scholarly journals Inactivation of cytosolic FUMARASE2 enhances growth and photosynthesis under simultaneous copper and iron deprivation in Arabidopsis

2021 ◽  
Author(s):  
Antoni Garcia‐Molina ◽  
Martin Lehmann ◽  
Katja Schneider ◽  
Andreas Klingl ◽  
Dario Leister
Keyword(s):  
Iron Deprivation

scholarly journals In vitro activities of novel catecholate siderophores against Plasmodium falciparum.

1996 ◽  
Vol 40 (9) ◽  
pp. 2094-2098 ◽  
Author(s):  
B Pradines ◽  
F Ramiandrasoa ◽  
L K Basco ◽  
L Bricard ◽  
G Kunesch ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Mechanism Of Action ◽  
Ribonucleotide Reductase ◽  
Antimalarial Activity ◽  
Iron Chelators ◽  
Resistant Clone ◽  
Iron Deprivation ◽  
Level Of Activity ◽  
Susceptible Clone

The activities of novel iron chelators, alone and in combination with chloroquine, quinine, or artemether, were evaluated in vitro against susceptible and resistant clones of Plasmodium falciparum with a semimicroassay system. N4-nonyl,N1,N8-bis(2,3-dihydroxybenzoyl) spermidine hydrobromide (compound 7) demonstrated the highest level of activity: 170 nM against a chloroquine-susceptible clone and 1 microM against a chloroquine-resistant clone (50% inhibitory concentrations). Compounds 6, 8, and 10 showed antimalarial activity with 50% inhibitory concentrations of about 1 microM. Compound 7 had no effect on the activities of chloroquine, quinine, and artemether against either clone, and compound 8 did not enhance the schizontocidal action of either chloroquine or quinine against the chloroquine-resistant clone. The incubation of compound 7 with FeCI3 suppressed or decreased the in vitro antimalarial activity of compound 7, while no effect was observed with incubation of compound 7 with CuSO4 and ZnSO4. These results suggest that iron deprivation may be the main mechanism of action of compound 7 against the malarial parasites. Chelator compounds 7 and 8 primarily affected trophozoite stages, probably by influencing the activity of ribonucleotide reductase, and thus inhibiting DNA synthesis.

scholarly journals The TonB system in Aeromonas hydrophila NJ-35 is essential for MacA2B2 efflux pump-mediated macrolide resistance

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Yuhao Dong ◽  
Qing Li ◽  
Jinzhu Geng ◽  
Qing Cao ◽  
Dan Zhao ◽  
...  
Keyword(s):  
Aeromonas Hydrophila ◽  
Efflux Pump ◽  
Fold Increase ◽  
Activity Level ◽  
Macrolide Resistance ◽  
Wild Type ◽  
Iron Deprivation ◽  
Pump Activity ◽  
Tonb System ◽  
Increased Sensitivity

AbstractThe TonB system is generally considered as an energy transporting device for the absorption of nutrients. Our recent study showed that deletion of this system caused a significantly increased sensitivity of Aeromonas hydrophila to the macrolides erythromycin and roxithromycin, but had no effect on other classes of antibiotics. In this study, we found the sensitivity of ΔtonB123 to all macrolides tested revealed a 8- to 16-fold increase compared with the wild-type (WT) strain, but this increase was not related with iron deprivation caused by tonB123 deletion. Further study demonstrated that the deletion of tonB123 did not damage the integrity of the bacterial membrane but did hinder the function of macrolide efflux. Compared with the WT strain, deletion of macA2B2, one of two ATP-binding cassette (ABC) types of the macrolide efflux pump, enhanced the sensitivity to the same levels as those of ΔtonB123. Interestingly, the deletion of macA2B2 in the ΔtonB123 mutant did not cause further increase in sensitivity to macrolide resistance, indicating that the macrolide resistance afforded by the MacA2B2 pump was completely abrogated by tonB123 deletion. In addition, macA2B2 expression was not altered in the ΔtonB123 mutant, indicating that any influence of TonB on MacA2B2-mediated macrolide resistance was at the pump activity level. In conclusion, inactivation of the TonB system significantly compromises the resistance of A. hydrophila to macrolides, and the mechanism of action is related to the function of MacA2B2-mediated macrolide efflux.

scholarly journals The Fish Pathogen Vibrio ordalii Under Iron Deprivation Produces the Siderophore Piscibactin

