scholarly journals Chloroplastic ATP synthase builds up a proton motive force preventing production of reactive oxygen species in photosystem I

2017 ◽  
Vol 91 (2) ◽  
pp. 306-324 ◽  
Author(s):  
Daisuke Takagi ◽  
Katsumi Amako ◽  
Masaki Hashiguchi ◽  
Hidehiro Fukaki ◽  
Kimitsune Ishizaki ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Atp Synthase ◽  
Photosystem I ◽  
Reactive Oxygen ◽  
Proton Motive Force ◽  
Motive Force ◽  
Oxygen Species

Proton motive force dissipation precludes interaction of microcin J25 with RNA polymerase, but enhances reactive oxygen species overproduction

2009 ◽  
Vol 1790 (10) ◽  
pp. 1307-1313 ◽  
Author(s):  
Fernando G. Dupuy ◽  
María V. Niklison Chirou ◽  
Beatriz Fernández de Arcuri ◽  
Carlos J. Minahk ◽  
Roberto D. Morero
Keyword(s):  
Reactive Oxygen Species ◽  
Rna Polymerase ◽  
Reactive Oxygen ◽  
Proton Motive Force ◽  
Motive Force ◽  
Oxygen Species ◽  
Microcin J25

Fe-S Cluster Biosynthesis Controls Uptake of Aminoglycosides in a ROS-Less Death Pathway

Science ◽  
2013 ◽  
Vol 340 (6140) ◽  
pp. 1583-1587 ◽  
Author(s):  
Benjamin Ezraty ◽  
Alexandra Vergnes ◽  
Manuel Banzhaf ◽  
Yohann Duverger ◽  
Allison Huguenot ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Proton Motive Force ◽  
Iron Limitation ◽  
Ros Production ◽  
Oxygen Species ◽  
Fenton Chemistry ◽  
Respiratory Complexes ◽  
Iron Sulfur ◽  
Cluster Biosynthesis

All bactericidal antibiotics were recently proposed to kill by inducing reactive oxygen species (ROS) production, causing destabilization of iron-sulfur (Fe-S) clusters and generating Fenton chemistry. We find that the ROS response is dispensable upon treatment with bactericidal antibiotics. Furthermore, we demonstrate that Fe-S clusters are required for killing only by aminoglycosides. In contrast to cells, using the major Fe-S cluster biosynthesis machinery, ISC, cells using the alternative machinery, SUF, cannot efficiently mature respiratory complexes I and II, resulting in impendence of the proton motive force (PMF), which is required for bactericidal aminoglycoside uptake. Similarly, during iron limitation, cells become intrinsically resistant to aminoglycosides by switching from ISC to SUF and down-regulating both respiratory complexes. We conclude that Fe-S proteins promote aminoglycoside killing by enabling their uptake.

scholarly journals The Antiapoptotic Herpes Simplex Virus Glycoprotein J Localizes to Multiple Cellular Organelles and Induces Reactive Oxygen Species Formation

2007 ◽  
Vol 82 (2) ◽  
pp. 617-629 ◽  
Author(s):  
Martine Aubert ◽  
Zheng Chen ◽  
Robin Lang ◽  
Chung H. Dang ◽  
Carla Fowler ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Atp Synthase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Transfected Cells ◽  
Cellular Effects ◽  
Herpes Simplex Virus Glycoprotein ◽  
Simplex Virus

ABSTRACT The Us5 gene of herpes simplex virus (HSV) encodes glycoprotein J (gJ). The only previously reported function of gJ was its ability to inhibit apoptosis. However, the mechanism by which gJ prevents apoptosis is not understood, and it is not known whether gJ mediates additional cellular effects. In this study, we evaluated the expression, localization, and cellular effects of Us5/gJ. Us5 was first expressed 4 h after infection. gJ was detectable at 6 h and was expressed in glycosylated and unglycosylated forms. Us5 was regulated as a late gene, with partial dependency on DNA replication for expression. Us5 expression was delayed in the absence of ICP22; furthermore, expression of Us5 in trans protected cells from apoptosis induced by an HSV mutant with deletion of ICP27, suggesting that the antiapoptotic effects of ICP22 and ICP27 are mediated in part through effects on gJ expression. Within HSV-infected or Us5-transfected cells, gJ was distributed widely, especially to the endoplasmic reticulum, trans-Golgi network, and early endosomes. gJ interacted with FoF1 ATP synthase subunit 6 by a yeast two-hybrid screen and had strong antiapoptotic effects, which were mediated by protein rather than mRNA. Antiapoptotic activity required the extracellular and transmembrane domains of gJ, but not the intracellular domain. Consistent with inhibition of FoF1 ATP synthase function, Us5 was required for HSV-induced reactive oxygen species (ROS) formation, and gJ was sufficient to induce ROS in Us5-transfected cells. Thus, HSV gJ is a multifunctional protein, modulating other cellular processes in addition to inhibition of apoptosis.

scholarly journals The antimicrobial action of polyaniline involves production of oxidative stress while functionalisation of polyaniline introduces additional mechanisms

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5135 ◽  
Author(s):  
Julia Robertson ◽  
Marija Gizdavic-Nikolaidis ◽  
Michel K. Nieuwoudt ◽  
Simon Swift
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Atp Synthase ◽  
Acid Stress ◽  
Reactive Oxygen ◽  
Antimicrobial Action ◽  
Oxygen Species ◽  
E Coli ◽  
Production Of Hydrogen

Polyaniline (PANI) and functionalised polyanilines (fPANI) are novel antimicrobial agents whose mechanism of action was investigated.Escherichia colisingle gene deletion mutants revealed that the antimicrobial mechanism of PANI likely involves production of hydrogen peroxide while homopolymer poly(3-aminobenzoic acid), P3ABA, used as an example of a fPANI, disrupts metabolic and respiratory machinery, by targeting ATP synthase and causes acid stress. PANI was more active againstE. coliin aerobic, compared to anaerobic, conditions, while this was apparent for P3ABA only in rich media. Greater activity in aerobic conditions suggests involvement of reactive oxygen species. P3ABA treatment causes an increase in intracellular free iron, which is linked to perturbation of metabolic enzymes and could promote reactive oxygen species production. Addition of exogenous catalase protectedE. colifrom PANI antimicrobial action; however, this was not apparent for P3ABA treated cells. The results presented suggest that PANI induces production of hydrogen peroxide, which can promote formation of hydroxyl radicals causing biomolecule damage and potentially cell death. P3ABA is thought to act as an uncoupler by targeting ATP synthase resulting in a futile cycle, which precipitates dysregulation of iron homeostasis, oxidative stress, acid stress, and potentially the fatal loss of proton motive force.

scholarly journals Opa1 relies on cristae preservation and ATP synthase to curtail reactive oxygen species accumulation in mitochondria

Redox Biology ◽  
2021 ◽  
pp. 101944
Author(s):  
Rubén Quintana-Cabrera ◽  
Israel Manjarrés-Raza ◽  
Carlos Vicente-Gutiérrez ◽  
Mauro Corrado ◽  
Juan P. Bolaños ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Atp Synthase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Accumulation ◽  
Species Accumulation

scholarly journals Reactive oxygen species target specific tryptophan site in the mitochondrial ATP synthase

2012 ◽  
Vol 1817 (2) ◽  
pp. 381-387 ◽  
Author(s):  
Sascha Rexroth ◽  
Ansgar Poetsch ◽  
Matthias Rögner ◽  
Andrea Hamann ◽  
Alexandra Werner ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Atp Synthase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Atp Synthase
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