Synechocystis Pcc6803 And

Total Page:16

File Type:pdf, Size:1020Kb

Synechocystis Pcc6803 And STUDIES ON THE PHOTOSYNTHETIC MICROORGANISM SYNECHOCYSTIS PCC6803 AND HOW IT RESPONDS TO THE EFFECTS OF SALT STRESS BY BRADLEY LYNN POSTIER Bachelor of Science Oklahoma State University Stillwater, OK 1996 Submitted to the Faculty of the Graduate College of the Oklahoma State University in partial fulfillment of the requirements for the Degree of DOCTOR OF PHILOSOPHY December, 2003 STUDIES ON THE PHOTOSYNTHETIC MICROORGANISM SYNECHOCYSTIS PCC6803 AND HOW IT RESPONDS TO THE EFFECTS OF SALT STRESS Thesis approved: Dean of the Graduate College 11 ACKNOWLEDGMENTS I would first like to thank my wife Sheridan for all of her support and motivation. Without her, I may have never even attempted graduate school. Since I met her in 1994, she has been everything I could ask for. I look forward to spending the rest of my life with you and our as of yet unborn son. I would also like to acknowledge all the work and effort put forth by my advisor - Dr. Burnap. Rob made every possible effort to support my research financially. He guided my intellectual'maturation throughout my experience here. I don't think anyone else could have shown the patience necessary to help me achieve my goals. I am truly appreciative for what he has helped me achieve and hope that some day I can do the same for other students working under me. To my parents, I would like to say thank you for all the great support guidance and memories. Y cm have been very supportive through all my years in school, allowing me to make all of the important decisions myself, good or bad. My brothers have provided many opportunities to escape from work when necessary and when not. I thank you for that. It helped keep me in excellent mental condition. I have had many coworkers and made many friends while in graduate school, too many to name.· I would like to thank all of you for your companionship; it has made my experience so much more enjoyable. I will remember the countless lunches at the Hideaway. Finally, I must thank my committee members: Dr. Miller, Dr. Prade, Dr. Melcher, and Dr. Henley. I would like to compliment (did I get it right this time?) you for all the work you have put into correcting my many mistakes. 111 TABLE OF CONTENTS Chapter Page I. Functional and Comparative Genomics of Cyanobacteria ............................ 1 Cyanobacterial Systems ...........................................................2 Genomics ...............................................................................7 Functional Genomics in a Cyanobacterium ...................................22 Outlook and Prospective ....................................................... .43 Bibliography ..................................................................... 4 7 II. The Construction and Use of Bacterial DNA Microarrays Based on an Optimized Two-stage PCR Strategy ................................................... 52 Abstract. .......................................................................... 53 Introduction ...................................................................... 55 Materials and Methods ..........................................................57 Results and Discussion .......................................................... 65 Bibliography ...................................................................... 77 III. Optimization of Fusion PCR for In Vitro Construction of Gene Knockout Fragments .............................................................. 78 Introduction ............................................................................. 79 Methods, Results and Discussion ................................................. 79 Bibliography ......................................................................90 IV. Global gene expression profiling and physiological analysis of salt stress and acclimation in Synechocystis sp PCC6803 ............................... 91 Abstract. ...........................................................................92 Introduction .......................................................................92 Materials and Methods ......................................................... 100 Results ............................................................................ 110 Discussion ....................................................................... 