2019 ◽  
Vol 7 (9) ◽  
pp. 313 ◽  
Author(s):  
Pamela Ruiz ◽  
Miguel Balado ◽  
Juan Carlos Fuentes-Monteverde ◽  
Alicia E. Toranzo ◽  
Jaime Rodríguez ◽  
...  
Keyword(s):  
Gene Cluster ◽  
Iron Uptake ◽  
Peptide Mass Fingerprinting ◽  
Iron Limitation ◽  
Fish Pathogen ◽  
Fish Pathogens ◽  
Iron Deprivation ◽  
Peptide Mass ◽  
Photobacterium Damselae ◽  
Vibrio Ordalii

Vibrio ordalii is the causative agent of vibriosis, mainly in salmonid fishes, and its virulence mechanisms are still not completely understood. In previous works we demonstrated that V. ordalii possess several iron uptake mechanisms based on heme utilization and siderophore production. The aim of the present work was to confirm the production and utilization of piscibactin as a siderophore by V. ordalii. Using genetic analysis, identification by peptide mass fingerprinting (PMF) of iron-regulated membrane proteins and chemical identification by LC-HRMS, we were able to clearly demonstrate that V. ordalii produces piscibactin under iron limitation. The synthesis and transport of this siderophore is encoded by a chromosomal gene cluster homologous to another one described in V. anguillarum, which also encodes the synthesis of piscibactin. Using β-galactosidase assays we were able to show that two potential promoters regulated by iron control the transcription of this gene cluster in V. ordalii. Moreover, biosynthetic and transport proteins corresponding to piscibactin synthesis and uptake could be identified in membrane fractions of V. ordalii cells grown under iron limitation. The synthesis of piscibactin was previously reported in other fish pathogens like Photobacterium damselae subsp. piscicida and V. anguillarum, which highlights the importance of this siderophore as a key virulence factor in Vibrionaceae bacteria infecting poikilothermic animals.

Hemolytic capability and expression of a putative haem oxygenase-encoding gene by blood isolates of Candida tropicalis are influenced by iron deprivation and the presence of hemoglobin and erythrocytes

2017 ◽  
Vol 105 ◽  
pp. 235-239 ◽  
Author(s):  
Emanuele Julio Galvão França ◽  
Luciana Furlaneto-Maia ◽  
Márcia Cristina Furlaneto
Keyword(s):  
Candida Tropicalis ◽  
Iron Deprivation ◽  
Haem Oxygenase ◽  
Encoding Gene

Immune Control of Chlamydial Growth in the Human Epithelial Cell Line RT4 Involves Multiple Mechanisms That Include Nitric Oxide Induction, Tryptophan Catabolism and Iron Deprivation

1998 ◽  
Vol 42 (9) ◽  
pp. 617-625 ◽  
Author(s):  
Joseph U. Igietseme ◽  
Godwin A. Ananaba ◽  
Debra H. Candal ◽  
Deborah Lyn ◽  
Carolyn M. Black
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cell ◽  
Cell Line ◽  
Epithelial Cell Line ◽  
Human Epithelial Cell ◽  
Immune Control ◽  
Iron Deprivation ◽  
Tryptophan Catabolism

The cyanotrophic bacterium Pseudomonas pseudoalcaligenes CECT5344 responds to cyanide by defence mechanisms against iron deprivation, oxidative damage and nitrogen stress

2007 ◽  
Vol 9 (6) ◽  
pp. 1541-1549 ◽  
Author(s):  
Victor M. Luque-Almagro ◽  
María J. Huertas ◽  
M. Dolores Roldán ◽  
Comrado Moreno-Vivián ◽  
Manuel Martínez-Luque ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Nitrogen Stress ◽  
Defence Mechanisms ◽  
Pseudomonas Pseudoalcaligenes ◽  
Iron Deprivation

scholarly journals Small RNA profiling in Mycobacterium tuberculosis identifies MrsI as necessary for an anticipatory iron sparing response

2018 ◽  
Vol 115 (25) ◽  
pp. 6464-6469 ◽  
Author(s):  
Elias R. Gerrick ◽  
Thibault Barbier ◽  
Michael R. Chase ◽  
Raylin Xu ◽  
Josie François ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Large Scale ◽  
Direct Interaction ◽  
Human Macrophage ◽  
Binding Interaction ◽  
Bacterial Gene ◽  
Rna Profiling ◽  
Iron Deprivation ◽  
Bacterial Gene Expression ◽  
Small Regulatory Rnas

