Symbol Gene Description ACVR1B activin A receptor, type IB ADCK2 aarF domain containing kinase 2 ADCK4 aarF domain containing kinase 4 AGK multiple substrate lipid kinase;MULK AK1 adenylate kinase 1 AK3 adenylate kinase 3 like 1 AK3L1 adenylate kinase 3 ALDH18A1 aldehyde dehydrogenase 18 family, member A1;ALDH18A1 ALK anaplastic lymphoma kinase (Ki-1) ALPK1 alpha-kinase 1 ALPK2 alpha-kinase 2 AMHR2 anti-Mullerian hormone receptor, type II ARAF v-raf murine sarcoma 3611 viral oncogene homolog 1 ARSG arylsulfatase G;ARSG AURKB aurora kinase B AURKC aurora kinase C BCKDK branched chain alpha-ketoacid dehydrogenase kinase BMPR1A bone morphogenetic protein receptor, type IA BMPR2 bone morphogenetic protein receptor, type II (serine/threonine kinase) BRAF v-raf murine sarcoma viral oncogene homolog B1 BRD3 bromodomain containing 3 BRD4 bromodomain containing 4 BTK Bruton agammaglobulinemia tyrosine kinase BUB1 BUB1 budding uninhibited by benzimidazoles 1 homolog (yeast) BUB1B BUB1 budding uninhibited by benzimidazoles 1 homolog beta (yeast) C9orf98 chromosome 9 open reading frame 98;C9orf98 CABC1 chaperone, ABC1 activity of bc1 complex like (S. pombe) CALM1 calmodulin 1 (phosphorylase kinase, delta) CALM2 calmodulin 2 (phosphorylase kinase, delta) CALM3 calmodulin 3 (phosphorylase kinase, delta) CAMK1 calcium/calmodulin-dependent protein kinase I CAMK2A calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha CAMK2B calcium/calmodulin-dependent
    [Show full text]
  • Genomic and Transcriptomic Alterations Associated with Drug Vulnerabilities and Prognosis in Adenocarcinoma at the Gastroesophageal Junction
    ARTICLE https://doi.org/10.1038/s41467-020-19949-6 OPEN Genomic and transcriptomic alterations associated with drug vulnerabilities and prognosis in adenocarcinoma at the gastroesophageal junction Yuan Lin1,8, Yingying Luo 2,8, Yanxia Sun 2,8, Wenjia Guo 2,3,8, Xuan Zhao2,8, Yiyi Xi2, Yuling Ma 2, ✉ ✉ Mingming Shao2, Wen Tan2, Ge Gao 1,4 , Chen Wu 2,5,6 & Dongxin Lin2,5,7 1234567890():,; Adenocarcinoma at the gastroesophageal junction (ACGEJ) has dismal clinical outcomes, and there are currently few specific effective therapies because of limited knowledge on its genomic and transcriptomic alterations. The present study investigates genomic and tran- scriptomic changes in ACGEJ from Chinese patients and analyzes their drug vulnerabilities and associations with the survival time. Here we show that the major genomic changes of Chinese ACGEJ patients are chromosome instability promoted tumorigenic focal copy- number variations and COSMIC Signature 17-featured single nucleotide variations. We provide a comprehensive profile of genetic changes that are potentially vulnerable to existing therapeutic agents and identify Signature 17-correlated IFN-α response pathway as a prog- nostic marker that might have practical value for clinical prognosis of ACGEJ. These findings further our understanding on the molecular biology of ACGEJ and may help develop more effective therapeutic strategies. 1 Beijing Advanced Innovation Center for Genomics (ICG), Biomedical Pioneering Innovation Center (BIOPIC), Peking University, Beijing, China. 2 Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. 3 Cancer Institute, Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi, China.
    [Show full text]
  • WO 2017/014762 Al 26 January 2017 (26.01.2017) P O P C T
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2017/014762 Al 26 January 2017 (26.01.2017) P O P C T (51) International Patent Classification: DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, C12Q 1/68 (2006.01) HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, (21) International Application Number: MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PCT/US201 5/0414 15 PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, (22) International Filing Date: SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, 2 1 July 20 15 (21 .07.2015) TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (25) Filing Language: English (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (26) Publication Language: English GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, (71) Applicant: OMNIOME, INC. [US/US]; 4225 Executive TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, Square, Suite 440, La Jolla, California 92037 (US). TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, IT, LT, LU, (72) Inventors: VIJAYAN, Kandaswamy; 4465 Vision Drive, LV, MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, Unit 6, San Diego, California 92121 (US).