146 Bibliography ..................................................................... 151 iv TABLE OF CONTENTS CONTINUED. Summary............................................................................. 154 Bibliography............................................................... 159 Appendix ............................................................................ 161 Vitae .................................................................................247 .v LIST OF TABLES 1.1 Statistical summary and comparison of cyanobacterial genome sequencing efforts .......................................................................... 12 . 1.2 Abbreviated list of web based genomic information services ........................... 19 1.3 Representative genes induced after one and five hours salt shock from 2mM to 684 mM NaCl in Synechocystis PCC6803 as determined through analysis with sub-genomic DNAmicroarrays .......................... ; ......................... 33 1.4 Synechocystis genes regulated by salt stress after 5 hours of treatement revealed through microarray differential expression profiling.................... 34-35 1.5 Hypothetical genes differentially expressed before and after salt shock. ............. .37 2.1 Construction of DNA microarray ............................................. ;., ............66 2.2 Synthesis and hybridization of fluorescently labeled cDNA derived from sample RNA ............................................................................ ~ .... 72 3 .1 Primer sequences for PCR mutagenesis .................................................... 81 4.1 Genes induced after acclimation to high salt conditions; ............................... 113 4.2 Genes repressed after acclimation to high salt conditions ............................... 120 A-1 Gene expression profiles for Synechocytis PCC6803 after acclimating to high salt conditions ....................................................................... 161 A-2 Gene expression profiles in response to 650 mM NaCl shock treatment By Synechocystis PCC6803 ................................................................................. 202 VI LIST OF FIGURES 1.1 Venn diagram presentation of genome homology clustering with various genome sequencing projects .................................................... 15 1.2 Functional genomics strategy for Synechocystis PCC6803 .............................. 24 1.3 PCR amplification strategy used to develop full genome arrays ........................ .38 2.1 Overall strategy for the production of bacterial DNA microarrays ..................... 59 2.2 Design and use of chimeric bipartite oligonucleotides for PCR amplification of each open reading frame of the genome from Synechocystis PCC6803 ......... 67 2.3 Thermal cycling conditions and resultant products from first and second round amplifications ....................................................................... 69 2.4 Scatter-plot of differential hybridization of fluorescently labeled cDNA from a 3-hour salt shock treated culture versus an untreated sample ................ 74 3 .1 Comparison of fusion PCR strategies for in vitro construction of gene knockout fragments developed in this study and elsewhere ......................... 82 3 .2 Optimization of fusion PCR steps for in vitro construction of gene knockout fragments .................................................................................... 84 3.3 Colony PCRs of Synechocystis with Taq or Herculase DNA polymerases ............ 88 4.1 The effect of an upshift in salt concentration (18 mM--+650 mM NaCl) On the autotrophic growth of Wild-type Synechocystis PCC6803 ............... 111 4.2 Hierarchical clustering of gene expression profiles ............................... 129-132 4.3 Polarographically measured rates of photosynthesis and respiration following salt shock of Synechocystis PCC6803 cells ........................................... 136 4.3 PAM Fluorometer measurements of PSII activity ....................................... 138 4.5 Salt shock reduces quantum efficiency of PSII ........................................... 139 4.6 Impact of salt shock on P700 content and P700+ re-reduction kinetics.; ............. 142 vu LIST OF FIGURES CONTINUED 4.7 Salt shock induced superoxide production ............................................... 