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Pneumoniae CG43
YjcC, a c-di-GMP Phosphodiesterase Protein, Regulates the Oxidative Stress Response and Virulence of Klebsiella pneumoniae CG43 Ching-Jou Huang1, Zhe-Chong Wang2, Hsi-Yuan Huang3, Hsien-Da Huang2,3, Hwei-Ling Peng1,2* 1 Institute of Molecular Medicine and Biological Technology, National Chiao Tung University, Hsin Chu, Taiwan, Republic of China, 2 Department of Biological Science and Technology, National Chiao Tung University, Hsin Chu, Taiwan, Republic of China, 3 Institute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsin Chu, Taiwan, Republic of China Abstract This study shows that the expression of yjcC, an in vivo expression (IVE) gene, and the stress response regulatory genes soxR, soxS, and rpoS are paraquat inducible in Klebsiella pneumoniae CG43. The deletion of rpoS or soxRS decreased yjcC expression, implying an RpoS- or SoxRS-dependent control. After paraquat or H2O2 treatment, the deletion of yjcC reduced bacterial survival. These effects could be complemented by introducing the DyjcC mutant with the YjcC-expression plasmid pJR1. The recombinant protein containing only the YjcC-EAL domain exhibited phosphodiesterase (PDE) activity; overexpression of yjcC has lower levels of cyclic di-GMP. The yjcC deletion mutant also exhibited increased reactive oxygen species (ROS) formation, oxidation damage, and oxidative stress scavenging activity. In addition, the yjcC deletion reduced capsular polysaccharide production in the bacteria, but increased the LD50 in mice, biofilm formation, and type 3 fimbriae major pilin MrkA production. Finally, a comparative transcriptome analysis showed 34 upregulated and 29 downregulated genes with the increased production of YjcC. The activated gene products include glutaredoxin I, thioredoxin, heat shock proteins, chaperone, and MrkHI, and proteins for energy metabolism (transporters, cell surface structure, and transcriptional regulation). -
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. -
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, -
The Escherichia Coli Narl Receiver Domain Regulates Transcription
Katsir et al. BMC Microbiology (2015) 15:174 DOI 10.1186/s12866-015-0502-9 RESEARCH ARTICLE Open Access The Escherichia coli NarL receiver domain regulates transcription through promoter specific functions Galit Katsir1,3,4, Michael Jarvis2,5, Martin Phillips1, Zhongcai Ma2,6 and Robert P. Gunsalus2,3* Abstract Background: The Escherichia coli response regulator NarL controls transcription of genes involved in nitrate respiration during anaerobiosis. NarL consists of two domains joined by a linker that wraps around the interdomain interface. Phosphorylation of the NarL N-terminal receiver domain (RD) releases the, otherwise sequestered, C-terminal output domain (OD) that subsequently binds specific DNA promoter sites to repress or activate gene expression. The aim of this study is to investigate the extent to which the NarL OD and RD function independently to regulate transcription, and the affect of the linker on OD function. Results: NarL OD constructs containing different linker segments were examined for their ability to repress frdA-lacZ or activate narG-lacZ reporter fusion genes. These in vivo expression assays revealed that the NarL OD, in the absence or presence of linker helix α6, constitutively repressed frdA-lacZ expression regardless of nitrate availability. However, the presence of the linker loop α5-α6reversedthisrepressionandalsoshowedimpairedDNAbindingin vitro.The OD alone could not activate narG-lacZ expression; this activity required the presence of the NarL RD. A footprint assay demonstrated that the NarL OD only partially bound recognition sites at the narG promoter, and the binding affinity was increased by the presence of the phosphorylated RD. Analytical ultracentrifugation used to examine domain oligomerization showed that the NarL RD forms dimers in solution while the OD is monomeric. -
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. -
Pleuropneumoniae Gene Expression
