Microbiology, Virology & Host Pathogen Interaction
- Endoplasmic reticulum chaperone Gp96 controls actomyosin dynamics and protects against pore‐forming toxins
- Francisco Sarmento Mesquita1,2,
- Cláudia Brito1,2,3,
- Maria J Mazon Moya4,
- Jorge Campos Pinheiro1,2,3,
- Serge Mostowy4,
- Didier Cabanes (didier{at}ibmc.up.pt)*,1,2 and
- Sandra Sousa (srsousa{at}ibmc.up.pt)*,1,2
- 1I3S‐Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
- 2Group of Molecular Microbiology, IBMC, Universidade do Porto, Porto, Portugal
- 3Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal
- 4Section of Microbiology, MRC Centre for Molecular Bacteriology and Infection (CMBI), Imperial College London, London, UK
- ↵*
Corresponding author. Tel: +351 220 408 800; E‐mail: didier{at}ibmc.up.pt
Corresponding author. Tel: +351 220 408 800; E‐mail: srsousa{at}ibmc.up.pt
Gp96 plays a role in actomyosin remodelling and coordination of plasma membrane blebbing triggered by pore‐forming toxins. This process protects membrane integrity and host survival during infection and has implications in cytoskeletal organization.
Synopsis
Gp96 plays a role in actomyosin remodelling and coordination of plasma membrane blebbing triggered by pore‐forming toxins. This process protects membrane integrity and host survival during infection and has implications in cytoskeletal organization.
Gp96 controls NMHCIIA network and NMII activity during PFT‐induced PM blebbing.
Gp96 and NMHCIIA protect PM integrity against bacterial PFT‐mediated damage.
Gp96–NMHCIIA interplay during PFT responses resembles polarized cell migration process.
Gp96 promotes host survival during in vivo Listeria infection.
EMBO Reports (2017) 18: 303–318
- Received June 3, 2016.
- Revision received November 16, 2016.
- Accepted November 18, 2016.
- © 2016 The Authors
- Domestication of a housekeeping transglycosylase for assembly of a Type VI secretion system
- 1Laboratoire d'Ingénierie des Systèmes Macromoléculaires (LISM), UMR 7255, Institut de Microbiologie de la Méditerranée, Aix‐Marseille Univ – CNRS, Marseille Cedex 20, France
- ↵*Corresponding author. Tel: +33 491164504; E‐mail: cascales{at}imm.cnrs.fr
The bacterial type VI secretion system (T6SS) comprises a contractile tail anchored to the cell envelope. This study shows that the housekeeping peptidoglycan hydrolase MltE is recruited to the T6SS and stimulated by the TssM subunit to create membrane lesions for the proper assembly of the trans‐envelope complex.
Synopsis
The bacterial Type VI secretion system (T6SS) comprises a contractile tail anchored to the cell envelope. This study shows that the housekeeping peptidoglycan hydrolase MltE is recruited to the T6SS and stimulated by the TssM subunit to create membrane lesions for the proper assembly of the trans‐envelope complex.
Proper function of the type VI secretion apparatus requires cell wall degradation.
The housekeeping transglycosylase MltE is recruited to and activated by the T6SS membrane complex.
A lytic transglycosylase encoded within the core bacterial genome is domesticated for the assembly of a secretion system.
EMBO Reports (2017) 18: 138–149
- Received August 19, 2016.
- Revision received October 27, 2016.
- Accepted October 28, 2016.
- © 2016 The Authors
- Una destinatio, viae diversaeDoes exposure to the vaginal microbiota confer health benefits to the infant, and does lack of exposure confer disease risk?
Does exposure to the vaginal microbiota confer health benefits to the infant, and does lack of exposure confer disease risk?
- 1Division of Maternal Fetal Medicine, Department of Obstetrics & Gynecology, Baylor College of Medicine and Texas Children's Hospital, Houston, TX, USA
- 2Center for Metagenomics & Microbiome Research, Baylor College of Medicine and Texas Children's Hospital, Houston, TX, USA
- 3Department of Molecular & Human Genetics, Baylor College of Medicine and Texas Children's Hospital, Houston, TX, USA
- 4Department of Molecular & Cell Biology, Baylor College of Medicine and Texas Children's Hospital, Houston, TX, USA
↵† These authors contributed equally to this work
There are lingering concerns that Cesarean surgery could impede on the child's health due to a lack of exposure to the mother's vaginal microbiota. However, the evidence so far is not sufficient to affirm whether the mode of birth influences disease risk or whether it is other causes.