143 4.8 Superoxide production during salt shock requires PSII activity during auto trophic growth ....................................................................... 145 Vlll NOMENCLATURE DNA deoxyribonucleic acid RNA ribonucleic acid DCMU 3-(3,4-dichlorophenyl)-1, 1-dimethylurea DCBQ 2,5-dichloro-1,4-benzo-quinone · PSI photosystem I PSII photosystem II DEPC diethyl pyrocarbonate DTT dithiothreitol ATP a:denosine triphosphate GTP guanosine triphosphate TTP thymidine triphosphate CTP cytidine triphosphate aa-dUTP amino-allyl deoxyuridine triphosphate IX CHAPTERI LITERATURE· REVIEW Bradley L. Postier and Robert L. Burnap Functional Geno mies of Plants and Fungi 2 CYANOBACTERIAL SYSTEMS Some of earth's oldest fossils derive from cyanobacteria-dominated mats that filled the shallow Archaean seas over 3.5 billion years ago (52). A significant factor in the ecological success
Recommended publications
  • WO 2007/084545 Al
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (43) International Publication Date (10) International Publication Number 26 July 2007 (26.07.2007) PCT WO 2007/084545 Al (51) International Patent Classification: (74) Agent: ZERULL, Susan, Moeller; The Dow Chemical C07C 227/32 (2006.01) C12P 41/00 (2006.01) Company, Intellectual Property Section, P.O. Box 1967, C07D 317/30 (2006.01) Midland, MI 48674-1967 (US). (21) International Application Number: (81) Designated States (unless otherwise indicated, for every PCT/US2007/001207 kind of national protection available): AE, AG, AL, AM, AT,AU, AZ, BA, BB, BG, BR, BW, BY, BZ, CA, CH, CN, (22) International Filing Date: 17 January 2007 (17.01.2007) CO, CR, CU, CZ, DE, DK, DM, DZ, EC, EE, EG, ES, FI, (25) Filing Language: English GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, KZ, LA, LC, LK, LR, LS, (26) Publication Language: English LT, LU, LV,LY,MA, MD, MG, MK, MN, MW, MX, MY, (30) Priority Data: MZ, NA, NG, NI, NO, NZ, OM, PG, PH, PL, PT, RO, RS, 11/333,937 18 January 2006 (18.01.2006) US RU, SC, SD, SE, SG, SK, SL, SM, SV, SY, TJ, TM, TN, (71) Applicant (for all designated States except US): DOW TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW GLOBAL TECHNOLOGIES INC. [US/US]; Washing (84) Designated States (unless otherwise indicated, for every ton Street, 1790 Building, Midland, MI 48674 (US).
    [Show full text]
  • Generated by SRI International Pathway Tools Version 25.0, Authors S
    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. Periplasmic (where appropriate) and extracellular reactions and proteins may also be shown. Pathways are colored according to their cellular function. Gcf_000238675-HmpCyc: Bacillus smithii 7_3_47FAA Cellular Overview Connections between pathways are omitted for legibility.
    [Show full text]
  • 1 Metabolic Dysfunction Is Restricted to the Sciatic Nerve in Experimental
    Page 1 of 255 Diabetes Metabolic dysfunction is restricted to the sciatic nerve in experimental diabetic neuropathy Oliver J. Freeman1,2, Richard D. Unwin2,3, Andrew W. Dowsey2,3, Paul Begley2,3, Sumia Ali1, Katherine A. Hollywood2,3, Nitin Rustogi2,3, Rasmus S. Petersen1, Warwick B. Dunn2,3†, Garth J.S. Cooper2,3,4,5* & Natalie J. Gardiner1* 1 Faculty of Life Sciences, University of Manchester, UK 2 Centre for Advanced Discovery and Experimental Therapeutics (CADET), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Sciences Centre, Manchester, UK 3 Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK 4 School of Biological Sciences, University of Auckland, New Zealand 5 Department of Pharmacology, Medical Sciences Division, University of Oxford, UK † Present address: School of Biosciences, University of Birmingham, UK *Joint corresponding authors: Natalie J. Gardiner and Garth J.S. Cooper Email: [email protected]; [email protected] Address: University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom Telephone: +44 161 275 5768; +44 161 701 0240 Word count: 4,490 Number of tables: 1, Number of figures: 6 Running title: Metabolic dysfunction in diabetic neuropathy 1 Diabetes Publish Ahead of Print, published online October 15, 2015 Diabetes Page 2 of 255 Abstract High glucose levels in the peripheral nervous system (PNS) have been implicated in the pathogenesis of diabetic neuropathy (DN). However our understanding of the molecular mechanisms which cause the marked distal pathology is incomplete. Here we performed a comprehensive, system-wide analysis of the PNS of a rodent model of DN.