    [Show full text]
  • Paraganglioma (PGL) Tumors in Patients with Succinate Dehydrogenase-Related PCC–PGL Syndromes: a Clinicopathological and Molecular Analysis
    T G Papathomas and others Non-PCC/PGL tumors in the SDH 170:1 1–12 Clinical Study deficiency Non-pheochromocytoma (PCC)/paraganglioma (PGL) tumors in patients with succinate dehydrogenase-related PCC–PGL syndromes: a clinicopathological and molecular analysis Thomas G Papathomas1, Jose Gaal1, Eleonora P M Corssmit2, Lindsey Oudijk1, Esther Korpershoek1, Ketil Heimdal3, Jean-Pierre Bayley4, Hans Morreau5, Marieke van Dooren6, Konstantinos Papaspyrou7, Thomas Schreiner8, Torsten Hansen9, Per Arne Andresen10, David F Restuccia1, Ingrid van Kessel6, Geert J L H van Leenders1, Johan M Kros1, Leendert H J Looijenga1, Leo J Hofland11, Wolf Mann7, Francien H van Nederveen12, Ozgur Mete13,14, Sylvia L Asa13,14, Ronald R de Krijger1,15 and Winand N M Dinjens1 1Department of Pathology, Josephine Nefkens Institute, Erasmus MC, University Medical Center, PO Box 2040, 3000 CA Rotterdam, The Netherlands, 2Department of Endocrinology, Leiden University Medical Center, Leiden,The Netherlands, 3Section for Clinical Genetics, Department of Medical Genetics, Oslo University Hospital, Oslo, Norway, 4Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands, 5Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands, 6Department of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, The Netherlands, 7Department of Otorhinolaryngology, Head and Neck Surgery, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany, 8Section for Specialized Endocrinology,
    [Show full text]
  • Supplementary Materials
    1 Supplementary Materials: Supplemental Figure 1. Gene expression profiles of kidneys in the Fcgr2b-/- and Fcgr2b-/-. Stinggt/gt mice. (A) A heat map of microarray data show the genes that significantly changed up to 2 fold compared between Fcgr2b-/- and Fcgr2b-/-. Stinggt/gt mice (N=4 mice per group; p<0.05). Data show in log2 (sample/wild-type). 2 Supplemental Figure 2. Sting signaling is essential for immuno-phenotypes of the Fcgr2b-/-lupus mice. (A-C) Flow cytometry analysis of splenocytes isolated from wild-type, Fcgr2b-/- and Fcgr2b-/-. Stinggt/gt mice at the age of 6-7 months (N= 13-14 per group). Data shown in the percentage of (A) CD4+ ICOS+ cells, (B) B220+ I-Ab+ cells and (C) CD138+ cells. Data show as mean ± SEM (*p < 0.05, **p<0.01 and ***p<0.001). 3 Supplemental Figure 3. Phenotypes of Sting activated dendritic cells. (A) Representative of western blot analysis from immunoprecipitation with Sting of Fcgr2b-/- mice (N= 4). The band was shown in STING protein of activated BMDC with DMXAA at 0, 3 and 6 hr. and phosphorylation of STING at Ser357. (B) Mass spectra of phosphorylation of STING at Ser357 of activated BMDC from Fcgr2b-/- mice after stimulated with DMXAA for 3 hour and followed by immunoprecipitation with STING. (C) Sting-activated BMDC were co-cultured with LYN inhibitor PP2 and analyzed by flow cytometry, which showed the mean fluorescence intensity (MFI) of IAb expressing DC (N = 3 mice per group). 4 Supplemental Table 1. Lists of up and down of regulated proteins Accession No.
    [Show full text]
  • Activation of Sphingosine Kinase 1 by ERK1/2Mediated Phosphorylation
    The EMBO Journal Vol. 22 No. 20 pp. 5491±5500, 2003 Activation of sphingosine kinase 1 by ERK1/2-mediated phosphorylation Stuart M.Pitson1,2, Paul A.B.Moretti1, second messenger and a ligand for cell-surface receptors Julia R.Zebol1, Helen E.Lynn1, Pu Xia1,3, (Hla et al., 2001; Spiegel and Milstien, 2002). MathewA.Vadas 1,3 and The cellular levels of S1P are controlled by its Binks W.Wattenberg1,4 formation from sphingosine through the activity of sphingosine kinase, and by its degradation by S1P lyase 1Hanson Institute, Division of Human Immunology, Institute of (Van Veldhoven et al., 2000) and S1P phosphatases Medical and Veterinary Science, Frome Road, Adelaide, SA 5000 and (Mandala, 2001). In the basal state, this balance between 3Department of Medicine, Adelaide University, Frome Road, Adelaide, Australia S1P generation and degradation results in low cellular levels of S1P (Pyne and Pyne, 2000). However, when cells 4Present address: James Graham Brown Cancer Center, Dehlia Baxter Research Building, 580 S. Preston Avenue, Louisville, KY 40202, are exposed to speci®c growth factors and other agonists USA like tumour necrosis factor-a (TNFa) or phorbol esters the cellular levels of S1P can increase rapidly and transiently 2Corresponding author e-mail: [email protected] (Pitson et al., 2000b). This results in the triggering of various signalling pathways through as yet unidenti®ed Sphingosine kinase 1 is an agonist-activated signalling intracellular S1P targets, as well as through the engage- enzyme that catalyses the formation of sphingosine ment of cell surface S1P receptors following its release 1-phosphate, a lipid second messenger that has been from cells (Hobson et al., 2001).