- © 2016 The Authors
- Peroxisomal protein PEX13 functions in selective autophagy
- Ming Y Lee1,
- Rhea Sumpter Jr1,
- Zhongju Zou1,2,
- Shyam Sirasanagandla1,
- Yongjie Wei1,2,
- Prashant Mishra3,
- Hendrik Rosewich4,
- Denis I Crane5 and
- Beth Levine (beth.levine{at}utsouthwestern.edu)*,1,2,6
- 1Center for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA
- 2Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA
- 3Children's Medical Center Research Institute at the University of Texas Southwestern Medical Center, Dallas, TX, USA
- 4Department of Pediatrics and Pediatric Neurology, Georg August University, Göttingen, Germany
- 5Eskitis Institute for Drug Discovery and School of Natural Sciences Griffith University, Nathan, Qld, Australia
- 6Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA
- ↵*Corresponding author. Tel: +1 214 648 2202; E‐mail: beth.levine{at}utsouthwestern.edu
PEX13 is a peroxisomal membrane protein that regulates matrix protein import during peroxisome biogenesis. This study shows that PEX13 and also PEX3 specifically regulate selective autophagy. Mutations in PEX13 lead to dysregulation of autophagy and might therefore contribute to the pathogenesis of Zellweger syndrome spectrum disorders.
Synopsis
PEX13 is a peroxisomal membrane protein that regulates matrix protein import during peroxisome biogenesis. This study shows that PEX13 and also PEX3 specifically regulate selective autophagy. Mutations in PEX13 lead to dysregulation of autophagy and might therefore contribute to the pathogenesis of Zellweger syndrome spectrum disorders.
PEX13 is required for selective virophagy and mitophagy, but not general autophagy.
The selective mitophagy function of PEX13 is shared with PEX3, another peroxin family member, but not with PEX14 and PEX19.
PEX13 mutants I326T and W313G associated with Zellweger syndrome spectrum disorders are defective in mitophagy.
EMBO Reports (2017) 18: 48–60
- Received March 26, 2016.
- Revision received October 4, 2016.
- Accepted October 7, 2016.
- © 2016 The Authors. Published under the terms of the CC BY NC ND 4.0 license
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
- Plant microbiomes and sustainable agricultureDeciphering the plant microbiome and its role in nutrient supply and plant immunity has great potential to reduce the use of fertilizers and biocides in agriculture
Deciphering the plant microbiome and its role in nutrient supply and plant immunity has great potential to reduce the use of fertilizers and biocides in agriculture
- Philip Hunter, Freelance journalist (ph{at}philiphunter.com)1
Plant microbiota play a crucial role by helping their host plant extract nutrients and defend against pathogens. Understanding these mutually beneficial relationships can greatly improve sustainable agriculture.
- © 2016 The Author
- Zika virus inhibits type‐I interferon production and downstream signaling
- Anil Kumar1,†,
- Shangmei Hou1,†,
- Adriana M Airo2,
- Daniel Limonta1,
- Valeria Mancinelli1,
- William Branton3,
- Christopher Power3 and
- Tom C Hobman (tom.hobman{at}ualberta.ca)*,1,2,4,5
- 1Department of Cell Biology, University of Alberta, Edmonton, Canada
- 2Department of Medical Microbiology & Immunology, University of Alberta, Edmonton, Canada
- 3Department of Medicine, University of Alberta, Edmonton, Canada
- 4Li Ka Shing Institute of Virology, University of Alberta, Edmonton, Canada
- 5Women & Childrens Health Research Institute, University of Alberta, Edmonton, Canada
- ↵*Corresponding author. Tel: +780 492 6485; E‐mail: tom.hobman{at}ualberta.ca
↵† These authors contributed equally to this work
Zika virus (ZIKV) is a mosquito‐borne pathogen that causes Guillain–Barré syndrome in adults and microcephaly in newborns. This report shows that ZIKV infection inhibits the induction of type‐I interferons by downregulating IRF3 and antiviral NF‐κB‐mediated signaling and targets STAT2 for proteasomal degradation.
