scholarly journals Role of the pJM1 plasmid-encoded transport proteins FatB, C and D in ferric anguibactin uptake in the fish pathogen Vibrio anguillarum

2009 ◽  
Vol 2 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Hiroaki Naka ◽  
Claudia S. López ◽  
Jorge H. Crosa
Keyword(s):  
Vibrio Anguillarum ◽  
Transport Proteins ◽  
Fish Pathogen

Influences of temperature, salinity and starvation on the motility and chemotactic response of Vibrio anguillarum

Microbiology ◽  
2004 ◽  
Vol 150 (5) ◽  
pp. 1283-1290 ◽  
Author(s):  
Marianne H. Larsen ◽  
Nicholas Blackburn ◽  
Jens L. Larsen ◽  
John E. Olsen
Keyword(s):  
Growth Factors ◽  
Rainbow Trout ◽  
Swimming Speed ◽  
Vibrio Anguillarum ◽  
Specific Inhibitor ◽  
Chemotactic Response ◽  
Fish Pathogen ◽  
Motile Cells ◽  
Bath Challenge

The role of growth factors for the motility and chemotaxis of the fish pathogen Vibrio anguillarum was determined. Cells of V. anguillarum were chemotactic to serine in the temperature range 5–25 °C and in 0·8–2·7 % NaCl. The chemotactic response was significantly higher at 25 °C than at 5 or 15 °C. Growth in medium with 1·5 % NaCl gave a higher response than growth with 3 % NaCl; when the salinity of the chemotaxis buffer was raised, the chemotactic response was reduced. The role of starvation was also studied; V. anguillarum showed a high chemotactic response after starvation for 2 and 8 days. Motility and chemotaxis are important virulence factors for this bacterium. Not only was the ability to perform chemotactic motility maintained after starvation, but also it was shown that starvation does not interfere with the ability of the organism to cause infection in rainbow trout after a bath challenge. The swimming speed was reduced at lower temperatures. Within the range of salinity and starvation studied, the motile cells swam with the same velocity, indicating that V. anguillarum under all the examined conditions has a functional flagellum and rotates it with constant speed. Phenamil, a specific inhibitor of Na+-driven flagella, reduced the motility of both starved and non-starved cells of V. anguillarum indicating that, in both cases, a Na+ motive force drives the flagellum.

ChemInform Abstract: Structure of Anguibactin (Ia), a Unique Plasmid-Related Bacterial Siderophore from the Fish Pathogen Vibrio anguillarum

ChemInform ◽  
1989 ◽  
Vol 20 (15) ◽  
Author(s):  
M. A. F. JALAL ◽  
M. B. HOSSAIN ◽  
D. VAN DER HELM ◽  
J. SANDERS-LOEHR ◽  
L. A. ACTIS ◽  
...  
Keyword(s):  
Vibrio Anguillarum ◽  
Fish Pathogen ◽  
Abstract Structure ◽  
Unique Plasmid

scholarly journals Localisation and regulation of cholesterol transporters in the human hair follicle: mapping changes across the hair cycle

2021 ◽  
Author(s):  
Megan A. Palmer ◽  
Eleanor Smart ◽  
Iain S. Haslam
Keyword(s):  
Hair Follicle ◽  
Human Hair ◽  
Vital Role ◽  
Transport Proteins ◽  
Hair Follicles ◽  
Regulatory Control ◽  
Cholesterol Transport ◽  
Hair Cycle ◽  
Human Hair Follicle

AbstractCholesterol has long been suspected of influencing hair biology, with dysregulated homeostasis implicated in several disorders of hair growth and cycling. Cholesterol transport proteins play a vital role in the control of cellular cholesterol levels and compartmentalisation. This research aimed to determine the cellular localisation, transport capability and regulatory control of cholesterol transport proteins across the hair cycle. Immunofluorescence microscopy in human hair follicle sections revealed differential expression of ATP-binding cassette (ABC) transporters across the hair cycle. Cholesterol transporter expression (ABCA1, ABCG1, ABCA5 and SCARB1) reduced as hair follicles transitioned from growth to regression. Staining for free cholesterol (filipin) revealed prominent cholesterol striations within the basement membrane of the hair bulb. Liver X receptor agonism demonstrated active regulation of ABCA1 and ABCG1, but not ABCA5 or SCARB1 in human hair follicles and primary keratinocytes. These results demonstrate the capacity of human hair follicles for cholesterol transport and trafficking. Future studies examining the role of cholesterol transport across the hair cycle may shed light on the role of lipid homeostasis in human hair disorders.