Global Effects of Catecholamines on Actinobacillus pleuropneumoniae Gene Expression Lu Li, Zhuofei Xu, Yang Zhou, Lili Sun, Ziduo Liu, Huanchun Chen, Rui Zhou* Division of Animal Infectious Diseases in State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China Abstract Bacteria can use mammalian hormones to modulate pathogenic processes that play essential roles in disease development. Actinobacillus pleuropneumoniae is an important porcine respiratory pathogen causing great economic losses in the pig industry globally. Stress is known to contribute to the outcome of A. pleuropneumoniae infection. To test whether A. pleuropneumoniae could respond to stress hormone catecholamines, gene expression profiles after epinephrine (Epi) and norepinephrine (NE) treatment were compared with those from untreated bacteria. The microarray results showed that 158 and 105 genes were differentially expressed in the presence of Epi and NE, respectively. These genes were assigned to various functional categories including many virulence factors. Only 18 genes were regulated by both hormones. These genes included apxIA (the ApxI toxin structural gene), pgaB (involved in biofilm formation), APL_0443 (an autotransporter adhesin) and genes encoding potential hormone receptors such as tyrP2, the ygiY-ygiX (qseC-qseB) operon and narQ-narP (involved in nitrate metabolism). Further investigations demonstrated that cytotoxic activity was enhanced by Epi but repressed by NE in accordance with apxIA gene expression changes. Biofilm formation was not affected by either of the two hormones despite pgaB expression being affected. Adhesion to host cells was induced by NE but not by Epi, suggesting that the hormones affect other putative adhesins in addition to APL_0443. This study revealed that A. -
Prokaryotic Genome Regulation: a Revolutionary Paradigm
No. 9] Proc. Jpn. Acad., Ser. B 88 (2012) 485 Review Prokaryotic genome regulation: A revolutionary paradigm † By Akira ISHIHAMA*1, (Communicated by Tasuku HONJO, M.J.A.) Abstract: After determination of the whole genome sequence, the research frontier of bacterial molecular genetics has shifted to reveal the genome regulation under stressful conditions in nature. The gene selectivity of RNA polymerase is modulated after interaction with two groups of regulatory proteins, 7 sigma factors and 300 transcription factors. For identification of regulation targets of transcription factors in Escherichia coli, we have developed Genomic SELEX system and subjected to screening the binding sites of these factors on the genome. The number of regulation targets by a single transcription factor was more than those hitherto recognized, ranging up to hundreds of promoters. The number of transcription factors involved in regulation of a single promoter also increased to as many as 30 regulators. The multi-target transcription factors and the multi-factor promoters were assembled into complex networks of transcription regulation. The most complex network was identified in the regulation cascades of transcription of two master regulators for planktonic growth and biofilm formation. Keywords: transcription regulation, genome regulation, transcription factor, regulation network, genomic SELEX, Escherichia coli developed and employed to reveal the expression of 1. Introduction the whole set of genes on the genome (the tran- In the early stage of molecular biology, Esche- scriptome) under a given culture condition. The high- richia coli served as a model organism of biochemical, throughput microarray has made a break-through biophysical, molecular genetic and biotechnological for providing transcription patterns of the whole set studies. -
Full Text Document (Pdf)
Kent Academic Repository Full text document (pdf) Citation for published version Dolata, Katarzyna M. and Montero, Isabel Guerrero and Miller, Wayne and Sievers, Susanne and Sura, Thomas and Wolff, Christian and Schlüter, Rabea and Riedel, Katharina and Robinson, Colin (2019) Far-reaching cellular consequences of tat deletion in Escherichia coli revealed by comprehensive proteome analyses. Microbiological Research, 218 . pp. 97-107. ISSN 0944-5013. DOI https://doi.org/10.1016/j.micres.2018.10.008 Link to record in KAR https://kar.kent.ac.uk/70187/ Document Version Publisher pdf Copyright & reuse Content in the Kent Academic Repository is made available for research purposes. Unless otherwise stated all content is protected by copyright and in the absence of an open licence (eg Creative Commons), permissions for further reuse of content should be sought from the publisher, author or other copyright holder. Versions of research The version in the Kent Academic Repository may differ from the final published version. Users are advised to check http://kar.kent.ac.uk for the status of the paper. Users should always cite the published version of record. Enquiries For any further enquiries regarding the licence status of this document, please contact: [email protected] If you believe this document infringes copyright then please contact the KAR admin team with the take-down information provided at http://kar.kent.ac.uk/contact.html Microbiological Research 218 (2019) 97–107 Contents lists available at ScienceDirect Microbiological Research journal homepage: www.elsevier.com/locate/micres Far-reaching cellular consequences of tat deletion in Escherichia coli revealed by comprehensive proteome analyses T Katarzyna M. -