Synopsis
Zika virus (ZIKV) is a mosquito‐borne pathogen that causes Guillain–Barré syndrome in adults and microcephaly in newborns. This report shows that ZIKV infection inhibits the induction of type‐I interferons by downregulating IRF3 and antiviral NF‐κB‐mediated signaling and targets STAT2 for proteasomal degradation.
ZIKV NS1, NS4A, and NS5 interfere with the induction of type‐I interferon.
ZIKV infection inhibits type‐I interferon signaling.
ZIKV infection results in depletion of STAT2 in human cells.
ZIKV NS5 interacts with STAT2 and induces proteasomal degradation of the protein.
EMBO Reports (2016) 17: 1766–1775
- Received April 27, 2016.
- Revision received September 13, 2016.
- Accepted September 22, 2016.
- © 2016 The Authors
- Transcription factor ANAC032 modulates JA/SA signalling in response to Pseudomonas syringae infection
- Annapurna Devi Allu1,2,
- Yariv Brotman2,
- Gang‐Ping Xue3 and
- Salma Balazadeh (balazadeh{at}mpimp-golm.mpg.de)*,1,2
- 1Institute of Biochemistry and Biology, University of Potsdam, Potsdam‐Golm, Germany
- 2Max‐Planck Institute of Molecular Plant Physiology, Potsdam‐Golm, Germany
- 3CSIRO Agriculture Flagship, St. Lucia, QLD, Australia
- ↵*Corresponding author. Tel: +49 331 567 8351; E‐mail: balazadeh{at}mpimp-golm.mpg.de
This study reports a novel NAC transcription factor ANAC032 in Arabidopsis as a positive regulator of plant defence against Pseudomonas syringae. ANAC032 promotes SA‐mediated defence signalling, but negatively regulates JA‐mediated responses.
Synopsis
This study reports a novel NAC transcription factor ANAC032 in Arabidopsis as a positive regulator of plant defence against Pseudomonas syringae. ANAC032 promotes SA‐mediated defence signalling, but negatively regulates JA‐mediated responses.
Arabidopsis ANAC032 enhances resistance to Pseudomonas syringae.
ANAC032 promotes SA‐mediated defence signalling by repressing NIMIN1, a negative regulator of SA‐dependent defence.
ANAC032 transcriptionally represses MYC2, a key JA activator, and restricts entry of bacteria into plant tissue.
EMBO Reports (2016) 17: 1578–1589
- Received February 12, 2016.
- Revision received August 19, 2016.
- Accepted August 23, 2016.
- © 2016 The Authors
- Xanthomonas campestris attenuates virulence by sensing light through a bacteriophytochrome photoreceptor
- Hernán R Bonomi (hbonomi{at}leloir.org.ar)*,1,
- Laila Toum2,
- Gabriela Sycz1,
- Rodrigo Sieira1,
- Andrés M Toscani3,
- Gustavo E Gudesblat2,
- Federico C Leskow3,
- Fernando A Goldbaum1,
- Adrián A Vojnov (avojnov{at}fundacioncassara.org.ar)*,2 and
- Florencia Malamud (fmalamud{at}iibintech.com.ar)*,2,4
- 1Fundación Instituto Leloir – IIBBA CONICET, Buenos Aires, Argentina
- 2Instituto de Ciencia y Tecnología Dr. Cesar Milstein, Fundación Pablo Cassará, CONICET, Buenos Aires, Argentina
- 3Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
- 4UNSAM Campus Miguelete IIB ‐ Instituto de Investigaciones Biotecnológicas, Buenos Aires, Argentina
- ↵*
Corresponding author. Tel: +54 11 5238 7500; E‐mail: hbonomi{at}leloir.org.ar
Corresponding author. Tel: +54 11 4105 4100; E‐mail: avojnov{at}fundacioncassara.org.ar
Corresponding author. Tel: +54 11 4006 1500; E‐mail: fmalamud{at}iibintech.com.ar
Upon sensing light, the XccBphP photoreceptor elicits a transcriptional response that suppresses virulence. This report establishes light as an important environmental cue, which ultimately governs plant–microbe interactions in the pathogen Xanthomonas campestris.
Synopsis
Upon sensing light, the XccBphP photoreceptor elicits a transcriptional response that suppresses virulence. This report establishes light as an important environmental cue, which ultimately governs plant–microbe interactions in the pathogen Xanthomonas campestris.