Abstract 16440: Cu Transporter ATP7A Protects Against Fibrosis Through Limiting Endothelial to Mesenchymal Transition

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Seock-Won Youn ◽  
Sudhahar Varadarajan ◽  
Archita Das ◽  
Ronald D McKinney ◽  
Tohru Fukai ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Inflammatory Diseases ◽  
Shape Change ◽  
Atherosclerotic Lesion ◽  
Transport Proteins ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Endothelial To Mesenchymal Transition

Background: Endothelial to mesenchymal transition (EndMT) is induced by inflammation and contributes to fibrosis; however, underlying mechanism is poorly understood. Cu plays an important role in physiological processes and pathophysiologies associated with inflammatory diseases. Since excess Cu is toxic, bioavailability of Cu is tightly controlled by Cu exporter ATP7A, which obtains Cu via Cu chaperone, Atox1, and exclude Cu. We reported that Atox1 also functions as a Cu dependent transcription factor. However, role of Cu transport proteins in EndMT is entirely unknown.[[Unable to Display Character: 
]] Results: Here we show that TNFα stimulation for 24hr in HUVEC significantly decreased ATP7A protein (80%) and increased intracellular Cu and Atox1 in nucleus, which was associated with shape change forming EndMT. ATP7A depletion with shRNA in EC significantly reduced EC markers (VE-cadherin and VEGFR2) and increased mesenchymal markers (αSMA, Calponin, SM22α, Collagen I/II). ATP7A siRNA also increased intracellular Cu and nuclear Atox1. These ATP7A knockdown-induced phenotype changes were inhibited by Cu chelators BCS and TTM. Mechanistically, microarray and qPCR based screening revealed that ATP7A knockdown in EC significantly increased miR21 (2.5 fold) and miR125b (1.5 fold) which induce EndMT in a Cu-dependent manner. Of note, promoters of both miR21 and miR125b have Cu dependent transcription factor Atox1 binding sites. Consistent with this, overexpression of Atox1 increased miR21 and miR125b expression as well as promoted EndMT. In vivo, ATP7A mutant (ATP7Amut) mice with reduced Cu export function showed impaired blood flow recovery and reduced arteriogenesis while increased αSMA+ cells and fibrosis in capillary network after ischemic injury. Moreover, ATP7Amut mice crossed with ApoE-/- mice with high fat diet (HFD) induced robust fibrosis and enhanced atherosclerotic lesion vs ApoE-/-/HFD mice.[[Unable to Display Character: 
]] Conclusions: ATP7A protects against fibrosis by preventing EndMT via nuclear Atox1-mediated upregulation of miR21 and miR125b which induce EndMT, in Cu dependent manner. These findings provide the foundation for novel protective role of Cu transport proteins against EndMT- and fibrosis-mediated cardiovascular diseases.

LuxS modulates motility and secretion of extracellular protease in fish pathogen Vibrio harveyi

2021 ◽  
Author(s):  
yaqiu Zhang ◽  
Yiqing Deng ◽  
Juan Feng ◽  
Jianmei Hu ◽  
Haoxiang Chen ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Stationary Growth Phase ◽  
Extracellular Protease ◽  
Fish Pathogen ◽  
Wild Type ◽  
Stationary Growth ◽  
Qrt Pcr ◽  
Reverse Transcription Pcr ◽  
Luxs Mutant

In this study, an in-frame deletion of the luxS gene was constructed to reveal the role of LuxS in the physiology and virulence of V. harveyi. The statistical analysis showed no significant differences in the growth ability, biofilm formation, antibiotic susceptibility, virulence by intraperitoneal injection, and the ability of V. harveyi to colonize the spleen and liver of the pearl gentian grouper between the wild-type (WT) and the luxS mutant. However, the deletion of luxS decreased the secretion of extracellular protease, while increased the ability of swimming and swarming. Simultaneously, a luxS-deleted mutant showed overproduction of lateral flagella, and an intact luxS complemented the defect. Since motility is flagella dependent, 16 of V. harveyi flagella biogenesis related genes were selected for further analysis. Based on quantitative real-time reverse transcription-PCR (qRT-PCR), the expression levels of these genes, including the polar flagella genes flaB, flhA, flhF, flhB, flhF, fliS, and flrA and the lateral flagella genes flgA, flgB, fliE, fliF, lafA, lafK, and motY, were significantly up-regulated in the ΔluxS: pMMB207 (ΔluxS+) strain as compared with the V. harveyi 345: pMMB207 (WT+) and C-ΔluxS strains during the early, mid-exponential, and stationary growth phase.

scholarly journals Sorting Mechanisms for MicroRNAs into Extracellular Vesicles and Their Associated Diseases

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1044 ◽  
Author(s):  
Michael Groot ◽  
Heedoo Lee
Keyword(s):  
Extracellular Vesicles ◽  
Potential Role ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Transport Proteins ◽  
Caveolin 1 ◽  
Argonaute 2 ◽  
Disease States ◽  
Mirna Content

Extracellular vesicles (EV) are secretory membranous elements used by cells to transport proteins, lipids, mRNAs, and microRNAs (miRNAs). While their existence has been known for many years, only recently has research begun to identify their function in intercellular communication and gene regulation. Importantly, cells have the ability to selectively sort miRNA into EVs for secretion to nearby or distant targets. These mechanisms broadly include RNA-binding proteins such as hnRNPA2B1 and Argonaute-2, but also membranous proteins involved in EV biogenesis such as Caveolin-1 and Neural Sphingomyelinase 2. Moreover, certain disease states have also identified dysregulated EV-miRNA content, shedding light on the potential role of selective sorting in pathogenesis. These pathologies include chronic lung disease, immune response, neuroinflammation, diabetes mellitus, cancer, and heart disease. In this review, we will overview the mechanisms whereby cells selectively sort miRNA into EVs and also outline disease states where EV-miRNAs become dysregulated.

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