scholarly journals High-Affinity Zn2+ Uptake System ZnuABC Is Required for Bacterial Zinc Homeostasis in Intracellular Environments and Contributes to the Virulence of Salmonella enterica

2007 ◽  
Vol 75 (12) ◽  
pp. 5867-5876 ◽  
Author(s):  
Serena Ammendola ◽  
Paolo Pasquali ◽  
Claudia Pistoia ◽  
Paola Petrucci ◽  
Patrizia Petrarca ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Infected Animal ◽  
Zinc Homeostasis ◽  
Elevated Concentration ◽  
Uptake System ◽  
Bacterial Physiology ◽  
High Affinity ◽  
Rich Media ◽  
Complex Functions ◽  
Mutant Strains

ABSTRACT To investigate the relevance of zinc in host-pathogen interactions, we have constructed Salmonella enterica mutant strains in which the znuA gene, which encodes the periplasmic component of the ZnuABC high-affinity Zn2+ transporter, was deleted. This mutation does not alter the ability of Salmonella to grow in rich media but drastically reduces its ability to multiply in media deprived of zinc. In agreement with this phenotype, ZnuA accumulates only in bacteria cultivated in environments poor in zinc. In spite of the nearly millimolar intracellular concentration of zinc, we have found that znuA is highly expressed in intracellular salmonellae recovered either from cultivated cells or from the spleens of infected mice. We have also observed that znuA mutants are impaired in their ability to grow in Caco-2 epithelial cells and that bacteria starved for zinc display decreased ability to multiply in phagocytes. A dramatic reduction in the pathogenicity of the znuA mutants was observed in Salmonella-susceptible (BALB/c) or Salmonella-resistant (DBA-2) mice infected intraperitoneally or orally. This study shows that the amount of free metals available for bacterial growth within the infected animal is limited, despite the apparent elevated concentration of free metals within cells and in plasma and suggests that Salmonella exploits the ZnuABC zinc transporter to maximize zinc availability in such conditions. These results shed new light on the complex functions of zinc in vertebrate and bacterial physiology and pave the way for a better comprehension of pathogenic mechanisms in Salmonella infections.

scholarly journals Role of the High-Affinity Zinc Uptake znuABC System in Salmonella enterica Serovar Typhimurium Virulence

2002 ◽  
Vol 70 (8) ◽  
pp. 4721-4725 ◽  
Author(s):  
Susana Campoy ◽  
Mónica Jara ◽  
Núria Busquets ◽  
Ana M. Pérez de Rozas ◽  
Ignacio Badiola ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Lethal Dose ◽  
Zinc Uptake ◽  
Uptake System ◽  
High Affinity ◽  
Knockout Mutants ◽  
Serovar Typhimurium ◽  
Genes Encoding

ABSTRACT The Salmonella enterica serovar Typhimurium znuABC genes encoding a high-affinity zinc uptake system and its regulatory zur gene have been cloned. Salmonella serovar Typhimurium zur and znuC knockout mutants have been constructed by marker exchange. The 50% lethal dose of the znuC mutant increased when either orally or intraperitoneally inoculated in BALB/c mice, while virulence of the zur mutant decreased only when mice were intraperitoneally challenged.

scholarly journals Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac+ enterotoxigenic E. coli (ETEC) under a zinc restricted environment

2020 ◽  
Vol 51 (1) ◽  
Author(s):  
Guomei Quan ◽  
Pengpeng Xia ◽  
Siqi Lian ◽  
Yunping Wu ◽  
Guoqiang Zhu
Keyword(s):  
Sharp Decrease ◽  
Zinc Uptake ◽  
Zinc Homeostasis ◽  
Data Sets ◽  
Uptake System ◽  
E Coli ◽  
High Affinity ◽  
Restricted Environment ◽  
Living Organisms

