scholarly journals Nitric oxide synthases from photosynthetic organisms improve growth and confer nitrosative stress tolerance in E. coli. Insights on the pterin cofactor

Nitric Oxide ◽  
2021 ◽  
Author(s):  
Natalia Correa-Aragunde ◽  
Andrés Nejamkin ◽  
Fiorella Del Castello ◽  
Noelia Foresi ◽  
Lorenzo Lamattina
Keyword(s):  
Nitric Oxide ◽  
Stress Tolerance ◽  
Nitrosative Stress ◽  
Nitric Oxide Synthases ◽  
E Coli ◽  
Photosynthetic Organisms ◽  
Pterin Cofactor

scholarly journals Nitric Oxide in Chemostat-Cultured Escherichia coli Is Sensed by Fnr and Other Global Regulators: Unaltered Methionine Biosynthesis Indicates Lack of S Nitrosation

2006 ◽  
Vol 189 (5) ◽  
pp. 1845-1855 ◽  
Author(s):  
Steven T. Pullan ◽  
Mark D. Gidley ◽  
Richard A. Jones ◽  
Jason Barrett ◽  
Tania M. Stevanin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Escherichia Coli ◽  
Nitrosative Stress ◽  
Adaptive Responses ◽  
Methionine Biosynthesis ◽  
Transcriptional Responses ◽  
No Donor ◽  
Global Regulators ◽  
E Coli ◽  
Cellular Effects

ABSTRACT We previously elucidated the global transcriptional responses of Escherichia coli to the nitrosating agent S-nitrosoglutathione (GSNO) in both aerobic and anaerobic chemostats, demonstrated the expression of nitric oxide (NO)-protective mechanisms, and obtained evidence of critical thiol nitrosation. The present study was the first to examine the transcriptome of NO-exposed E. coli in a chemostat. Using identical conditions, we compared the GSNO stimulon with the stimulon of NO released from two NO donor compounds {3-[2-hydroxy-1-(1-methyl-ethyl)-2-nitrosohydrazino]-1-propanamine (NOC-5) and 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamine (NOC-7)} simultaneously and demonstrated that there were marked differences in the transcriptional responses to these distinct nitrosative stresses. Exposure to NO did not induce met genes, suggesting that, unlike GSNO, NO does not elicit homocysteine S nitrosation and compensatory increases in methionine biosynthesis. After entry into cells, exogenous methionine provided protection from GSNO-mediated killing but not from NO-mediated killing. Anaerobic exposure to NO led to up-regulation of multiple Fnr-repressed genes and down-regulation of Fnr-activated genes, including nrfA, which encodes cytochrome c nitrite reductase, providing strong evidence that there is NO inactivation of Fnr. Other global regulators apparently affected by NO were IscR, Fur, SoxR, NsrR, and NorR. We tried to identify components of the NorR regulon by performing a microarray comparison of NO-exposed wild-type and norR mutant strains; only norVW, encoding the NO-detoxifying flavorubredoxin and its cognate reductase, were unambiguously identified. Mutation of norV or norR had no effect on E. coli survival in mouse macrophages. Thus, GSNO (a nitrosating agent) and NO have distinct cellular effects; NO more effectively interacts with global regulators that mediate adaptive responses to nitrosative stress but does not affect methionine requirements arising from homocysteine nitrosation.

scholarly journals Time course of nitric oxide synthases, nitrosative stress, and poly(ADP ribosylation) in an ovine sepsis model

Critical Care ◽  
2010 ◽  
Vol 14 (4) ◽  
pp. R129 ◽  
Author(s):  
Matthias Lange ◽  
Rhykka Connelly ◽  
Daniel L Traber ◽  
Atsumori Hamahata ◽  
Yoshimitsu Nakano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Time Course ◽  
Nitrosative Stress ◽  
Nitric Oxide Synthases ◽  
Adp Ribosylation ◽  
Sepsis Model

Nitric oxide-sensing mechanisms in Escherichia coli

2006 ◽  
Vol 34 (1) ◽  
pp. 200-202 ◽  
Author(s):  
S. Spiro
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Escherichia Coli ◽  
Nitrosative Stress ◽  
Current Understanding ◽  
Array Data ◽  
E Coli ◽  
Regulatory Systems

Exposure of Escherichia coli to nitric oxide (NO) or nitrosating agents causes significant changes in patterns of gene expression. Three recent studies have used microarrays to analyse the response of the E. coli transcriptome to NO and nitrosative stress. Drawing on the array data, I review our current understanding of the E. coli regulatory systems that are involved.

Comparative Effects of Substrates and Pterin Cofactor on the Heme Midpoint Potential in Inducible and Neuronal Nitric Oxide Synthases

1998 ◽  
Vol 120 (37) ◽  
pp. 9460-9465 ◽  
Author(s):  
Anthony Presta ◽  
Anne M. Weber-Main ◽  
Marian T. Stankovich ◽  
Dennis J. Stuehr
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthases ◽  
Midpoint Potential ◽  
Pterin Cofactor

scholarly journals HcpR of Porphyromonas gingivalis Is Required for Growth under Nitrosative Stress and Survival within Host Cells

2012 ◽  
Vol 80 (9) ◽  
pp. 3319-3331 ◽  
Author(s):  
Janina P. Lewis ◽  
Sai S. Yanamandra ◽  
Cecilia Anaya-Bergman
Keyword(s):  
Nitric Oxide ◽  
Porphyromonas Gingivalis ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Transcriptional Response ◽  
Promoter Sequence ◽  
Host Cells ◽  
Content Type ◽  
E Coli ◽  
Gene Coding