XccBphP is a bathy‐type photoreceptor that photoconverts between red‐absorbing (Pr) and far‐red‐absorbing (Pfr) states in vitro.
XccBphP negatively regulates Xcc virulence in a light‐dependent manner.
Light sensed by XccBphP downregulates xanthan production and biofilm formation.
Far‐red light or XccBphP overexpression produces genomewide transcriptional changes, including downregulation of virulence systems.
EMBO Reports (2016) 17: 1565–1577
- Received November 2, 2015.
- Revision received July 27, 2016.
- Accepted August 2, 2016.
- © 2016 The Authors
- Natural mutations in IFITM3 modulate post‐translational regulation and toggle antiviral specificity
- Alex A Compton (alex.compton{at}pasteur.fr)*,1,
- Nicolas Roy1,
- Françoise Porrot1,
- Anne Billet1,
- Nicoletta Casartelli1,
- Jacob S Yount2,
- Chen Liang3 and
- Olivier Schwartz (schwartz{at}pasteur.fr)*,1,4,5
- 1Virus & Immunity Unit, Institut Pasteur, Paris, France
- 2Department of Microbial Infection & Immunity, The Ohio State University, Columbus, OH, USA
- 3Lady Davis Institute, McGill University, Montreal, QC, Canada
- 4CNRS‐URA 3015, Paris, France
- 5Vaccine Research Institute, Creteil, France
- ↵*
Corresponding author. Tel: +33 1456 88576; E‐mail: alex.compton{at}pasteur.fr
Corresponding author. Tel: +33 1456 88353; E‐mail: schwartz{at}pasteur.fr
By analyzing synthetic and naturally occurring mutations of interferon‐induced transmembrane 3 (IFITM3), this study provides novel insight into the antiviral mechanisms at play during HIV‐1 infection. The authors further show that the diversification of IFITM3 genes during evolution may boost the antiviral coverage of host cells and provides selective functional advantages.
Synopsis
By analyzing synthetic and naturally occurring mutations of interferon‐induced transmembrane 3 (IFITM3), this study provides novel insight into the antiviral mechanisms at play during HIV‐1 infection. The authors further show that the diversification of IFITM3 genes during evolution may boost the antiviral coverage of host cells and provides selective functional advantages.
Amino‐terminal mutations of IFITM3 result in an enhanced incorporation into HIV‐1 virions and promote the inhibition of virus–cell fusion.
Two adjacent regulatory motifs that control ubiquitination and endocytosis of IFITM3 regulate its potency and antiviral specificity.
IFITM3 shows recurrent gene duplication and divergence during primate evolution.
EMBO Reports (2016) 17: 1657–1671
- Received May 24, 2016.
- Revision received August 3, 2016.
- Accepted August 3, 2016.
- © 2016 The Authors
- Pseudouridylation of 7SK snRNA promotes 7SK snRNP formation to suppress HIV‐1 transcription and escape from latency
- 1Department of Molecular and Cell Biology, University of California, Berkeley, CA, USA
- 2Department of Plant and Microbial Biology, University of California, Berkeley, CA, USA
- 3Howard Hughes Medical Institute, University of California, Berkeley, CA, USA
- ↵*Corresponding author. Tel: +1 510 643 1697; E‐mail: qzhou{at}berkeley.edu
↵† These authors contributed equally to this work
7SK snRNA function is regulated by pseudouridylation, which stabilizes P‐TEFb‐sequestering 7SK snRNP and suppresses the transcription of HIV‐1 and cellular genes.
Synopsis
The 7SK RNA is an abundant non‐coding nuclear RNA that is highly conserved in vertebrates. This study indicates that its function can be modulated by pseudouridylation, which in turn controls transcription of both HIV‐1 and cellular genes.
The vast majority of cellular 7SK snRNA is pseudouridylated on U250 by the predominant cellular pseudouridine synthase machinery, the DKC1–box H/ACA RNP.
Pseudouridylation of 7SK RNA promotes formation of the 7SK snRNP that sequesters the general transcription elongation factor P‐TEFb into the catalytically inactive form to suppress HIV‐1 transcription and escape from latency.
EMBO Reports (2016) 17: 1441–1451
- Received May 5, 2016.
- Revision received July 27, 2016.
- Accepted July 28, 2016.
- © 2016 The Authors
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