Abstract Zinc is the second trace element of living organisms after iron. Given its crucial importance, mammalian hosts restrict the bioavailability of Zinc ions (Zn2+) to bacterial pathogens. As a countermeasure, pathogens utilize high affinity Zn2+ transporters, such as ZnuACB to compete with the host for zinc. It is essential for bacteria to maintain zinc homeostasis and thus maintain their physiology and pathogenesis. In an attempt to uncover the zinc transporter in F4+ enterotoxigenic E. coli (ETEC) C83902, we analyzed two RNA-seq data sets of bacteria samples when different zinc treatments (restriction or abundance) were applied. Considering data revealing that the high affinity zinc uptake system ZnuACB acts as the main transporter in ETEC C83902 to resist zinc deficiency, we deleted znuACB genes to study the role of them in ETEC C83902. The deletion of znuACB genes results in growth perturbation and a sharp decrease in the ability of biofilm formation and adhesion of bacteria in vitro. Taking the data together, this study demonstrates that the ZnuACB system is required for ETEC C83902 to acquire zinc, which highly contributes to ETEC pathogenicity as well.

scholarly journals Regulation of Copper Metabolism by Nitrogen Utilization in Saccharomyces cerevisiae

2021 ◽  
Vol 7 (9) ◽  
pp. 756
Author(s):  
Suzie Kang ◽  
Hyewon Seo ◽  
Min-Gyu Lee ◽  
Cheol-Won Yun
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Iron Uptake ◽  
Nitrogen Starvation ◽  
Copper Metabolism ◽  
Nitrogen Utilization ◽  
Deletion Mutants ◽  
Uptake System ◽  
Wild Type ◽  
High Affinity ◽  
Uptake Activity

To understand the relationship between carbon or nitrogen utilization and iron homeostasis, we performed an iron uptake assay with several deletion mutants with partial defects in carbon or nitrogen metabolism. Among them, some deletion mutants defective in carbon metabolism partially and the MEP2 deletion mutant showed lower iron uptake activity than the wild type. Mep2 is known as a high-affinity ammonia transporter in Saccharomyces cerevisiae. Interestingly, we found that nitrogen starvation resulted in lower iron uptake activity than that of wild-type cells without downregulation of the genes involved in the high-affinity iron uptake system FET3/FTR1. However, the gene expression of FRE1 and CTR1 was downregulated by nitrogen starvation. The protein level of Ctr1 was also decreased by nitrogen starvation, and addition of copper to the nitrogen starvation medium partially restored iron uptake activity. However, the expression of MAC1, which is a copper-responsive transcriptional activator, was not downregulated by nitrogen starvation at the transcriptional level but was highly downregulated at the translational level. Mac1 was downregulated dramatically under nitrogen starvation, and treatment with MG132, which is an inhibitor of proteasome-dependent protein degradation, partially attenuated the downregulation of Mac1. Taken together, these results suggest that nitrogen starvation downregulates the high-affinity iron uptake system by degrading Mac1 in a proteasome-dependent manner and eventually downregulates copper metabolism.

The uptake of sulfate by excised roots of rape seedlings (Brassica napus var. Target)

1975 ◽  
Vol 53 (9) ◽  
pp. 914-920 ◽  
Author(s):  
P. D. Shargool ◽  
T. T. Ngo
Keyword(s):  
Brassica Napus ◽  
Chloride Solution ◽  
Liquid Scintillation ◽  
Sodium Cyanide ◽  
Calcium Chloride Solution ◽  
Scintillation Counting ◽  
Uptake System ◽  
Counting Method ◽  
Brassica Napus L ◽  
High Affinity

Excised roots from 5-day-old seedlings of Brassica napus L. var. Target, which had been grown in 2 × 10−4 M calcium chloride solution, were incubated in medium containing various concentrations of sulfate. The uptake of this ion by the roots was measured with the aid of [35S]-labelled sulfate and a liquid scintillation counting method. The membrane uptake system was shown to be sensitive to sodium cyanide and dinitrophenol. Kinetic examination of the process demonstrated that it was mediated by two separate systems each of which operated in a specific sulfate concentration range. One system was shown to have a low affinity for sulfate and was thought to remain inoperative until the second high-affinity system became saturated.

scholarly journals Multiple Factors Independently RegulatehilA and Invasion Gene Expression in Salmonella enterica Serovar Typhimurium