    [Show full text]
  • The Histone Deacetylase HDA15 Interacts with MAC3A and MAC3B to Regulate Intron
    bioRxiv preprint doi: https://doi.org/10.1101/2020.11.17.386672; this version posted November 17, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 The histone deacetylase HDA15 interacts with MAC3A and MAC3B to regulate intron 2 retention of ABA-responsive genes 3 4 Yi-Tsung Tu1#, Chia-Yang Chen1#, Yi-Sui Huang1, Ming-Ren Yen2, Jo-Wei Allison Hsieh2,3, 5 Pao-Yang Chen2,3*and Keqiang Wu1* 6 7 1Institute of Plant Biology, National Taiwan University, Taipei 10617, Taiwan 8 2 Institute of Plant and Microbial Biology, Academia Sinica, Taipei 11529, Taiwan 9 3 Genome and Systems Biology Degree Program, Academia Sinica and National Taiwan 10 University, Taipei, Taiwan 11 12 # These authors contributed equally to this work. 13 * Corresponding authors: Keqiang Wu ([email protected], +886-2-3366-4546) and Pao-Yang 14 Chen ([email protected], +886-2-2787-1140) 15 16 Short title: HDA15 and MAC3A/MAC3B coregulate intron retention 17 One sentence summary: HDA15 and MAC3A/MAC3B coregulate intron retention and reduce 18 the histone acetylation level of the genomic regions near ABA-responsive retained introns. 19 20 The author responsible for distribution of materials integral to the findings presented in this 21 article in accordance with the policy described in the Instructions for Authors (www.plantcell.org) 22 is: Keqiang Wu ([email protected]) 23 24 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.11.17.386672; this version posted November 17, 2020.
    [Show full text]
  • 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]
  • Natural Products That Target the Arginase in Leishmania Parasites Hold Therapeutic Promise
    microorganisms Review Natural Products That Target the Arginase in Leishmania Parasites Hold Therapeutic Promise Nicola S. Carter, Brendan D. Stamper , Fawzy Elbarbry , Vince Nguyen, Samuel Lopez, Yumena Kawasaki , Reyhaneh Poormohamadian and Sigrid C. Roberts * School of Pharmacy, Pacific University, Hillsboro, OR 97123, USA; cartern@pacificu.edu (N.S.C.); stamperb@pacificu.edu (B.D.S.); fawzy.elbarbry@pacificu.edu (F.E.); nguy6477@pacificu.edu (V.N.); lope3056@pacificu.edu (S.L.); kawa4755@pacificu.edu (Y.K.); poor1405@pacificu.edu (R.P.) * Correspondence: sroberts@pacificu.edu; Tel.: +1-503-352-7289 Abstract: Parasites of the genus Leishmania cause a variety of devastating and often fatal diseases in humans worldwide. Because a vaccine is not available and the currently small number of existing drugs are less than ideal due to lack of specificity and emerging drug resistance, the need for new therapeutic strategies is urgent. Natural products and their derivatives are being used and explored as therapeutics and interest in developing such products as antileishmanials is high. The enzyme arginase, the first enzyme of the polyamine biosynthetic pathway in Leishmania, has emerged as a potential therapeutic target. The flavonols quercetin and fisetin, green tea flavanols such as catechin (C), epicatechin (EC), epicatechin gallate (ECG), and epigallocatechin-3-gallate (EGCG), and cinnamic acid derivates such as caffeic acid inhibit the leishmanial enzyme and modulate the host’s immune response toward parasite defense while showing little toxicity to the host. Quercetin, EGCG, gallic acid, caffeic acid, and rosmarinic acid have proven to be effective against Leishmania Citation: Carter, N.S.; Stamper, B.D.; in rodent infectivity studies.