Transcription Regulation of the Expression of the Plasmid Encoded Toxin of Enteroaggregative Escherichia Coli
TRANSCRIPTION REGULATION OF THE EXPRESSION OF THE PLASMID ENCODED TOXIN OF ENTEROAGGREGATIVE ESCHERICHIA COLI by Jacob Henry Duddy A thesis submitted to The University of Birmingham for the degree of MASTER OF PHILOSOPHY February 2013 School of Biosciences The University of Birmingham University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. Abstract The pathogenic properties of Enteroaggregative Escherichia coli strain 042 results from the synchronised expression of virulence factors, which include the Plasmid Encoded Toxin. Pet is a member of the serine protease autotransporter of the Enterobacteriaceae family and contributes to infection by cleaving α-fodrin, disrupting the actin cytoskeleton of host cells. The expression of Pet is induced by global transcription factor CRP with further enhancement by the nucleoid associated protein Fis. This study identifies the residues of RNA polymerase, Fis and CRP required for the induction of transcription, thereby clarifying the mechanism of activation employed by the transcription factors. Fis activates transcription from the Fis binding site via a direct interaction with RNA polymerase, facilitated by protein specific determinants. This interaction is dependent on the position of the Fis binding site on the DNA and it subsequent orientation on the helical face of the DNA. -
La Réponse Au NO Au Centre De La Pathogenèse Bactérienne Et Cible D’Antibiotiques Innovants Constance Porrini
La réponse au NO au centre de la pathogenèse bactérienne et cible d’antibiotiques innovants Constance Porrini To cite this version: Constance Porrini. La réponse au NO au centre de la pathogenèse bactérienne et cible d’antibiotiques innovants. Médecine humaine et pathologie. Université Paris-Saclay, 2020. Français. NNT : 2020UP- ASA008. tel-03175216 HAL Id: tel-03175216 https://pastel.archives-ouvertes.fr/tel-03175216 Submitted on 19 Mar 2021 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. La réponse au NO au centre de la pathogenèse bactérienne et cible d’antibiotiques innovants Thèse de doctorat de l'université Paris-Saclay École doctorale n°581, Agriculture, Alimentation, Biologie, Environnement, Santé - ABIES Spécialité de doctorat : Microbiologie INRAE, AgroParisTech, Micalis Institute, 78350, Jouy-en-Josas, France Référent : AgroParisTech Thèse présentée et soutenue à Paris-Saclay, le 12 juin 2020, par Constance PORRINI Composition du Jury Stéphanie BURY-MONE Présidente Professeure, Université Paris-Saclay Véronique BROUSSOLLE Rapporteur et -
Multiple Endocrine Neoplasia Type 2: an Overview Jessica Moline, MS1, and Charis Eng, MD, Phd1,2,3,4
GENETEST REVIEW Genetics in Medicine Multiple endocrine neoplasia type 2: An overview Jessica Moline, MS1, and Charis Eng, MD, PhD1,2,3,4 TABLE OF CONTENTS Clinical Description of MEN 2 .......................................................................755 Surveillance...................................................................................................760 Multiple endocrine neoplasia type 2A (OMIM# 171400) ....................756 Medullary thyroid carcinoma ................................................................760 Familial medullary thyroid carcinoma (OMIM# 155240).....................756 Pheochromocytoma ................................................................................760 Multiple endocrine neoplasia type 2B (OMIM# 162300) ....................756 Parathyroid adenoma or hyperplasia ...................................................761 Diagnosis and testing......................................................................................756 Hypoparathyroidism................................................................................761 Clinical diagnosis: MEN 2A........................................................................756 Agents/circumstances to avoid .................................................................761 Clinical diagnosis: FMTC ............................................................................756 Testing of relatives at risk...........................................................................761 Clinical diagnosis: MEN 2B ........................................................................756 -
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