2000 ◽  
Vol 182 (7) ◽  
pp. 1872-1882 ◽  
Author(s):  
Robin L. Lucas ◽  
C. Phoebe Lostroh ◽  
Concetta C. DiRusso ◽  
Michael P. Spector ◽  
Barry L. Wanner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Salmonella Enterica ◽  
Inorganic Phosphate ◽  
Response Regulator ◽  
Regulatory System ◽  
Negative Control ◽  
Host Cells ◽  
Uptake System ◽  
Intracellular Signals ◽  
Serovar Typhimurium

HilA activates the expression of Salmonella entericaserovar Typhimurium invasion genes. To learn more about regulation ofhilA, we isolated Tn5 mutants exhibiting reduced hilA and/or invasion gene expression. In addition to expected mutations, we identified Tn5 insertions inpstS, fadD, flhD, flhC, and fliA. Analysis of the pstS mutant indicates that hilA and invasion genes are repressed by the response regulator PhoB in the absence of the Pst high-affinity inorganic phosphate uptake system. This system is required for negative control of the PhoR-PhoB two-component regulatory system, suggesting thathilA expression may be repressed by PhoR-PhoB under low extracellular inorganic phosphate conditions. FadD is required for uptake and degradation of long-chain fatty acids, and our analysis of the fadD mutant indicates that hilA is regulated by a FadD-dependent, FadR-independent mechanism. Thus, fatty acid derivatives may act as intracellular signals to regulatehilA expression. flhDC and fliAencode transcription factors required for flagellum production, motility, and chemotaxis. Complementation studies with flhCand fliA mutants indicate that FliZ, which is encoded in an operon with fliA, activates expression of hilA, linking regulation of hilA with motility. Finally, epistasis tests showed that PhoB, FadD, FliZ, SirA, and EnvZ act independently to regulate hilA expression and invasion. In summary, our screen has identified several distinct pathways that can modulate S. enterica serovar Typhimurium's ability to express hilA and invade host cells. Integration of signals from these different pathways may help restrict invasion gene expression during infection.

scholarly journals Blockage of High-Affinity Choline Transporter Increases Visceral Hypersensitivity in Rats with Chronic Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Chen Zhao ◽  
Mengjuan Lin ◽  
Yasi Pan ◽  
Baoping Yu
Keyword(s):  
Normal Saline ◽  
Specific Inhibitor ◽  
Visceral Hypersensitivity ◽  
Choline Uptake ◽  
Uptake System ◽  
Threshold Intensity ◽  
Choline Transporter ◽  
High Affinity ◽  
Acetylcholine Concentration ◽  
High Affinity Choline Transporter

Background. Visceral hypersensitivity is a common feature of irritable bowel syndrome. Cholinergic system involves in the development of visceral hypersensitivity, and high-affinity choline transporter (CHT1) is of crucial importance in choline uptake system. However, involvement of CHT1 in visceral hypersensitivity remains unknown. The research aimed to study the CHT1 expression in dorsal root ganglions (DRGs) and the role of CHT1 in visceral hypersensitivity. Methods. Repetitive water avoidance stress (WAS) was used to induce visceral hypersensitivity in rats. Colorectal distension (CRD) was determined, and the abdominal withdrawal reflex (AWR) and threshold intensity data were recorded to measure the visceral sensitivity. After intraperitoneal injection of hemicholinium-3 (HC-3), the specific inhibitor of CHT1, CRD data were also recorded. The CHT1 expression of DRGs was investigated by Western blotting, immunohistochemistry, and quantitative RT-PCR. Acetylcholine levels in the DRGs were detected by the assay kit. Results. Repetitive WAS increased the AWR score of CRD at high distension pressure and decreased the mean threshold of rats. The CHT1 expression and acetylcholine concentration of DRG were significantly increased in WAS rats. After the administration of HC-3, the AWR score in WAS group was significantly increased at higher distension pressure while the threshold intensity was significantly reduced compared to the normal saline group. Acetylcholine concentration was significantly lower than the normal saline rats. Conclusion. Our research firstly reports that CHT1 is overexpressed in noninflammatory visceral hypersensitivity, and blockage of CHT1 can enhance the visceral hypersensitivity. CHT1 may play an inhibitory role in visceral hypersensitivity.

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