    [Show full text]
  • Nitrilase 1 Modulates Lung Tumor Progression in Vitro and in Vivo
    www.impactjournals.com/oncotarget/ Oncotarget, Vol. 7, No. 16 Nitrilase 1 modulates lung tumor progression in vitro and in vivo Yong Antican Wang1, Yunguang Sun2,5, Justin M. Le Blanc1, Charalambos Solomides3, Tingting Zhan4, Bo Lu1 1Department of Radiation Oncology, Thomas Jefferson University, Philadelphia, PA, 19107, USA 2Department of Cancer Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA 3Department of Pathology, Thomas Jefferson University, Philadelphia, PA, 19107, USA 4Department of Pharmacology, Thomas Jefferson University, Philadelphia, PA, 19107, USA 5Department of Pathology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA Correspondence to: Bo Lu, e-mail: [email protected]. Keywords: NIT1, lung cancer, KRAS, NSCLC, tumor suppressor Received: October 01, 2015 Accepted: January 23, 2016 Published: March 10, 2016 ABSTRACT Uncovering novel growth modulators for non-small cell lung cancer (NSCLC) may lead to new therapies for these patients. Previous studies suggest Nit1 suppresses chemically induced carcinogenesis of the foregut in a mouse model. In this study we aimed to determine the role of Nit1 in a transgenic mouse lung cancer model driven by a G12D Kras mutation. Nit1 knockout mice (Nit1−/−) were crossed with KrasG12D/+ mice to investigate whether a G12D Kras mutation and Nit1 inactivation interact to promote or inhibit the development of NSCLC. We found that lung tumorigenesis was suppressed in the Nit1-null background (Nit1−/−:KrasG12D/+). Micro-CT scans and gross tumor measurements demonstrated a 5-fold reduction in total tumor volumes compared to Nit1+/+KrasG12D/+ (p<0.01). Furthermore, we found that Nit1 is highly expressed in human lung cancer tissues and cell lines and use of siRNA against Nit1 decreased overall cell survival of lung cancer cells in culture.
    [Show full text]
  • ASPA Gene Aspartoacylase
    ASPA gene aspartoacylase Normal Function The ASPA gene provides instructions for making an enzyme called aspartoacylase. In the brain, this enzyme breaks down a compound called N-acetyl-L-aspartic acid (NAA) into aspartic acid (an amino acid that is a building block of many proteins) and another molecule called acetic acid. The production and breakdown of NAA appears to be critical for maintaining the brain's white matter, which consists of nerve fibers surrounded by a myelin sheath. The myelin sheath is the covering that protects nerve fibers and promotes the efficient transmission of nerve impulses. The precise function of NAA is unclear. Researchers had suspected that it played a role in the production of the myelin sheath, but recent studies suggest that NAA does not have this function. The enzyme may instead be involved in the transport of water molecules out of nerve cells (neurons). Health Conditions Related to Genetic Changes Canavan disease More than 80 mutations in the ASPA gene are known to cause Canavan disease, which is a rare inherited disorder that affects brain development. Researchers have described two major forms of this condition: neonatal/infantile Canavan disease, which is the most common and most severe form, and mild/juvenile Canavan disease. The ASPA gene mutations that cause the neonatal/infantile form severely impair the activity of aspartoacylase, preventing the breakdown of NAA and allowing this substance to build up to high levels in the brain. The mutations that cause the mild/juvenile form have milder effects on the enzyme's activity, leading to less accumulation of NAA.
    [Show full text]
  • 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
    [Show full text]
  • Structures, Functions, and Mechanisms of Filament Forming Enzymes: a Renaissance of Enzyme Filamentation