One key to the success of Mycobacterium tuberculosis as a pathogen is its ability to reside in the hostile environment of the human macrophage. Bacteria adapt to stress through a variety of mechanisms, including the use of small regulatory RNAs (sRNAs), which posttranscriptionally regulate bacterial gene expression. However, very little is currently known about mycobacterial sRNA-mediated riboregulation. To date, mycobacterial sRNA discovery has been performed primarily in log-phase growth, and no direct interaction between any mycobacterial sRNA and its targets has been validated. Here, we performed large-scale sRNA discovery and expression profiling in M. tuberculosis during exposure to five pathogenically relevant stresses. From these data, we identified a subset of sRNAs that are highly induced in multiple stress conditions. We focused on one of these sRNAs, ncRv11846, here renamed mycobacterial regulatory sRNA in iron (MrsI). We characterized the regulon of MrsI and showed in mycobacteria that it regulates one of its targets, bfrA, through a direct binding interaction. MrsI mediates an iron-sparing response that is required for optimal survival of M. tuberculosis under iron-limiting conditions. However, MrsI is induced by multiple host-like stressors, which appear to trigger MrsI as part of an anticipatory response to impending iron deprivation in the macrophage environment.

scholarly journals An iron-regulated LysR-type element mediates antimicrobial peptide resistance and virulence in Yersinia pseudotuberculosis

Microbiology ◽  
2009 ◽  
Vol 155 (7) ◽  
pp. 2168-2181 ◽  
Author(s):  
Sonia Arafah ◽  
Marie-Laure Rosso ◽  
Linda Rehaume ◽  
Robert E. W. Hancock ◽  
Michel Simonet ◽  
...  
Keyword(s):  
Antimicrobial Peptide ◽  
Yersinia Pseudotuberculosis ◽  
Polymyxin B ◽  
Uptake System ◽  
Mesenteric Lymph Nodes ◽  
Iron Starvation ◽  
Iron Deprivation ◽  
Genes Encoding ◽  
Antimicrobial Peptide Resistance

During the course of its infection of the mammalian digestive tract, the entero-invasive, Gram-negative bacterium Yersinia pseudotuberculosis must overcome various hostile living conditions (notably, iron starvation and the presence of antimicrobial compounds produced in situ). We have previously reported that in vitro bacterial growth during iron deprivation raises resistance to the antimicrobial peptide polymyxin B; here, we show that this phenotype is mediated by a chromosomal gene (YPTB0333) encoding a transcriptional regulator from the LysR family. We determined that the product of YPTB0333 is a pleiotropic regulator which controls (in addition to its own expression) genes encoding the Yfe iron-uptake system and polymyxin B resistance. Lastly, by using a mouse model of oral infection, we demonstrated that YPTB0333 is required for colonization of Peyer's patches and mesenteric lymph nodes by Y. pseudotuberculosis.

Kinetics of iron transport into the leaf symplast during recovery from iron stress

1983 ◽  
Vol 61 (9) ◽  
pp. 2496-2499 ◽  
Author(s):  
Terry Forrest Young ◽  
Norman Terry
Keyword(s):  
Sugar Beet ◽  
Leaf Blade ◽  
Iron Transport ◽  
Iron Stress ◽  
Manganese Zinc ◽  
Iron Deprivation ◽  
Kinetics Of ◽  
Iron Concentrations

The iron concentrations of chloroplasts (isolated by nonaqueous methods) and of chloroplast lamellae (isolated by aqueous procedures) were determined and used to investigate the kinetics of iron transport across the plasmalemma into the leaf symplast during the recovery of sugar beet plants from iron stress due to iron deprivation. Iron concentrations in chloroplasts isolated by the nonaqueous procedure were greatly reduced during iron stress and recovered to over 200% of control levels within 24 h. Iron concentrations in lamellae from aqueous isolations increased significantly within 24 h of resupply and reached values in excess of control levels in 48–72 h. These results indicate that a substantial quantity of the iron that entered the leaf blade during the first 24–48 h of iron resupply crossed the plasmalemma. The effect appeared to be specific to iron because there was no evidence that manganese, zinc, and copper were transported into chloroplasts and lamellae in enhanced amounts.

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