    [Show full text]
  • Download Via Github on RNA-Seq and Chip-Seq Data Analysis and the University of And/Or Bioconductor [33–35, 38–40]
    Kumka and Bauer BMC Genomics (2015) 16:895 DOI 10.1186/s12864-015-2162-4 RESEARCH ARTICLE Open Access Analysis of the FnrL regulon in Rhodobacter capsulatus reveals limited regulon overlap with orthologues from Rhodobacter sphaeroides and Escherichia coli Joseph E. Kumka and Carl E. Bauer* Abstract Background: FNR homologues constitute an important class of transcription factors that control a wide range of anaerobic physiological functions in a number of bacterial species. Since FNR homologues are some of the most pervasive transcription factors, an understanding of their involvement in regulating anaerobic gene expression in different species sheds light on evolutionary similarity and differences. To address this question, we used a combination of high throughput RNA-Seq and ChIP-Seq analysis to define the extent of the FnrL regulon in Rhodobacter capsulatus and related our results to that of FnrL in Rhodobacter sphaeroides and FNR in Escherichia coli. Results: Our RNA-seq results show that FnrL affects the expression of 807 genes, which accounts for over 20 % of the Rba. capsulatus genome. ChIP-seq results indicate that 42 of these genes are directly regulated by FnrL. Importantly, this includes genes involved in the synthesis of the anoxygenic photosystem. Similarly, FnrL in Rba. sphaeroides affects 24 % of its genome, however, only 171 genes are differentially expressed in common between two Rhodobacter species, suggesting significant divergence in regulation. Conclusions: We show that FnrL in Rba. capsulatus activates photosynthesis while in Rba. sphaeroides FnrL regulation reported to involve repression of the photosystem. This analysis highlights important differences in transcriptional control of photosynthetic events and other metabolic processes controlled by FnrL orthologues in closely related Rhodobacter species.
    [Show full text]
  • Supplementary Materials
    Supplementary Materials Figure S1. Differentially abundant spots between the mid-log phase cells grown on xylan or xylose. Red and blue circles denote spots with increased and decreased abundance respectively in the xylan growth condition. The identities of the circled spots are summarized in Table 3. Figure S2. Differentially abundant spots between the stationary phase cells grown on xylan or xylose. Red and blue circles denote spots with increased and decreased abundance respectively in the xylan growth condition. The identities of the circled spots are summarized in Table 4. S2 Table S1. Summary of the non-polysaccharide degrading proteins identified in the B. proteoclasticus cytosol by 2DE/MALDI-TOF. Protein Locus Location Score pI kDa Pep. Cov. Amino Acid Biosynthesis Acetylornithine aminotransferase, ArgD Bpr_I1809 C 1.7 × 10−4 5.1 43.9 11 34% Aspartate/tyrosine/aromatic aminotransferase Bpr_I2631 C 3.0 × 10−14 4.7 43.8 15 46% Aspartate-semialdehyde dehydrogenase, Asd Bpr_I1664 C 7.6 × 10−18 5.5 40.1 17 50% Branched-chain amino acid aminotransferase, IlvE Bpr_I1650 C 2.4 × 10−12 5.2 39.2 13 32% Cysteine synthase, CysK Bpr_I1089 C 1.9 × 10−13 5.0 32.3 18 72% Diaminopimelate dehydrogenase Bpr_I0298 C 9.6 × 10−16 5.6 35.8 16 49% Dihydrodipicolinate reductase, DapB Bpr_I2453 C 2.7 × 10−6 4.9 27.0 9 46% Glu/Leu/Phe/Val dehydrogenase Bpr_I2129 C 1.2 × 10−30 5.4 48.6 31 64% Imidazole glycerol phosphate synthase Bpr_I1240 C 8.0 × 10−3 4.7 22.5 8 44% glutamine amidotransferase subunit Ketol-acid reductoisomerase, IlvC Bpr_I1657 C 3.8 × 10−16
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2014/0155567 A1 Burk Et Al
    US 2014O155567A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2014/0155567 A1 Burk et al. (43) Pub. Date: Jun. 5, 2014 (54) MICROORGANISMS AND METHODS FOR (60) Provisional application No. 61/331,812, filed on May THE BIOSYNTHESIS OF BUTADENE 5, 2010. (71) Applicant: Genomatica, Inc., San Diego, CA (US) Publication Classification (72) Inventors: Mark J. Burk, San Diego, CA (US); (51) Int. Cl. Anthony P. Burgard, Bellefonte, PA CI2P 5/02 (2006.01) (US); Jun Sun, San Diego, CA (US); CSF 36/06 (2006.01) Robin E. Osterhout, San Diego, CA CD7C II/6 (2006.01) (US); Priti Pharkya, San Diego, CA (52) U.S. Cl. (US) CPC ................. CI2P5/026 (2013.01); C07C II/I6 (2013.01); C08F 136/06 (2013.01) (73) Assignee: Genomatica, Inc., San Diego, CA (US) USPC ... 