    Structures, Functions, and Mechanisms of Filament Forming Enzymes: A Renaissance of Enzyme Filamentation A Review By Chad K. Park & Nancy C. Horton Department of Molecular and Cellular Biology University of Arizona Tucson, AZ 85721 N. C. Horton ([email protected], ORCID: 0000-0003-2710-8284) C. K. Park ([email protected], ORCID: 0000-0003-1089-9091) Keywords: Enzyme, Regulation, DNA binding, Nuclease, Run-On Oligomerization, self-association 1 Abstract Filament formation by non-cytoskeletal enzymes has been known for decades, yet only relatively recently has its wide-spread role in enzyme regulation and biology come to be appreciated. This comprehensive review summarizes what is known for each enzyme confirmed to form filamentous structures in vitro, and for the many that are known only to form large self-assemblies within cells. For some enzymes, studies describing both the in vitro filamentous structures and cellular self-assembly formation are also known and described. Special attention is paid to the detailed structures of each type of enzyme filament, as well as the roles the structures play in enzyme regulation and in biology. Where it is known or hypothesized, the advantages conferred by enzyme filamentation are reviewed. Finally, the similarities, differences, and comparison to the SgrAI system are also highlighted. 2 Contents INTRODUCTION…………………………………………………………..4 STRUCTURALLY CHARACTERIZED ENZYME FILAMENTS…….5 Acetyl CoA Carboxylase (ACC)……………………………………………………………………5 Phosphofructokinase (PFK)……………………………………………………………………….6
    [Show full text]
  • Lineage-Specific Programming Target Genes Defines Potential for Th1 Temporal Induction Pattern of STAT4
    Downloaded from http://www.jimmunol.org/ by guest on October 1, 2021 is online at: average * The Journal of Immunology published online 26 August 2009 from submission to initial decision 4 weeks from acceptance to publication J Immunol http://www.jimmunol.org/content/early/2009/08/26/jimmuno l.0901411 Temporal Induction Pattern of STAT4 Target Genes Defines Potential for Th1 Lineage-Specific Programming Seth R. Good, Vivian T. Thieu, Anubhav N. Mathur, Qing Yu, Gretta L. Stritesky, Norman Yeh, John T. O'Malley, Narayanan B. Perumal and Mark H. Kaplan Submit online. Every submission reviewed by practicing scientists ? is published twice each month by http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://www.jimmunol.org/content/suppl/2009/08/26/jimmunol.090141 1.DC1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* • Why • • Material Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of October 1, 2021. Published August 26, 2009, doi:10.4049/jimmunol.0901411 The Journal of Immunology Temporal Induction Pattern of STAT4 Target Genes Defines Potential for Th1 Lineage-Specific Programming1 Seth R. Good,2* Vivian T. Thieu,2† Anubhav N. Mathur,† Qing Yu,† Gretta L.
    [Show full text]
  • Neutrophils Regulate Humoral Autoimmunity by Restricting Interferon-Γ Production Via the Generation of Reactive Oxygen Species
    UCSF UC San Francisco Previously Published Works Title Neutrophils Regulate Humoral Autoimmunity by Restricting Interferon-γ Production via the Generation of Reactive Oxygen Species Permalink https://escholarship.org/uc/item/3dn9r8j2 Journal Cell Reports, 12(7) ISSN 0022-1767 Authors Huang, X Li, J Dorta-Estremera, S et al. Publication Date 2015-08-18 DOI 10.1016/j.celrep.2015.07.021 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Article Neutrophils Regulate Humoral Autoimmunity by Restricting Interferon-g Production via the Generation of Reactive Oxygen Species Graphical Abstract Authors Xinfang Huang, Jingjing Li, Stephanie Dorta-Estremera, ..., Kimberly S. Schluns, Lewis L. Lanier, Wei Cao Correspondence [email protected] In Brief Huang et al. find that IFN-a/b produced by plasmacytoid dendritic cells (pDCs) stimulates NK cells to secrete IFN-g, which is essential for the development of autoantibodies. ROS-producing neutrophils negatively regulate this NK- IFN-g pathway and control autoimmune progression in lupus-prone mice. Highlights d Mice pre-depleted of neutrophils develop more autoantibodies after pDC activation d The pDC-IFN-a/b pathway stimulates NK cells to produce IFN-g by inducing IL-15 d ROS released by neutrophils decreases IL-15 and thus inhibits IFN-g production d Neutrophils in male NZB/W F1 mice suppress NK cell and autoimmune B cell activation Huang et al., 2015, Cell Reports 12, 1120–1132 August 18, 2015 ª2015 The Authors http://dx.doi.org/10.1016/j.celrep.2015.07.021 Cell Reports Article Neutrophils Regulate Humoral Autoimmunity by Restricting Interferon-g Production via the Generation of Reactive Oxygen Species Xinfang Huang,1,2,7 Jingjing Li,1,7 Stephanie Dorta-Estremera,1,3 Jeremy Di Domizio,1,8 Scott M.
    [Show full text]