ABSTRACTAlthough the Gram-negative, anaerobic periodontopathogenPorphyromonas gingivalismust withstand nitrosative stress, which is particularly high in the oral cavity, the mechanisms allowing for protection against such stress are not known in this organism. In this study, microarray analysis ofP. gingivalistranscriptional response to nitrite and nitric oxide showed drastic upregulation of the PG0893 gene coding for hybrid cluster protein (Hcp), which is a putative hydroxylamine reductase. Although regulation ofhcphas been shown to be OxyR dependent inEscherichia coli, here we show that inP. gingivalisits expression is dependent on the Fnr-like regulator designated HcpR. Growth of the isogenic mutant V2807, containing anermF-ermAMinsertion within thehcpR(PG1053) gene, was significantly reduced in the presence of nitrite (P< 0.002) and nitric oxide-generating nitrosoglutathione (GSNO) (P< 0.001), compared to that of the wild-type W83 strain. Furthermore, the upregulation of PG0893 (hcp) was abrogated in V2807 exposed to nitrosative stress. In addition, recombinant HcpR bound DNA containing thehcppromoter sequence, and the binding was hemin dependent. Finally, V2807 was not able to survive with host cells, demonstrating that HcpR plays an important role inP. gingivalisvirulence. This work gives insight into the molecular mechanisms of protection against nitrosative stress inP. gingivalisand shows that the regulatory mechanisms differ from those inE. coli.

scholarly journals Nitric oxide synthases from photosynthetic organisms improve growth and confer nitrosative stress tolerance in E. coli. Insights on the pterin cofactor

2021 ◽  
Author(s):  
Natalia Correa-Aragunde ◽  
Andrés Nejamkin ◽  
Fiorella Del Castello ◽  
Noelia Foresi ◽  
Lorenzo Lamattina
Keyword(s):  
Nitric Oxide ◽  
Bacterial Growth ◽  
Nitrosative Stress ◽  
Biochemical Properties ◽  
Ligand Docking ◽  
List Type ◽  
No Donor ◽  
E Coli ◽  
Bioinformatic Tools ◽  
Photosynthetic Microorganisms

AbstractNitric oxide synthase (NOS) synthesizes NO from the substrate L-arginine (Arg). NOS with distinct biochemical properties were characterized from two photosynthetic microorganisms, the unicellular algae Ostreococcus tauri (OtNOS) and the cyanobacteria Synechococcus PCC 7335 (SyNOS). In this work we studied OtNOS and SyNOS recombinantly expressed in E. coli and analyzed bacterial growth and tolerance to nitrosative stress. Results show that the expression of OtNOS and SyNOS promotes bacterial growth and allows metabolizing Arg as N source. In accordance to a high NO producing activity, OtNOS expression induces the hmp flavohemoglobin in E. coli, suggesting that this strain is sensing nitrosative stress. The addition of 1 mM of the NO donor sodium nitroprusside (SNP) is toxic and generates a strong nitrosative stress. The expression of OtNOS or SyNOS reduced SNP toxicity restoring bacterial growth. Finally, using bioinformatic tools and ligand docking analyses, we propose tetrahydromonapterin (MH4), an endogenous pterin found in E. coli, as potential cofactor required for NOS catalytic activity. Our findings could be useful for the development of biotechnological applications using NOS expression to improve growth in bacteria.Key points- The NO synthase (NOS) from photosynthetic microorganisms were expressed in E. coli- Expression of NOS increases bacterial growth and tolerance to nitrosative stress.- Ligand docking analyses indicate tetrahydromonapterin (MH4) as potential NOS cofactor in E. coli.

scholarly journals Cerebral Microvascular Damage Occurs Early after Hypoxia–Ischemia via nNOS Activation in the Neonatal Brain

2014 ◽  
Vol 34 (4) ◽  
pp. 668-676 ◽  
Author(s):  
Yi-Ching Hsu ◽  
Ying-Chao Chang ◽  
Yung-Chieh Lin ◽  
Chun-I Sze ◽  
Chao-Ching Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Damage ◽  
Cerebral Perfusion ◽  
Nitrosative Stress ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Nitric Oxide Synthases ◽  
Neonatal Brain ◽  
Microvascular Damage ◽  
Vascular Lumen

Microvascular injury early after hypoxic ischemia (HI) may contribute to neonatal brain damage. N-methyl-D-aspartate receptor overstimulation activates neuronal nitric oxide synthases (nNOS). We hypothesized that microvascular damage occurs early post-HI via nNOS activation and contributes to brain injury. Postpartum day-7 rat pups were treated with 7-nitroindazole (7-NI) or aminoguanidine (AG) before or after HI. Electron microscopy was performed to measure neuronal and endothelial cell damage. There were vascular lumen narrowing at 1 hour, pyknotic neurons at 3 hours, and extensive neuronal damage and loss of vessels at 24 hours post HI. Early after reoxygenation, there were neurons with heterochromatic chromatin and endothelial cells with enlarged nuclei occluding the lumen. There was also increased 3-nitrotyrosin in the microvessels and decreased cerebral blood perfusion. 7-NI and AG treatment before hypoxia provided complete and partial neuroprotection, respectively. Early post-reoxygenation, the AG group showed significantly increased microvascular nitrosative stress, microvascular interruptions, swollen nuclei that narrowed the vascular lumen, and decreased cerebral perfusion. The 7-NI group showed significantly decreased microvascular nitrosative stress, patent vascular lumen, and increased cerebral perfusion. Our results indicate that microvascular damage occurs early and progressively post HI. Neuronal nitric oxide synthases activation contributes to microvascular damage and decreased cerebral perfusion early after reoxygenation and worsens brain damage.

Sign in / Sign up

Export Citation Format

Share Document