526/335; 435/252.3:435/167; 435/254.2: (21) Appl. No.: 14/059,131 435/254.11: 435/252.33: 435/254.21:585/16 (22) Filed: Oct. 21, 2013 (57) ABSTRACT O O The invention provides non-naturally occurring microbial Related U.S. Application Data organisms having a butadiene pathway. The invention addi (63) Continuation of application No. 13/101,046, filed on tionally provides methods of using Such organisms to produce May 4, 2011, now Pat. No. 8,580,543. butadiene. Patent Application Publication Jun. 5, 2014 Sheet 1 of 4 US 2014/O155567 A1 ?ueudos!SMS |?un61– Patent Application Publication Jun. 5, 2014 Sheet 2 of 4 US 2014/O155567 A1 VOJ OO O Z?un61– Patent Application Publication US 2014/O155567 A1 {}}} Hººso Patent Application Publication Jun.
    [Show full text]
  • DNA Methylation Seeing the Forest for the Trees: a Wide Perspective on RNA-Directed
    Downloaded from genesdev.cshlp.org on August 16, 2012 - Published by Cold Spring Harbor Laboratory Press Seeing the forest for the trees: a wide perspective on RNA-directed DNA methylation Huiming Zhang and Jian-Kang Zhu Genes Dev. 2012 26: 1769-1773 Access the most recent version at doi:10.1101/gad.200410.112 References This article cites 31 articles, 9 of which can be accessed free at: http://genesdev.cshlp.org/content/26/16/1769.full.html#ref-list-1 Related Content Spatial and functional relationships among Pol V-associated loci, Pol IV-dependent siRNAs, and cytosine methylation in the Arabidopsis epigenome Andrzej T. Wierzbicki, Ross Cocklin, Anoop Mayampurath, et al. Genes Dev. August 15, 2012 26: 1825-1836 Email alerting Receive free email alerts when new articles cite this article - sign up in the box at the service top right corner of the article or click here Topic Articles on similar topics can be found in the following collections Collections Chromatin and Gene Expression (146 articles) Plant Biology (29 articles) To subscribe to Genes & Development go to: http://genesdev.cshlp.org/subscriptions Copyright © 2012 by Cold Spring Harbor Laboratory Press Downloaded from genesdev.cshlp.org on August 16, 2012 - Published by Cold Spring Harbor Laboratory Press PERSPECTIVE Seeing the forest for the trees: a wide perspective on RNA-directed DNA methylation Huiming Zhang1 and Jian-Kang Zhu1,2,3 1Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, Indiana 47907, USA; 2Shanghai Center for Plant Stress Biology, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China In this issue of Genes & Development, Wierzbicki and remaining subunits of Pol IV and/or Pol V are different but colleagues (pp.
    [Show full text]
  • About SDHD Gene Mutations
    About SDHD Gene Mutations About Genes Recommendations Genes are in every cell in our bodies. Genes are made Knowing if you have an SDHD mutation can help you of DNA, which gives instructions to cells about how to grow manage your medical care. and work together. We have two copies of each gene in each cell—one from our mother and one from our father. When MEN AND WOMEN genes work right, they help stop cancer cells from developing. If you know you have an SDHD mutation, it is important If one copy of a gene has a mutation, it cannot function as it to find tumors early. It is also important to tell your doctor should. This increases the risk for certain cancers. that you have this mutation before any medical procedures. TheSDH genes have instructions for turning food into energy Recommendations may vary according to your age. and helping fix mistakes in DNA. The four genes involved are Ages 8-18: SDHA, SDHB, SDHC, and SDHD. If there is a mutation in one • MRI of the whole body every 2-3 years of these genes, it can cause cells to grow and divide too much. This • Neck MRI every 2-3 years can lead to tumors called paragangliomas and pheochromocytomas. These tumors are often benign (non-cancerous) but can be Adults: cancer and spread in some cases. This condition is called • PET/CT scan as your doctor recommends hereditary paraganglioma/pheochromocytoma syndrome. All ages: Paragangliomas and Pheochromocytomas • Physical exam every year with blood pressure check Paragangliomas (PGLs) are slow-growing tumors that develop • Blood test every year along nerves or blood vessels.
    [Show full text]